糖尿病肾病患者相比于肾小球肾炎患者，长期预后更差

研究表明NLR、PLR不仅参与CKD的炎症反应，更与疾病的进展和预后息息相关。同时，NLR、PLR也影响着糖尿病肾病、狼疮性肾炎等疾病的发生与发展。因此，本文就NLR、PLR在CKD ...

因此早期发现并干预治疗不仅可能延缓肾功能的衰竭[6]，而且还有助于减少其他系统的累及，从而使患者获益。尽管终末期肾脏病(End stage renal disease, ESRD)患者的死亡率较前 ...

研究结果表明，慢性肾病患者的adropin水平显著降低，其中终末期肾病(ESRD)患者降低幅度最大。此外，肌酐水平的升高与阿多林浓度呈显著负相关。随后针对进展至肾病的2型糖尿病 ...

... 肾小球血流动力学来促进慢性肾病的进展。Yan [36] 等人对3212例糖尿病患者的研究表明，高尿酸血症患者的糖尿病肾病患病率要高于正常尿酸患者。DKD的患病率随着尿酸的 ...

... 率和更快的肾功能丢失显著相关[1]。另一项国内的队列研究提示，大多数患者在15年内进展至终末期肾病，蛋白尿水平≥ 0.5 g/d的患者肾脏结局更差。[2]. 然而，该病发病 ...

据流行病学调查，我国CKD患病率在8.2%~13.8%，且随着人口老龄化及糖尿病、高血压等疾病的增加，其发病率和负担仍在持续攀升[2] [3]。临床上一半以上的患者仍处于非透析阶段，但 ...

结果：共纳入PD患者246例，其中DM患者50例(20.33%)，N-DM患者196例(79.67%)。与N-DM组患者相比，DM组患者年龄较大，残余肾功能较好(P < 0.05)。Kaplan-Meier分析显示，两组技术 ...

采用COX比例风险模型筛选影响预后的危险因素，其中性别以男性为参照，开始透析时年龄以<60岁组为参照，MHD的原发病因以原发性肾小球疾病为参照。为了避免漏掉重要因素，将单 ...

Dapagliflozin reduces the risk of kidney failure and heart failure in patients with chronic kidney disease. We aimed to investigate the effects of dapagliflozin on kidney, cardiovascular, and mortality outcomes according to presence or absence of type 2 diabetes and according to underlying cause of chronic kidney disease, reported as diabetic nephropathy, chronic glomerulonephritides, ischaemic or hypertensive chronic kidney disease, or chronic kidney disease of other or unknown cause. DAPA-CKD was a multicentre, double-blind, placebo-controlled, randomised trial done at 386 study sites in 21 countries, in which participants with a urinary albumin-to-creatinine ratio of 200-5000 mg/g and an estimated glomerular filtration rate (eGFR) of 25-75 mL/min per 1·73m The study took place between Feb 2, 2017, and June 12, 2020. 4304 participants were randomly assigned (2152 to dapagliflozin and 2152 to placebo) and were followed up for a median of 2·4 years (IQR 2·0-2·7). Overall, 2906 (68%) participants had a diagnosis of type 2 diabetes, of whom 396 (14%) had chronic kidney disease ascribed to causes other than diabetic nephropathy. The relative risk reduction for the primary composite outcome with dapagliflozin was consistent in participants with type 2 diabetes (hazard ratio [HR] 0·64, 95% CI 0·52-0·79) and those without diabetes (0·50, 0·35-0·72; p Dapagliflozin reduces the risks of major adverse kidney and cardiovascular events and all-cause mortality in patients with diabetic and non-diabetic chronic kidney disease. AstraZeneca.

The Dapagliflozin and Prevention of Adverse outcomes in Chronic Kidney Disease (DAPA-CKD; NCT03036150) trial was designed to assess the effect of the sodium-glucose co-transporter 2 (SGLT2) inhibitor dapagliflozin on kidney and cardiovascular events in participants with CKD with and without type 2 diabetes (T2D). This analysis reports the baseline characteristics of those recruited, comparing them with those enrolled in other trials. In DAPA-CKD, 4304 participants with a urinary albumin:creatinine ratio (UACR) ≥200 mg/g and estimated glomerular filtration rate (eGFR) between 25 and 75 mL/min/1.73 m2 were randomized to dapagliflozin 10 mg once daily or placebo. Mean eGFR was 43.1 mL/min/1.73 m2 and median UACR was 949 mg/g (108 mg/mmol). Overall, 2906 participants (68%) had a diagnosis of T2D and of these, 396 had CKD ascribed to a cause other than diabetes. The most common causes of CKD after diabetes (n = 2510) were ischaemic/hypertensive nephropathy (n = 687) and chronic glomerulonephritis (n = 695), of which immunoglobulin A nephropathy (n = 270) was the most common. A total of 4174 participants (97%) were receiving an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, 1882 (43.7%) diuretics, 229 (5.3%) mineralocorticoid receptor antagonists and 122 (2.8%) glucagon-like peptide 1 receptor agonists. In contrast to the Canagliflozin and Renal Events in Diabetes with Established Nephropathy Clinical Evaluation (CREDENCE), the DAPA-CKD trial enrolled participants with CKD due to diabetes and to causes other than diabetes. The mean eGFR of participants in the DAPA-CKD trial was 13.1 mL/min/1.73 m2 lower than in CREDENCE, similar to that in the Finerenone in Reducing Kidney Failure and Disease Progression in DKD (FIDELIO-DKD) trial and the Study Of diabetic Nephropathy with AtRasentan (SONAR). Participants with a wide range of underlying kidney diseases receiving renin-angiotensin system blocking therapy have been enrolled in the DAPA-CKD trial. The trial will examine the efficacy and safety of dapagliflozin in participants with CKD Stages 2-4 and increased albuminuria, with and without T2D.

Finerenone, a non-steroidal mineralocorticoid receptor antagonist, improved kidney and cardiovascular outcomes in patients with chronic kidney disease (CKD) and type 2 diabetes in two phase 3 outcome trials. The Finerenone, in addition to standard of care, on the progression of kidney disease in patients with Non-Diabetic Chronic Kidney Disease (FIND-CKD) study investigates the effect of finerenone in adults with CKD without diabetes. FIND-CKD (NCT05047263 and EU CT 2023-506897-11-00) is a randomized, double-blind, placebo-controlled phase 3 trial in patients with CKD of non-diabetic aetiology. Adults with a urinary albumin:creatinine ratio (UACR) ≥200-≤3500 mg/g and an estimated glomerular filtration rate (eGFR) ≥25-<90 ml/min/1.73 m2 receiving a maximum tolerated dose of a renin-angiotensin system inhibitor were randomized 1:1 to once-daily placebo or finerenone 10 or 20 mg depending on eGFR >60 or <60 ml/min/1.73 m2. The primary efficacy outcome is total eGFR slope, defined as the mean annual rate of change in eGFR from baseline to month 32. Secondary efficacy outcomes include a combined cardiorenal composite outcome comprising time to kidney failure, sustained ≥57% decrease in eGFR, hospitalization for heart failure or cardiovascular death, as well as separate kidney and cardiovascular composite outcomes. Adverse events are recorded to assess tolerability and safety. Across 24 countries, 3231 patients were screened and 1584 were randomized to study treatment. The most common causes of CKD were chronic glomerulonephritis (57.0%) and hypertensive/ischaemic nephropathy (29.0%). Immunoglobulin A nephropathy was the most common glomerulonephritis (26.3% of the total population). At baseline, mean eGFR and median UACR were 46.7 ml/min/1.73 m2 and 818.9 mg/g, respectively. Diuretics were used by 282 participants (17.8%), statins by 851 (53.7%) and calcium channel blockers by 794 (50.1%). Sodium-glucose co-transporter 2 (SGLT2) inhibitors were used in 16.9% of patients; these individuals had a similar mean eGFR (45.6 versus 46.8 ml/min/1.73 m2) and a slightly higher median UACR (871.9 versus 808.3 mg/g) compared with those not using SGLT2 inhibitors at baseline. FIND-CKD is the first phase 3 trial of finerenone in patients with CKD of non-diabetic aetiology.

Diabetes mellitus (DM) is the leading cause of chronic kidney disease (CKD) in the population. In patients with diabetes mellitus, the incidence of non-diabetic nephropathy (NDNP) has been estimated to range from 3% to 69.5%. Personal judgment is frequently employed while deciding whether or not to do a kidney biopsy (KB) on diabetic patients. NDNP alters the prognosis and course of treatment for people with DM. In our study, we examined the incidence of NDNP concurrent with the progression of diabetes mellitus, as well as the laboratory and clinical indicators that could be utilized to forecast it. A retrospective analysis of 76 diabetic patients who underwent KB was conducted. Based on the pathological diagnoses of these patients, they were categorized as DNP (diabetic nephropathy) or NDNP. The definition of HbA1c variability was determined by calculating the mean HbA1c and the average value of the HbA1c measurements, as well as the standard deviation (SD) for each participant. NDNP was detected in 50% of 76 patients. Among patients with NDNP, 36.8% had focal segmental glomerulosclerosis (FSGS), 23.6% had membranous glomerulonephritis, and 7.8% had IgA nephritis. The NDNP group exhibited significantly higher rates of female gender, absence of diabetic retinopathy, shorter time to diagnosis of diabetes mellitus, chronic kidney disease, and proteinuria, less intensive medication for diabetes mellitus, presence of hematuria and leukociduria, immunological serological marker positivity, and non-HbA1C variability. Risk factors for predicting non-diabetic nephropathy, as determined by multivariate analysis, included female gender, the absence of diabetic retinopathy, non-HbA1c variability and a positive immunological serological test. In this study, a significant number of diabetic patients with chronic kidney disease were diagnosed with NDNP. Identifying these patients allows for treatment of the specific underlying disease. Factors such as the absence of DR, non-HbA1c variability, female gender, and immunological serological test positivity can predict NDNP and guide the clinician's decision on kidney biopsy. Further prospective studies are warranted to validate the efficacy of potential predictive factors like HbA1c variability.

Renal biopsies were obtained from 164 patients with diabetes mellitus. Their histological changes were evaluated together with clinical findings and prognosis. In 36 patients, various types of glomerulonephritis were complicated: mesangial proliferative glomerulonephritis (17 patients), membranous glomerulonephritis (8), endocapillary proliferative glomerulonephritis (5), membranoproliferative glomerulonephritis (4) and minimal change nephrotic syndrome (2). Superimposed glomerulonephritis was suspected in diabetic patients with a short history of less than 5 years, persistent proteinuria, occasional hematuria and no retinopathy. They may, however, produce little effects on the long-term prognosis of diabetic patients except membranoproliferative glomerulonephritis.

Diabetic nephropathy (DMN) is usually diagnosed clinically without pathology, and the prognosis of which compared to non-diabetic renal diseases has rarely been investigated especially in ethnic Chinese population. Here we reported the outcome of patients with biopsy-proved DMN compared to those with isolated crescentic glomerulonephritis (GN) or lupus nephritis (LN). This retrospective observational study included patients with DMN (n = 55), crescentic GN (n = 48) and LN (n = 82) from an original cohort of 987 adult patients who underwent kidney biopsy. The median follow-up period was 8.3 years. The Cox regression model was used to identify factors associated with the outcome measures of end-stage renal disease (ESRD) and all-cause mortality. Patients with DMN and crescentic GN exhibited higher rates of ESRD than LN group (65.5%, 66.7% versus 32.9%, p < 0.001). After accounting for the competing risk of death, DMN versus LN, along with lower hemoglobin values, lower estimated glomerular filtration rates and severe proteinuria were independent predictors for ESRD. Patients with DMN and crescentic GN displayed higher mortality rates than LN patients following the development of ESRD (38.2% and 29.2% versus 9.8%, p < 0.001). Multivariate analysis showed old age (≧65 years) and lower serum albumin levels were independently associated with overall death. Patients with biopsy-proved DMN, but not crescentic GN, showed a greater risk of ESRD than LN counterparts. Given the grave renal prognosis of DMN, more meticulous follow-up is critical to ensure that best therapeutic strategies are used to avert progression to ESRD.

Patients with both diabetes mellitus (DM) and kidney disease could have diabetic nephropathy (DN) or non-diabetic renal disease (NDRD). IgA nephropathy (IgAN) and membranous nephropathy (MN) are the major types of NDRD. No ideal noninvasive diagnostic model exists for differentiating them. Our study sought to construct diagnostic models for these diseases and to identify noninvasive biomarkers that can reflect the severity and prognosis of DN. The diagnostic models were constructed using logistic regression analysis and were validated in an external cohort by receiver operating characteristic curve analysis method. The associations between these microRNAs and disease severity and prognosis were explored using Pearson correlation analysis, Cox regression, Kaplan-Meier survival curves, and log-rank tests. Our diagnostic models showed that miR-95-3p, miR-185-5p, miR-1246, and miR-631 could serve as simple and noninvasive tools to distinguish patients with DM, DN, DM with IgAN, and DM with MN. The areas under the curve of the diagnostic models for the four diseases were 0.995, 0.863, 0.859, and 0.792, respectively. The miR-95-3p level was positively correlated with the estimated glomerular filtration rate (p < 0.001) but was negatively correlated with serum creatinine (p < 0.01), classes of glomerular lesions (p < 0.05), and scores of interstitial and vascular lesions (p < 0.05). However, the miR-631 level was positively correlated with proteinuria (p < 0.001). A low miR-95-3p level and a high miR-631 level increased the risk of progression to end-stage renal disease (p = 0.002, p = 0.011). These four microRNAs could be noninvasive tools for distinguishing patients with DN and NDRD. The levels of miR-95-3p and miR-631 could reflect the severity and prognosis of DN.

Globally, Type 2 diabetes mellitus (T2DM) is one of the most prevalent chronic diseases, which poses a great potential threat to the human body. Diabetic nephropathy (DN), a very common complication in T2DM, is also the main trigger for end-stage renal disease. A thorough understanding of the pathogenesis is the key as well as the breakthrough for future diagnosis and treatment of DN. This investigation aims to provide more in-depth and accurate guidance for future follow-up research by analyzing the role of vascular endothelial growth factor (VEGF) in the kidney tissue of DN patients. Seventy-nine patients with suspected DN who underwent renal needle biopsy in our hospital from January 2015 to June 2019 were selected as the research participants. After the biopsy, 36 cases were confirmed as DN, and the other 43 were T2DM with primary glomerulonephritis. Determination of VEGF mRNA and protein expression in renal tissue employed PCR and Western blot, and the connection between VEGF mRNA level and clinical pathology (such as renal function, inflammatory factors and pathological manifestations) was discussed. The disease recurrence in DN patients was recorded through the 3-year prognostic followed up, and the related influencing factors were analyzed. In kidney tissue, VEGF mRNA level and protein expression were notably higher in DN patients than in diabetic patients (P<0.05). Pearson correlation coefficient analysis identified that VEGF mRNA and protein had a positive connection with blood urea nitrogen (BUN), serum creatinine (Scr), 24-hour urine total protein (24hUTP) and C-reactive protein (CRP) (P<0.05). Among the various clinicopathological features of DN patients, age, BMI, sex, family history, smoking, drinking, exercise habits, clinical presentations and pathological changes had no significant relationship with VEGF level (P>0.05), but the course of the disease, fasting blood glucose (FBG), glycosylated hemoglobin (HBALC) and pathological stages of nephropathy had a close connection with VEGF level (P<0.05). Prognostic follow-up revealed that VEGF mRNA was noticeably higher in patients with recurrence than in those without (P<0.05). When VEGF mRNA >5.20 in kidney tissue, the sensitivity and specificity for predicting the 3-year recurrence were 85.71% and 84.00% respectively (P<0.05). Finally, Logistic regression analysis identified the independence of FBG, HBALC and VEGF levels as the influencing factors for the prognostic recurrence of DN (P<0.05).VEGF expression in kidney tissue of DN patients is closely linked to renal function and increases as the disease progresses, which is an independent risk factor associated with the prognostic recurrence of DN, with great potential significance for future DN diagnosis and treatment.

Diabetic renal lesions can only be diagnosed by kidney biopsy. These biopsies have a high prevalence of non-diabetic lesions. The aims of the study were to determine the predictability of non-diabetic nephropathy (NDN) in diabetics and study differences in survival and renal prognosis. In addition, we evaluated histological lesions and the effect of proteinuria on survival and renal prognosis in patients with diabetic nephropathy (DN). A descriptive, retrospective study of kidney biopsies of diabetics between 1990 and 2013 in our centre. 110 patients were included in the study: 87 men (79%), mean age 62 years (50-74), mean serum creatinine 2.6mg/dl (0.9-4.3) and proteinuria 3.5g/24hours (0.5-6.5). 61.8% showed NDN, 34.5% showed DN and 3,6% showed DN+NDN. The most common NDN was IgA nephropathy (13,2%). In the multivariate analysis, creatinine (OR: 1.48, 1.011-2.172, p=0.044), proteinuria/24hours (OR: 0.813, 0.679-0.974, p=0.025), duration of diabetes (OR: 0.992, 0.987-0.998, p=0.004), age (OR: 1.068, 95% CI: 1.010-1.129, p=0.022), and diabetic retinopathy (OR: 0.23, 0.066-0.808, p=0.022) were independently associated with NDN. We did not find any differences in survival or renal prognosis. Concerning patients with DN, increased nodular mesangial expansion (p=0.02) and worse renal prognosis (p=0.004) were observed in nephrotic proteinuria as compared to non-nephrotic proteinuria. We did not find differences in patient survival. The most common cause of NDN was IgA nephropathy. Higher creatinine levels, shorter duration of diabetes, absence of diabetic retinopathy, lower proteinuria, and older age were risk factors for NDN. Patients with DN and nephrotic-range proteinuria had worse renal prognosis.

No abstract

This study aimed to analyze the clinical and prognostic differences in immune-mediated membranous nephropathy (MN) concurrent with other forms of glomerulonephritis. A retrospective cohort study at Jinling Hospital from 2015 to 2023 included patients with PLA2R antibody levels ≥ 14RU/mL who underwent renal biopsy. Those with immune-mediated MN and concurrent glomerulonephritides were compared to a control group with isolated MN diagnosed in 2015. Concurrent glomerulonephritis was found in 5.53% of the MN cohort, including 61 patients with IgA nephropathy (IgAN-MN), 49 with diabetic nephropathy (DN-MN), and 131 with focal segmental glomerulosclerosis (FSGS-MN). Compared to the control group, those with IgAN-MN showed increased severity of glomerular injury yet had a reduced degree of interstitial fibrosis. The DN-MN group exhibited intensified glomerular damage; however, no significant difference was observed in the extent of tubulointerstitial damage. Additionally, the FSGS-MN group displayed more severe damage to both glomerular and tubulointerstitial structures. Both the DN-MN group and the FSGS-MN group exhibited a significantly lower complete remission rate compared to the control group. The renal endpoint event rates were 29.51% for IgAN-MN, 46.94% for DN-MN, and 33.59% for FSGS-MN, which were all significantly higher than the 18.99% rate in the control group. Patients with MN who test positive for serum Anti-PLA2R antibodies may present with other forms of glomerulonephritis. The prognostic outcomes of MN in the presence of concurrent IgAN, DN, or FSGS are notably poorer than those of isolated MN. Renal biopsy is valuable for definitive diagnosis and prognostic evaluation.

Prognosis in chronic kidney disease (CKD) for adverse outcomes differs substantially based on the etiology of CKD. We examined whether the biomarker profile differed based on CKD etiology and whether they were associated with mortality. Prospective observational study of 1,157 patients, 663 with diabetic kidney disease (DKD), 273 with glomerulonephritis (GN), and 221 with cystic/interstitial disease (polycystic kidney disease, pyelonephritis or chronic tubulointerstitial nephritis [PCK/TIN]) were identified in the Canadian Study of Prediction of Dialysis, Death and Interim Cardiovascular events over Time cohort. The outcome of interest was mortality before commencing dialysis. The biomarker profile consisted of N-terminal pro-brain natriuretic peptide (NT-proBNP), troponin I (TnI), asymmetric dimethylarginine (ADMA), interleukin (IL)-6, high sensitivity C-reactive protein, fibroblast growth factor-23 (FGF23), transforming growth factor-beta, 25-hydroxylvitamin D, and cystatin C (CysC). The mean estimated glomerular filtration rate was 27 mL/min/1.73 m2 and median follow-up time was 44 months. Mortality before dialysis commencement was the greatest in DKD (20%), followed by PCK/TIN (13%), and was least in those GN (8%). The majority of deaths were cardiovascular in nature, 17, 9, and 5.5% for DKD, PCK/TIN, GN, respectively. Those with DKD had higher hazard for mortality, unadjusted (hazard ratio [HR] 2.7, 95% CI 1.7-4.3) and adjusted (HR 1.7, 95% CI 1.1-2.8). The biomarker profiles associated with mortality differed significantly by CKD etiology as follows: DKD was associated with CysC (HR 1.3, 95% CI 1.0-1.6), ADMA (HR 1.3, 95% CI 1.1-1.6), and NT-proBNP (HR 1.7, 95% CI 1.4-2.1), GN was associated with FGF23 (HR 1.8, 95% CI 1.1-2.8), TnI (HR 3.6, 95% CI 1.3-9.5), and transforming growth factor-beta (HR 0.6, 95% CI 0.4-0.9) and PCK/TIN was associated with ADMA (HR 1.5, 95% CI 1.3-1.8) and IL-6 (HR 2.1, 95% CI 1.5-3.1). Biomarkers profiles differ according to the etiology of CKD and are associated with mortality.

End-stage kidney disease (ESKD) is now a worldwide pandemic. In concert with this, ESKD in Libya has also increased exponentially in recent decades. This review aims to define the magnitude of and risks for this ESKD epidemic among Libyans as there is a dearth of published data on this subject. A systematic review was conducted by searching PubMed, EMBASE and Google scholar databases to identify all relevant papers published in English from 2003 to 2012, using the following keywords: end stage, terminal, chronic, renal, kidney, risk factors, Arab, North Africa and Libya. In 2003, the reported incidence of ESKD and prevalence of dialysis-treated ESKD in Libya were the same at 200 per million population (pmp). In 2007, the prevalence of dialysis-treated ESKD was 350 pmp, but the true incidence of ESKD was not available. The most recent published WHO data in 2012 showed the incidence of dialysis-treated ESKD had risen to 282 pmp and the prevalence of dialysis-treated ESKD had reached 624 pmp. The leading causes of ESKD were diabetic kidney disease (26.5 %), chronic glomerulonephritis (21.1 %), hypertensive nephropathy (14.6 %) and congenital/hereditary disease (12.3 %). The total number of dialysis centers was 40 with 61 nephrologists. Nephrologist/internist to patient ratio was 1:40, and nurse to patient ratio was 1:3.7. Only 135 living-related kidney transplants had been performed between 2004 and 2007. There were no published data on most macroeconomic and renal service factors. ESKD is a major public health problem in Libya with diabetic kidney disease and chronic glomerulonephritis being the leading causes. The most frequent co-morbidities were hypertension, obesity and the metabolic syndrome. In addition to provision of RRT, preventive strategies are also urgently needed for a holistic integrated renal care system.

The kidney failure risk equation is a clinical tool commonly used for prediction of progression from CKD to kidney failure. The kidney failure risk equation's accuracy in advanced CKD and whether this varies by CKD etiology remains unknown. This study examined the kidney failure risk equation's discrimination and calibration at 2 and 5 years among a large tertiary care population with advanced CKD from heterogeneous etiologies. This retrospective cohort study included 1293 patients with advanced CKD (median eGFR 15 ml/min per 1.73 m The kidney failure risk equation provided adequate to excellent discrimination in identifying patients with CKD likely to progress to kidney failure at the 2- and 5-year time points both overall (2-year area under the curve, 0.83; 95% confidence interval, 0.81 to 0.85; 5-year area under the curve, 0.81; 95% confidence interval, 0.77 to 0.84) and across CKD etiologies. The kidney failure risk equation displayed adequate calibration at the 2- and 5-year time points both overall and across CKD etiologies (Hosmer-Lemeshow The kidney failure risk equation provides adequate discrimination and calibration in advanced CKD and across CKD etiologies.

Despite increasing prevalence of end-stage renal disease (ESRD), little attention has been directed to how occupational exposures may contribute to risk. Our objective was to investigate the relationship between metalworking fluids (MWF) and ESRD in a cohort of 36 703 male autoworkers. We accounted for competing risk of death, using the subdistribution hazard approach to estimate subhazard ratios (sHRs) and 95% CIs in models with cubic splines for cumulative exposure to MWF (straight, soluble or synthetic). Based on 501 ESRD cases and 13 434 deaths, we did not observe an association between MWF and ESRD overall. We observed modest associations between MWF and ESRD classification of glomerulonephritis and diabetic nephropathy. For glomerulonephritis, the 60th percentile of straight MWF was associated with an 18% increased subhazard (sHR=1.18, 95% CI: 0.99 to 1.41). For diabetic nephropathy, the subhazard increased 28% at the 60th percentile of soluble MWF (sHR=1.28, 95% CI: 1.00 to 1.64). Differences by race suggest that black males may have higher disease rates following MWF exposure. Exposure to straight and soluble MWF may be related to ESRD classification, though this relationship should be further examined.

This study tested the hypothesis that progression of chronic kidney disease (CKD) is less aggressive in patients whose primary cause of CKD was nephrectomy, compared with non-surgical causes. A sample of 5983 patients from five specialist nephrology practices was ascertained from the Queensland CKD Registry. Rates of kidney failure/death were compared on primary aetiology of CKD using multivariable Cox proportional hazards models. CKD progression was compared using multivariable linear and logistic regression analyses. Of 235 patients with an acquired single kidney as their primary cause of CKD, 24 (10%) and 38 (17%) developed kidney failure or died at median [IQR] follow-up times of 12.9 [2.5-31.0] and 33.6 [18.0-57.9] months after recruitment. Among patients with an eGFR < 45 mL/min per 1.73m Patients who developed CKD after nephrectomy had similar rates of adverse events to most other causes of CKD, except for diabetic nephropathy which was consistently associated with worse outcomes. While CKD after nephrectomy is not the most aggressive cause of kidney disease, it is by no means benign, and is associated with a tangible risk of kidney failure and death, which is comparable to other major causes of CKD.

In non-dialysis chronic kidney disease (CKD), absolute proteinuria (Uprot) depends on the extent of kidney damage and residual glomerular filtration rate (GFR). We therefore evaluated, as compared with Uprot, the strength of association of proteinuria indexed to estimated GFR (eGFR) with end-stage renal disease (ESRD) risk. In a multi-cohort prospective study in 3957 CKD patients of Stages G3-G5 referred to nephrology clinics, we tested two multivariable Cox models for ESRD risk, with either Uprot (g/24 h) or filtration-adjusted proteinuria (F-Uprot) calculated as Uprot/eGFR ×100. Mean ± SD age was 67 ± 14 years, males 60%, diabetics 29%, cardiovascular disease (CVD) 34%, eGFR 32 ± 13 mL/min/1.73 m2, median (interquartile range) Uprot 0.41 (0.12-1.29) g/24 h and F-Uprot 1.41 (0.36-4.93) g/24 h per 100 mL/min/1.73 m2 eGFR. Over a median follow-up of 44 months, 862 patients reached ESRD. At competing risk analysis, ESRD risk progressively increased when F-Uprot was 1.0-4.9 and ≥5.0 versus <1.0 g/24 h per 100 mL/min/1.73 m2 eGFR in Stages G3a-G4 (P < 0.001) and Stage G5 (P = 0.002). Multivariable Cox analysis showed that Uprot predicts ESRD in Stages G3a-G4 while in G5 the effect was not significant; conversely, F-Uprot significantly predicted ESRD at all stages. The F-Uprot model allowed a significantly better prediction versus the Uprot model according to Akaike information criterion. Net reclassification improvement was 12.2% (95% confidence interval 4.2-21.1), with higher reclassification in elderly, diabetes and CVD, as well as in diabetic nephropathy and glomerulonephritis, and in CKD Stages G4 and G5. In patients referred to nephrology clinics, F-Uprot predicts ESRD at all stages of overt CKD and improves, as compared with Uprot, reclassification of patients for renal risk, especially in more advanced and complicated disease.

Inferences about late risk of end-stage renal disease (ESRD) in live kidney donors have been extrapolated from studies averaging <10 years of follow-up. Because early (<10 years) and late (≥10 years) postdonation ESRD may differ by causal mechanism, it is possible that extrapolations are misleading. To better understand postdonation ESRD, we studied patterns of common etiologies including diabetes, hypertension and glomerulonephritis (GN; as reported by providers) using donor registry data linked to ESRD registry data. Overall, 125 427 donors were observed for a median of 11.0 years (interquartile range 5.3-15.7 years; maximum 25 years). The cumulative incidence of ESRD increased from 10 events per 10 000 at 10 years after donation to 85 events per 10 000 at 25 years after donation (late vs. early ESRD, adjusted for age, race and sex: incidence rate ratio [IRR]

This study intends to investigate the causes and risk factors for withdrawal from peritoneal dialysis (PD) in patients with end stage renal disease (ESRD). Two hundred ninety-three patients admitted to the peritoneal dialysis center in nephrology department for PD treatment were divided into 175 cases in group A (continuous treatment group) and 118 cases in group B (withdrawal group). The proportion of patients in group B whose primary disease was glomerulonephritis was significantly lower than that in group A (p <0.05), whereas the proportion of patients with diabetic nephropathy was significantly higher in group B than in group A (p <0.05). Group A received better emotional support and care services from family members than group B. Family care was mostly severely impaired in patients who died and were lost to follow-up. Diabetes mellitus, level of knowledge regarding PD, depression, and family care are risk factors for withdrawal from PD.

Patients with lupus nephritis could progress to end-stage renal disease (10-22%); hence, kidney transplants should be considered as the treatment of choice for these patients. To evaluate the clinical outcomes after kidney transplants in patients with chronic kidney diseases secondary to lupus nephritis, polycystic kidney disease and diabetes nephropathy at Pablo Tobon Uribe Hospital. A descriptive and retrospective study performed at one kidney transplant center between 2005 and 2013. A total of 136 patients, 27 with lupus nephritis (19.9%), 31 with polycystic kidney disease (22.8%) and 78 with diabetes nephropathy (57.4%), were included in the study. The graft survivals after one, three and five years were 96.3%, 82.5% and 82.5% for lupus nephritis; 90%, 86% and 76.5% for polycystic kidney disease and 91.7%, 80.3% and 67.9% for diabetes nephropathy, respectively, with no significant differences (p= 0.488); the rate of lupus nephritis recurrence was 0.94%/person-year. The etiology of lupus vs diabetes vs polycystic disease was not a risk factor for a decreased time of graft survival (Hazard ratio: 1.43; 95% CI: 0.52-3.93). Kidney transplant patients with end stage renal disease secondary to lupus nephritis has similar graft and patient survival success rates to patients with other kidney diseases. The complication rate and risk of recurrence for lupus nephritis are low. Kidney transplants should be considered as the treatment of choice for patients with end stage renal disease secondary to lupus nephritis. Pacientes con nefritis lúpica pueden progresar a enfermedad renal crónica terminal (10-22%); en estos pacientes el trasplante renal debe ser considerado como la terapia de elección. Objetivo: Evaluar los desenlaces clínicos de un grupo de pacientes con enfermedad renal crónica terminal por nefropatía lúpica, enfermedad renal poliquística y nefropatía diabética que fueron sometidos a trasplante renal en el Hospital Pablo Tobón Uribe. Estudio retrospectivo, descriptivo, realizado en un solo centro de trasplante renal, durante el período 2005-2013. Se evaluaron 136 pacientes: 27 con nefritis lúpica (19.9%), 31 con enfermedad renal poliquística (22.8%) y 78 con nefropatía diabética (57.4%). La supervivencia del injerto a uno, tres y cinco años fue de de 96.3%, 82.5% y 82.5% en nefropatía lúpica, 90%, 86% y 76.5% en enfermedad renal poliquística y 91.7%, 80.3% y 67.9% en nefropatía diabética respectivamente, sin diferencias estadísticas significativas (Long Rank test= 0.488). La tasa de recurrencia de nefritis lúpica posterior al trasplante renal fue de 0.94%/persona-año. Tener lupus vs diabetes o enfermedad renal poliquística no fue un factor de riesgo para disminución del tiempo de supervivencia del injerto (Hazard ratio= 1.43; 95% IC= 0.52-3.93). Los pacientes enfermedad renal crónica terminal secundaria a nefritis lúpica, que son llevados a trasplante renal tienen tasas de éxito similar en cuanto a supervivencia del injerto y del paciente, al compararlos con otras enfermedades renales. La tasa de complicaciones y el riesgo de recurrencia de la nefropatía lúpica son bajos. El trasplante renal debe ser considerado como la terapia de elección para los pacientes con enfermedad renal crónica estadio terminal secundaria a nefritis lúpica.

Numerous kidney diseases progress to end-stage kidney disease (ESKD); however, a limited number of cohort studies have evaluated the underlying kidney diseases through kidney biopsy (KB). We retrospectively evaluated all patients who initiated dialysis at Toranomon Hospital, Japan, from 1985 to 2019, and whose underlying kidney disease had been diagnosed by KB. The data on histopathological diagnosis and various clinical characteristics were collected and analyzed for 357 patients. The most prevalent underlying diseases, which constituted the primary endpoint of this study, were diabetic nephropathy (DN; n = 100, 28.0%), IgA nephropathy (IgAN; n = 99, 27.7%), and focal segmental glomerulosclerosis (n = 34, 9.5%). Benign nephrosclerosis (BNS; n = 1, 0.3%), that is, arteriosclerosis/arteriolosclerosis without distinct glomerulopathy, was rare. As the secondary endpoint, Cox regression analysis revealed that lower eGFR (p < 0.0001), higher proteinuria (p < 0.0001), older age (p = 0.005) and presence of DN (p = 0.008) were significant independent risk factors for early dialysis initiation. In the subgroup analysis, when comparing DN and IgAN, significantly earlier dialysis initiation was observed in DN than in IgAN by log-rank analysis (p < 0.0001), as well as after adjustment for baseline clinical characteristics using propensity score matching (n = 45 each) (p = 0.023). We identified a list of kidney diseases that were at risk for ESKD at the time of KB through a long-term follow-up. DN and IgAN are the two primary causes of ESKD, whereas BNS is an infrequent direct cause of ESKD in patients requiring kidney biopsy.

The Kidney Failure Risk Equation (KFRE) predicts the 2- and 5-year risk of end-stage renal disease (ESRD) in patients with chronic kidney disease (CKD) stages 3a-5. Its predictive performance in advanced CKD and in specific disease aetiologies requires further exploration. This study validates the 4- and 8-variable KFREs in an advanced CKD population in the United Kingdom by evaluating discrimination, calibration and clinical utility. Patients enrolled in the Salford Kidney Study who were referred to the Advanced Kidney Care Service (AKCS) clinic at Salford Royal NHS Foundation Trust between 2011 and 2018 were included. The 4- and 8-variable KFREs were calculated on the first AKCS visit and the observed events of ESRD (dialysis or pre-emptive transplantation) within 2- and 5-years were the primary outcome. The area under the receiver operator characteristic curve (AUC) and calibration plots were used to evaluate discrimination and calibration respectively in the whole cohort and in specific disease aetiologies: diabetic nephropathy, hypertensive nephropathy, glomerulonephritis, autosomal dominant polycystic kidney disease (ADPKD) and other diseases. Clinical utility was assessed with decision curve analyses, comparing the net benefit of using the KFREs against estimated glomerular filtration rate (eGFR) cut-offs of < 20 ml/min/1.73m A total of 743 patients comprised the 2-year analysis and 613 patients were in the 5-year analysis. Discrimination was good in the whole cohort: the 4-variable KFRE had an AUC of 0.796 (95% confidence interval [CI] 0.762-0.831) for predicting ESRD at 2-years and 0.773 (95% CI 0.736-0.810) at 5-years, and there was good-to-excellent discrimination across disease aetiologies. Calibration plots revealed underestimation of risk at 2-years and overestimation of risk at 5-years, especially in high-risk patients. There was, however, underestimation of risk in patients with ADPKD for all KFRE calculations. The predictive accuracy was similar between the 4- and 8-variable KFREs. Finally, compared to eGFR-based thresholds, the KFRE was the optimal tool to guide further care based on decision curve analyses. The 4- and 8-variable KFREs demonstrate adequate discrimination and calibration for predicting ESRD in an advanced CKD population and, importantly, can provide better clinical utility than using an eGFR-based strategy to inform decision-making.

Chronic kidney disease (CKD) is a global health problem with increasing prevalence. Several sex-specific differences have been reported for disease progression and mortality. Selection and survival bias might have influenced the results of previous cohort studies. The objective of this study was to investigate sex-specific differences of CKD progression and mortality among patients with CKD not receiving maintenance dialysis. Observational cohort study. Adult patients with incident CKD glomerular filtration rate categories 3b to 5 (G3b-G5) identified between 2010 and 2018 within the nationwide Swedish Renal Registry-CKD (SRR-CKD). Sex. Time to CKD progression (defined as a change of at least 1 CKD stage or initiation of kidney replacement therapy [KRT]) or death. Repeated assessments of estimated glomerular filtration rate (eGFR). CKD progression and mortality before KRT were assessed by the cumulative incidence function methods and Fine and Gray models, with death handled as a competing event. Sex differences in eGFR slope were estimated using mixed effects linear regression models. 7,388 patients with incident CKD G3b, 18,282 with incident CKD G4, and 9,410 with incident CKD G5 were identified. Overall, 19.6 (95% CI, 19.2-20.0) patients per 100 patient-years progressed, and 10.1 (95% CI, 9.9-10.3) patients per 100 person-years died. Women had a lower risk of CKD progression (subhazard ratio [SHR], 0.88 [95% CI, 0.85-0.92]), and a lower all-cause (SHR, 0.90 [95% CI, 0.85-0.94]) and cardiovascular (SHR, 0.83 [95% CI, 0.76-0.90]) mortality risk. Risk factors related to a steeper decline in eGFR included age, sex, albuminuria, and type of primary kidney disease. Incomplete data for outpatient visits and laboratory measurements and regional differences in reporting. Compared to women, men had a higher rate of all-cause and cardiovascular mortality, an increased risk of CKD progression, and a steeper decline in eGFR.

Diabetes and chronic kidney diseases are associated with a large health burden in the USA and globally. To estimate age-standardized mortality rates by county from diabetes mellitus and chronic kidney disease. Validated small area estimation models were applied to de-identified death records from the National Center for Health Statistics (NCHS) and population counts from the census bureau, NCHS, and the Human Mortality Database to estimate county-level mortality rates from 1980 to 2014 from diabetes mellitus and chronic kidney disease (CKD). County of residence. Age-standardized mortality rates by county, year, sex, and cause. Between 1980 and 2014, 2,067,805 deaths due to diabetes were recorded in the USA. The mortality rate due to diabetes increased by 33.6% (95% UI: 26.5%-41.3%) between 1980 and 2000 and then declined by 26.4% (95% UI: 22.8%-30.0%) between 2000 and 2014. Counties with very high mortality rates were found along the southern half of the Mississippi river and in parts of South and North Dakota, while very low rates were observed in central Colorado, and select counties in the Midwest, California, and southern Florida. A total of 1,659,045 deaths due to CKD were recorded between 1980 and 2014 (477,332 due to diabetes mellitus, 1,056,150 due to hypertension, 122,795 due to glomerulonephritis, and 2,768 due to other causes). CKD mortality varied among counties with very low mortality rates observed in central Colorado as well as some counties in southern Florida, California, and Great Plains states. High mortality rates from CKD were observed in counties throughout much of the Deep South, and a cluster of counties with particularly high rates was observed around the Mississippi river. This study found large inequalities in diabetes and CKD mortality among US counties. The findings provide insights into the root causes of this variation and call for improvements in risk factors, access to medical care, and quality of medical care.

Diabetic kidney disease (DKD) is the primary cause of end‐stage renal disease globally, yet reliable biomarkers for its diagnosis and progression assessment are lacking. This study employed artificial intelligence techniques, including weighted gene co‐expression network analysis (WGCNA) and machine learning, to identify crucial genes associated with DKD. Validation was conducted using online databases such as Nephroseq and KIT, alongside biological samples from human serum, urine, peripheral blood mononuclear cell (PBMC) mRNA, kidney tissues, DKD rat models, and high glucose‐treated HK‐2 cells. Statistical analyses evaluated the correlations. The study revealed that C‐X‐C motif chemokine ligand 3 (CXCL3) was markedly upregulated in the serum and urine of DKD patients compared to healthy controls and those with type 2 diabetes mellitus, primary glomerulonephritis (e.g., IgA nephropathy, membranous nephropathy, minimal change disease). Immunohistochemistry showed significantly higher CXCL3 in both the glomeruli and tubulointerstitium of DKD patient kidneys than in those from controls. Elevated CXCL3 mRNA levels were also noted in PBMCs from DKD patients, STZ‐induced DKD rat kidneys, and high glucose‐treated HK‐2 cells. Furthermore, urinary CXCL3 protein levels positively correlated with the pathological grade, serum blood urea nitrogen (BUN), serum creatinine, and HbA1c percentage, while inversely correlating with estimated glomerular filtration rate (eGFR) in DKD patients. Mechanically, high glucose stimulation significantly upregulates the expression of inflammatory factors (including IL‐6 and IL‐1β) and fibrosis markers (α‐SMA and CTGF) in HK‐2 cells overexpressing CXCL3. Conversely, CXCL3 knockout in HK‐2 cells led to substantial downregulation of these inflammatory and fibrotic markers in the same high glucose conditions. Elevated CXCL3 levels in the serum, urine, and kidney tissues, alongside increased mRNA in PBMCs, suggest its potential as a biomarker for diagnosing and monitoring DKD. Correlations of urinary CXCL3 with disease severity indicators further support its diagnostic and prognostic utility. Mechanically, CXCL3 promotes inflammation and fibrosis in DKD.

Primary kidney disease is suggested to affect renal prognosis of CKD patients; however, whether nephrology care modifies this association is unknown. We studied patients with CKD stage I-IV treated in a renal clinic and with established diagnosis of CKD cause to evaluate whether the risk of renal event (composite of end-stage renal disease and eGFR decline ≥40%) linked to the specific diagnosis is modified by the achievement or maintenance in the first year of nephrology care of therapeutic goals for hypertension (BP ≤130/80 mmHg in patients with proteinuria ≥150 mg/24h and/or diabetes and ≤140/90 in those with proteinuria <150 mg/24h and without diabetes) anemia (hemoglobin, Hb ≥11 g/dL), and proteinuria (≤0.5 g/24h). Survival analysis started after first year of nephrology care. We studied 729 patients (age 64±15 y; males 59.1%; diabetes 34.7%; cardiovascular disease (CVD) 44.9%; hypertensive nephropathy, HTN 53.8%; glomerulonephritis, GN 17.3%; diabetic nephropathy, DN 15.9%; tubule-interstitial nephropathy, TIN 9.5%; polycystic kidney disease, PKD 3.6%). During first year of Nephrology care, therapy was overall intensified in most patients and prevalence of main therapeutic goals generally improved. During subsequent follow up (median 3.3 years, IQR 1.9-5.1), 163 renal events occurred. Cox analysis disclosed a higher risk for PKD (Hazard Ratio 5.46, 95% Confidence Intervals 2.28–10.6) and DN (1.28,2.99–3.05), versus HTN (reference), independently of age, gender, CVD, BMI, eGFR or CKD stage, use of RAS inhibitors and achievement or maintenance in the first year of nephrology care of each of the three main therapeutic goals. No interaction was found on the risk of CKD progression between diagnostic categories and month-12 eGFR (P=0.737), as with control of BP (P=0.374), Hb (P=0.248) or proteinuria (P=0.590). Therefore, in CKD patients under nephrology care, diagnosis of kidney disease should be considered in conjunction with the main risk factors to refine renal risk stratification.

Background The relevance of the cause of kidney disease to prognosis among patients with chronic kidney disease is uncertain. Study Design Observational study. Settings & Participants 6,245 nondialysis participants in the Study of Heart and Renal Protection (SHARP). Predictor Baseline cause of kidney disease was categorized into 4 groups: cystic kidney disease, diabetic nephropathy, glomerulonephritis, and other recorded diagnoses. Outcomes End-stage renal disease (ESRD; dialysis or transplantation) and death. Results During an average 4.7 years' follow-up, 2,080 participants progressed to ESRD, including 454 with cystic kidney disease (23% per year), 378 with glomerulonephritis (10% per year), 309 with diabetic nephropathy (12% per year), and 939 with other recorded diagnoses (8% per year). By comparison with patients with cystic kidney disease, other disease groups had substantially lower adjusted risks of ESRD (relative risks of 0.28 [95% CI, 0.24-0.32], 0.40 [95% CI, 0.34-0.47], and 0.29 [95% CI, 0.25-0.32] for glomerulonephritis, diabetic nephropathy, and other recorded diagnoses, respectively). Albuminuria and baseline estimated glomerular filtration rate were associated more weakly with risk of ESRD in patients with cystic kidney disease than the 3 other diagnostic categories (P for interaction, <0.001 and 0.01, respectively). Death before ESRD was uncommon in patients with cystic kidney disease, but was a major competing risk for participants with diabetic nephropathy, whose adjusted risk of death was 2-fold higher than that of the cystic kidney disease group (relative risk, 2.35 [95% CI, 1.73-3.18]). Limitations Exclusion of patients with prior myocardial infarction or coronary revascularization. Conclusions The cause of kidney disease has substantial prognostic implications. Other things being equal, patients with cystic kidney disease are at much higher risk of ESRD (and much lower risk of death before ESRD) than other patients. Patients with diabetic nephropathy are at particularly high risk of death prior to reaching ESRD.

Abstract Introduction: The Kidney Disease: Improving Global Outcomes guidelines recognize the importance of causes of chronic kidney disease (CKD), glomerular filtration rate, and albuminuria as predictors of kidney outcome and prognosis. However, compared with biopsy-proven causes, there has been limited research regarding the relationship between clinically diagnosed causes of CKD and patient prognosis. Methods: We examined 3,119 patients with non-dialysis-dependent CKD who participated in the Fukuoka Kidney disease Registry Study, a multicenter prospective cohort study. Patients were divided into six groups: IgA nephropathy, chronic glomerulonephritis (non-biopsy-proven), diabetic nephropathy, hypertensive nephrosclerosis, chronic interstitial nephritis, and polycystic kidney disease. The primary outcomes included a composite kidney outcome, defined as a 1.5-fold increase in serum creatinine and/or the development of end-stage kidney disease, and all-cause mortality. The risks of these outcomes were estimated using a Fine-Gray proportional subdistribution hazards model. Patients with IgA nephropathy, the most prevalent primary glomerulonephritis, served as the reference group. Results: During the median follow-up period of 5 years, 1,221 patients developed the composite kidney outcome, and 346 patients died. Compared with IgA nephropathy, the multivariable-adjusted subdistribution hazard ratios (sHRs) for the composite kidney outcome were significantly higher in diabetic nephropathy (sHR 1.45) and polycystic kidney disease (sHR 2.07) groups, whereas the chronic interstitial nephritis group had a significantly lower risk (sHR 0.71). The risk of all-cause mortality was significantly higher in the hypertensive nephrosclerosis group (sHR 1.90). Conclusion: The causes of CKD were associated with risks of the composite kidney outcome and all-cause mortality, highlighting their clinical relevance in predicting prognosis. These findings suggest that different causes of CKD have distinct impacts on patient outcomes, emphasizing the importance of tailoring management strategies according to the underlying causes.

Background Patients with end-stage kidney disease (ESKD) face higher risks of life-threatening events including cardiovascular disease. Various risk factors are identified as agents influencing the life prognosis of ESKD patients. Herein, we evaluated the risk factors related to the outcomes of Japanese patients with dialysis induction. We present the study protocol, the patients’ baseline characteristics, and their outcomes. Methods The Ibaraki Dialysis Initiation Cohort (iDIC) Study is a prospective multi-center cohort study in collaboration with 60 tertiary-care facilities in Ibaraki Prefecture, Japan. We collected baseline data from clinical records and analyzed blood and urine samples of these facilities’ patients with diabetic nephropathy, hypertensive nephrosclerosis, and chronic glomerulonephritis (CGN). The study’s primary outcome was the survival rate at 24 months after dialysis induction. We performed a Kaplan-Meier analysis for cumulative survival and a Cox proportional hazards analysis for all-cause mortality and hospitalization. Results We analyzed 636 patients’ cases (424 males, 212 females, age 67.4 ± 13.1 yrs. [mean ± SD]). We compared the patients’ baseline data with those of similar cohort studies. As the primary kidney disease, 327 cases (51.4%) were diagnosed as diabetic nephropathy, 101 (15.9%) as hypertensive nephrosclerosis, and 114 (17.9%) as CGN. The mean serum creatinine value was 9.1 ± 2.9 mg/dL. The mean estimated glomerular filtration rate was 5.6 ± 1.8 mL/min/1.73m 2 . The cumulative survival rates at 6 months and 24 months after dialysis induction were 95.2 and 87.7%, respectively. The cumulative survival rate was significantly lower with increasing age. A Cox proportional hazards regression analysis demonstrated that high age was significantly associated with all-cause mortality. Conclusions Regarding the clinical characteristics of these newly induced dialysis patients, the same trend as in other cohort studies was observed. Another study is underway to explore prognostic factors based on the iDIC Study’s findings.

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Abstract Background AA amyloidosis is a rare but significant cause of chronic kidney disease (CKD). We aimed to characterize the clinical profile of patients with AA amyloidosis affecting the kidneys in the Indian subcontinent. Methodology In this retrospective cohort study, we evaluated patients with kidney biopsy-confirmed AA amyloidosis and compared them with a control group of patients with diabetic kidney disease (DKD). Primary outcome was defined as a composite of ≥50% decline in estimated glomerular filtration rate (eGFR) and/or progression to end-stage kidney disease (ESKD). Results AA amyloidosis (n = 91) accounted for 1.9% of all kidney biopsies. The median age was 45 years, and 75.8% were male. Chronic infections or inflammatory diseases were reported in 58.2%, tuberculosis being most common (35.2%). Baseline median eGFR was 66.0 mL/min/1.73 m2 and urine protein creatinine ratio was 4.9 g/g. During median follow-up of 5.58 years, 38.6% experienced worsening kidney outcomes. Adjusted analyses showed significantly better kidney survival than DKD (0.29 (95% CI: 0.14–0.66, p = 0.002). Conclusion AA amyloidosis is an uncommon but important cause of CKD. Tuberculosis is the leading predisposing factor in Indian patients. These patients exhibit slower eGFR decline compared to DKD despite progressive proteinuria, suggesting distinct pathophysiology.

Abstract Background There are many causes of kidney disease in dogs. The association of the diagnostic category with survival is unknown. Objective Determine survival outcomes for biopsy‐determined diagnostic categories of kidney disease in dogs. Animals Six hundred forty‐nine dogs were biopsied for evaluation of kidney disease. Methods Retrospective study. Survival information was obtained for dogs whose kidney biopsy was submitted to the International Veterinary Renal Pathology Service between 2008 and 2018. Signalment, serum creatinine (sCr), urine protein : creatinine ratio (UPCR), and serum albumin (sAlb) were reported at the time of biopsy. Cox proportional hazards analysis was performed for the 14 categories with >10 cases having follow‐up to determine hazard ratios (HR), using focal segmental glomerulosclerosis (FSGS) as baseline. Results The median survival time (MST) for all dogs with follow‐up (n = 649) was 608 days (interquartile range [IQR]: 109‐1475 days). The most follow‐up was obtained for FSGS (n = 138, MST 536 days). Dogs with renal amyloidosis (n = 80) had the shortest survival (MST 76 days, IQR 8‐299 days) and, in the multivariate analysis including age, sCr, sAlb, and UPCR, an increased risk of death (HR 1.79 [95% CI: 1.22‐2.65], P < .01). Dogs with podocytopathy, membranous glomerulonephritis (MGN), mixed MGN, membranoproliferative GN (MPGN), and mixed MPGN had decreased risk of death. Regardless of category, increasing age, sCr, and UPCR and decreased sAlb were associated with a greater risk of death. Conclusions The diagnostic category is associated with survival in dogs with kidney disease. Survival of individual dogs within each category was highly variable.

There is no evidence-based definition for diagnosing crescentic glomerulonephritis. The prognostic implications of crescentic lesions on kidney biopsy have not been quantified. Our objective was to determine risk factors for end-stage kidney disease (ESKD) in patients with glomerulonephritis and crescents on kidney biopsy. A query of the Pediatric Nephrology Research Consortium’s Pediatric Glomerulonephritis with Crescents registry identified 305 patients from 15 centers. A retrospective cohort study was performed with ESKD as the primary outcome. Median age at biopsy was 11 years (range 1–21). The percentage of crescents was 3–100% (median 20%). Etiologies included IgA nephropathy (23%), lupus (21%), IgA vasculitis (19%) and ANCA-associated GN (13%), post-infectious GN (5%), and anti-glomerular basement membrane disease (3%). The prevalence of ESKD was 12% at one year and 16% at last follow-up (median = 3 years, range 1–11). Median time to ESKD was 100 days. Risk factors for ESKD included %crescents, presence of fibrous crescents, estimated GFR, and hypertension at biopsy. For each 1% increase in %crescents, there was a 3% decrease in log odds of 1-year renal survival (p = 0.003) and a 2% decrease in log odds of renal survival at last follow-up (p < 0.001). These findings provide an evidence base for enrollment criteria for crescentic glomerulonephritis in future clinical trials.

Visual Abstract Background C3 glomerulopathy and idiopathic immunoglobulin-mediated membranoproliferative GN (Ig-MPGN) are rare complement-mediated kidney diseases. Inherited forms of C3 glomerulopathy/Ig-MPGN are rarely described. Methods Three hundred ninety-eight patients with C3 glomerulopathy (n=296) or Ig-MPGN (n=102) from a national registry were screened for three complement genes: factor H (CFH), factor I (CFI), and C3. Patients with rare variant (minor allele frequency <0.1%) were included. Epidemiologic, clinical, and immunologic data at diagnosis and kidney outcomes of patients were retrospectively collected. Results Fifty-three different rare variants, including 30 (57%), 13 (24%), and ten (19%) in CFH, CFI, and C3 variants, were identified in 66/398 (17%) patients. Thirty-eight (72%) variants were classified as pathogenic, including 20/30 (66%) and 11/13 (84%) variants in CFH and CFI, respectively, impairing synthesis of factor H or factor I regulators. Fifteen of 53 (27%) variants were of unknown significance. At diagnosis, 69% of patients were adult (median age of 31 years). With the exception of biologic stigma of thrombotic microangiopathy, which was more frequent in patients with CFI variants (5/14 [36%] versus 1/37 [3%] and 0% in the CFH group and C3 group, respectively, P < 0.001), the clinical and histologic features were similar among the three variants groups. The kidney outcome was poor regardless of the age at onset and treatment received. Sixty-five percent (43/66) of patients with rare variant reach kidney failure after a median delay of 41 (19–104) months, compared with 28% (55/195) after a median delay of 34 (12–143) months in the nonvariant group. Among 36 patients who received a kidney transplant, 2-year recurrence was frequent, occurring in 39% (12/31), without difference between variant groups, and led to graft failure in three cases. Conclusions In our cohort, 17% of C3 glomerulopathy/Ig-MPGN cases were associated with rare variants in the CFH, CFI, or C3 genes. In most cases, a quantitative deficiency in factor H or factor I was identified. The presence of a rare variant was associated with poor kidney survival. Podcast This article contains a podcast at https://dts.podtrac.com/redirect.mp3/www.asn-online.org/media/podcast/CJASN/2023_11_08_CJN0000000000000252.mp3

Visual Abstract Background and objectives C3 glomerulopathy and idiopathic Ig-associated membranoproliferative GN are kidney diseases characterized by abnormal glomerular complement C3 deposition. These conditions are heterogeneous in outcome, but approximately 50% of patients develop kidney failure within 10 years. Design, setting, participants, & measurements To improve identification of patients with poor prognosis, we performed a detailed analysis of percutaneous kidney biopsies in a large cohort of patients. Using a validated histologic scoring system, we analyzed 156 native diagnostic kidney biopsies from a retrospective cohort of 123 patients with C3 glomerulopathy and 33 patients with Ig-associated membranoproliferative GN. We used linear regression, survival analysis, and Cox proportional hazards models to assess the relationship between histologic and clinical parameters with outcome. Results Frequent biopsy features were mesangial expansion and hypercellularity, glomerular basement membrane double contours, and endocapillary hypercellularity. Multivariable analysis showed negative associations between eGFR and crescents, interstitial inflammation, and interstitial fibrosis/tubular atrophy. Proteinuria positively associated with endocapillary hypercellularity and glomerular basement membrane double contours. Analysis of second native biopsies did not demonstrate associations between immunosuppression treatment and improvement in histology. Using a composite outcome, risk of progression to kidney failure associated with eGFR and proteinuria at the time of biopsy, cellular/fibrocellular crescents, segmental sclerosis, and interstitial fibrosis/tubular atrophy scores. Conclusions Our detailed assessment of kidney biopsy data indicated that cellular/fibrocellular crescents and interstitial fibrosis/tubular atrophy scores were significant determinants of deterioration in kidney function.

ABSTRACT Background Three different histological scores—histopathologic classification (Berden), Renal Risk Score (RRS) and the Mayo Clinic Chronicity Score (MCCS)—for anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis (ANCA-GN) were compared to evaluate their association with patient and kidney prognosis of ANCA-GN. Methods Patients aged >18 years with at least 1 year of follow-up and biopsy-proven ANCA-GN entered this retrospective study. Renal biopsies were classified according to Berden's classification, RRS and MCCS. The first endpoint was end-stage kidney disease (ESKD), defined as chronic dialysis or estimated glomerular filtration rate <15 mL/min/1.73 m2. The second endpoint was ESKD or death. Results Of 152 patients 84 were males, with median age of 63.8 years and followed for 46.9 (interquartile range 12.8–119) months, 59 (38.8%) reached the first endpoint and 20 died. The Kaplan–Meier curves showed that Berden and RRS were associated with first (Berden: P = .004, RRS: P < .001) and second (Berden: P = .001, RRS: P < .001) endpoint, MCCS with the first endpoint only when minimal + mild vs moderate + severe groups were compared (P = .017), and with the second endpoint (P < .001). Among the clinical/histological presentation features, arterial hypertension [odds ratio (OR) = 2.75, confidence interval (95% CI) 1.50–5.06; P = .0011], serum creatinine (OR = 1.17, 95% CI 1.09–1.25; P < .0001), and the percentage of normal glomeruli (OR = 0.97, 95% CI 0.96–0.99; P = .009) were the independent predictors of ESKD at multivariate analysis. When the three scores were included in multivariate analysis, RRS (OR = 2.21, 95% CI 1.15–4.24; P = .017) and MCCS (OR = 2.03, 95% CI 1.04–3.95; P = .037) remained predictive of ESKD, but Berden (OR = 1.17, 95% CI 0.62–2.22; P = .691) did not. Conclusion RRS and MCCS scores were independent predictors of kidney survival together with high serum creatinine and arterial hypertension at diagnosis, while Berden classification was not.

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are a group of multisystemic autoimmune diseases characterized by necrotizing inflammation of small vessels, with a predilection for the kidney. The prognostic value of histological classification of ANCA-glomerulonephritis (ANCA-GN) is discussed. In 2010, Berden and colleagues proposed a prognostic classification based on glomerular involvement; in 2018, Brix et al. introduced the ANCA Renal Risk Score, which includes histological features and glomerular filtration rate; in 2017 the Mayo Clinic Chronicity Score, that considers chronic histological lesions, was designed and assessed in ANCA-GN. We aimed to identify which score is the best tool to predict end-stage kidney disease or death in a cohort of ANCA-GN patients. Patients who underwent kidney biopsy in two Italian centers within 32 years were retrospectively collected. Inclusion criteria: age >18 years, and at least one year of follow-up. A minimum of 10 glomeruli was considered adequate for a biopsy. Renal biopsies were classified according to Berden's classification, Renal Risk Score and Mayo Clinic Chronicity Score. The primary end point of the study was the development of end-stage kidney disease (ESKD) at 5 years, defined as the chronic need of renal replacement therapy (RRT) or glomerular filtration rate (GFR) <15 ml/min. The secondary endpoint was a composite endpoint of ESKD or death for all causes. Of the 152 patients 84 were male, the median age was 63.8 years (Figure 1). Mean eGFR at diagnosis was 21.32 ml/min/1.73 m2. 32.2% of patients were PR-3 positive, 50.6% were MPO positive, 17.2% were ANCA-negative. After a mean follow-up of 71.7 ± 66.7 months, 59 patients (38.8%) were on chronic dialysis or with a GFR <15 ml/min; among them, 20 patients died. The pure kidney survival rate (without ESKD or GFR<15 ml/min) was 79% at 1 year, 65% at 5 years, 59.8% at 10 years. Figure 2 reported the pure kidney survival rates of the patients assigned to every class of the three scores that we considered in this study. Fig. 3, Fig. 4, Fig. 5 show Kaplan-Meyer curves for the secondary outcome (ESKD+death); patients are classified according to the Berden's score (Fig. 2), the Renal Risk Score (Fig. 3) and Mayo Clinic Chronicity Score (Fig. 4). Berden histopathological classification and Renal Risk Score are predictive of renal prognosis when we consider the primary outcome (ESKD or eGFR<15 ml/min) and when we consider the composite outcome (ESKD + death). The Mayo Clinic Chronicity Score allows a reliable stratification of the patients only when we consider the composite outcome (ESKD and death).

Background Comorbidities are associated with increased mortality among patients receiving long-term kidney replacement therapy (KRT). However, it is not known whether primary kidney disease modifies the effect of comorbidities on KRT patients’ survival. Methods An incident cohort of all patients (n = 8696) entering chronic KRT in Finland in 2000–2017 was followed until death or end of 2017. All data were obtained from the Finnish Registry for Kidney Diseases. Information on comorbidities (coronary artery disease, peripheral vascular disease, left ventricular hypertrophy, heart failure, cerebrovascular disease, malignancy, obesity, underweight, and hypertension) was collected at the start of KRT. The main outcome measure was relative risk of death according to comorbidities analyzed in six groups of primary kidney disease: type 2 diabetes, type 1 diabetes, glomerulonephritis (GN), polycystic kidney disease (PKD), nephrosclerosis, and other or unknown diagnoses. Kaplan-Meier estimates and Cox regression were used for survival analyses. Results In the multivariable model, heart failure increased the risk of death threefold among PKD and GN patients, whereas in patients with other kidney diagnoses the increased risk was less than twofold. Obesity was associated with worse survival only among GN patients. Presence of three or more comorbidities increased the age- and sex-adjusted relative risk of death 4.5-fold in GN and PKD patients, but the increase was only 2.5-fold in patients in other diagnosis groups. Conclusions Primary kidney disease should be considered when assessing the effect of comorbidities on survival of KRT patients as it varies significantly according to type of primary kidney disease.

OBJECTIVES Antineutrophil cytoplasmic antibody (ANCA) may appear in the course of rheumatic diseases (RD) but the kidney involvement is very rare and the prognosis poorly defined. METHODS We retrospectively identified patients with RD among 153 patients with ANCA glomerulonephritis (ANCA-GN). Their clinical/histological presentation and outcome were compared with that of primitive ANCA-GN patients (1:4) matched for sex, age, ANCA type and follow-up. RESULTS Nine patients (5.9%) were included: three had rheumatoid arthritis, two systemic sclerosis, two psoriatic arthritis, one ankylosing spondylitis and one seronegative spondylarthritis. Seven patients were MPO positive, two PR3 positive. ANCA-GN developed 74 months after RD with microscopic haematuria and acute kidney dysfunction in all but two patients. After 68-month follow-up, four patients (44.4%) achieved response to therapy defined as eGFR >60/min/1,73 m2 or stable, no microscopic haematuria and negative ANCA. At ANCA-GN diagnosis, serum creatinine and C-reactive protein were significantly lower in RD-ANCA-GN (2.38 vs. 3.34mg/dl, p=0.05 and 2.3mg/dl vs. 7.2mg/dl; p=0.05, respectively) while haemoglobin was higher (12.3g/dl vs. 9.3g/dl p<0.01) than in the 36 primitive ANCA-GN patients of control group. At kidney biopsy, focal forms were more frequent in RD patients (44.45% vs. 18.75%, p=0.11). The treatment between the two groups was not significantly different. At last observation, the percentage of patients with ESKD was lower in RD than in controls (11.1%vs. 30.5%; p=0.23). CONCLUSIONS Patients with RD seem to develop ANCA-GN with less severe clinical/histological kidney involvement, and better long-term kidney survival than primitive ANCA-GN. This is probably due to the strict monitoring of RD patients that allows a prompter ANCA-GN diagnosis and treatment.

Background and objective Infection-related glomerulonephritis (IRGN) in adults, particularly the diabetic population, has a grave prognosis with many patients progressing to dialysis-dependent renal failure. Indian data on this entity are very scarce. This study attempts to correlate the clinicopathological factors related to diabetic IRGN and its short-term outcomes. Subjects and methods A retrospective analysis of all diabetic patients with biopsy-proven IRGN between January 2017 and August 2021 was conducted. Factors affecting outcomes such as clinical characteristics, urine examination, complete blood count, serum biochemistry, renal biopsy, and follow-up data were obtained and analyzed to determine the risk of progression to chronic kidney disease (CKD)/end-stage renal disease (ESRD). Univariate/multivariate analysis and receiver operating characteristic (ROC) curve were performed to identify independent risk factors affecting outcomes. Results A total of 40 diabetic patients with IRGN was included in the study, with a mean age of 53.08 ± 10 years, comprising predominantly males (60%). Infective foci were occult in majority (37.5%). Isolated low C3 levels were documented in the majority, while three patients (7.5%) had normal complement levels. Complete renal recovery was noted in 15 patients (37.5%), while 12 patients (30%) progressed to ESRD. Anuria or uremia at presentation, glomerulosclerosis >28.6%, interstitial fibrosis with tubular atrophy (IFTA) >17.5%, and diabetic nephropathy correlated to poor renal recovery. No correlation was observed between endocapillary proliferation, the pattern of deposits, the prevalence of crescents, and complement levels with the outcome. Conclusion IRGN is a common immune-mediated clinical entity among diabetics and often requires renal replacement therapy. Anuria or uremia at presentation, diabetic nephropathy, elevated glomerulosclerosis, and IFTA were associated with poor renal recovery. Complement levels and crescents had no impact on the outcome.

Chronic kidney disease can progress to end-stage chronic renal disease (ESRD), which requires the use of replacement therapy (dialysis or kidney transplant) in life-threatening conditions. In ESRD, irreversible changes in the kidneys are associated with systemic changes of proinflammatory nature and dysfunctions of internal organs, skeletal muscles, and integumentary tissues. The common components of ESRD pathogenesis, regardless of the initial nosology, are (1) local (in the kidneys) and systemic chronic low-grade inflammation (ChLGI) as a risk factor for diabetic kidney disease and its progression to ESRD, (2) inflammation of the classical type characteristic of primary and secondary autoimmune glomerulonephritis and infectious recurrent pyelonephritis, as well as immune reactions in kidney allograft rejection, and (3) chronic systemic inflammation (ChSI), pathogenetically characterized by latent microcirculatory disorders and manifestations of paracoagulation. The development of ChSI is closely associated with programmed hemodialysis in ESRD, as well as with the systemic autoimmune process. Consideration of ESRD pathogenesis from the standpoint of the theory of general pathological processes opens up the scope not only for particular but also for universal approaches to conducting pathogenetic therapies and diagnosing and predicting systemic complications in severe nephropathies.

AIM: The basic aim of this study was to discover the association of End Stage Renal Disease (ESRD) with various risk factors. End Stage Renal Failure is the last stage of the chronic renal failure in which kidneys become completely fail to function. MATERIALS AND METHODS: The data were collected from the patients of renal diseases from three major hospitals in Peshawar, Pakistan. Odds ratio analysis was performed to examine the relationship of ESRD (a binary response variable) with various risk factors: Gender, Diabetic, Hypertension, Glomerulonephritis, Obstructive Nephropathy, Polycystic kidney disease, Myeloma, SLE Nephritis, Heredity, Hepatitis, Excess use of Drugs, heart problem and Anemia. RESULTS: Using odds ratio analysis, the authors found that the ESRD in diabetic patients was 11.04 times more than non-diabetic patients and the ESRD were 7.29 times less in non-hypertensive patients as compared to hypertensive patients. Similarly, glomerulonephritis patients had 3.115 times more risk of having ESRD than non-glomerulonephritis. Other risk factors may also, to some extent, were causes of ESRD but turned out insignificant due to stochastic sample. CONCLUSION: The authors concluded that there is a strong association between ESRD and three risk factors, namely diabetes, hypertension and glomerulonephritis.

The purpose of this study was to determine the prevalence, etiology and risk factors of treated end-stage renal disease (ESRD) in the region of Tabuk, Saudi Arabia. We studied 460 renal replacement therapy patients through a review of medical records and patient interviews and obtained patient demographics, family history, risk factors for ESRD, environmental exposure to toxins, work conditions, social history and causes of death. The estimated prevalence of treated ESRD was 460 per million populations (PMP); 350 (76%) were treated by hemodialysis, 30 (7%) by peritoneal dialysis and 80 (17%) by kidney transplantation. The mean age was 48 ± 17 years, body mass index was 25 ± 2 kg/m 2 and the male vs. female ratio was 64% vs. 36%. Most patients (55%) were living in rural areas. Etiology of the ESRD was unknown in 33%, hypertension in 24%, chronic glomerulonephritis in 8%, obstructive uropathy in 3.5%, analgesic nephropathy in 5%, Bilhaziasis in 0.5%, chronic pyelonephritis in 2% and diabetic nephropathy in 18%. Other causes such as gouty nephropathy, collagen diseases, toxemia of pregnancy and lupus nephritis constituted 6% of the cases. We conclude that the epidemiology of the treated ESRD in Tabuk area is similar to that in Egypt, but very different from that in the United States.

No abstract available

BACKGROUND In previous reports of end-stage renal disease (ESRD) patients, family history of ESRD was associated with race, younger age, higher education levels and ESRD etiology. This study aimed to analyze how often Polish caucasian dialysis patients reported relatives with ESRD, and to evaluate which risk factors are associated with family history of ESRD. METHODS 4808 ESRD patients provided data about renal disease etiology, diabetes and hypertensive status of first- and second-degree relatives, socioeconomic status and education level. RESULTS Reported ESRD etiologies were: chronic glomerular disease, 19.4 %; diabetic nephropathy, 11.3%; interstitial nephritris, 11.2%; hypertension, 7.8%; polycystic kidney disease (PKD), 7.1%; other or no response, 40.0%. Positive ESRD family history was reported by 745 patients (15.5%); positive history of diabetes, 932 (19.4%); hypertension, 1904 (39%). Positive ESRD family history according to kidney disease etiology was: PKD, 53.1%; glomerulonephritis, 12%; diabetic nephropathy, 11.9%; hypertension, 11.8%; interstitial nephritis, 10.8%. PKD as ESRD etiology (odds ratio (OR) 8.06, 95% confidence interval (CI) 6.35-10.23, p < 0.0001), positive family history of diabetes (OR 1.64, 95% CI 1.34-1.99, p < 0.0001) and positive history of hypertension (OR 1.64, 95% CI 1.39-1.95, p < 0.0001), were independently associated with positive ESRD history. Patients with later ESRD onset had a less frequent positive ESRD family history: for ESRD < 45 yrs, 16% (OR 1.0); 45-64 yrs, 14.4% (OR 0.83, 95% CI 0.70-0.99); > or = 65 yrs, 9.2 % (OR 0.5, 95% CI 0.35-0.72). CONCLUSIONS Results of our study strongly support the contention that familial predisposition contributes to ESRD development.

In this issue of CKJ, McQuarrie et al. have explored the relationship between socioeconomic status and outcomes among Scottish patients with a renal biopsy diagnosis of primary glomerulonephritis. Patients in the lower socioeconomic category had a twofold higher risk of death. No significant differences were observed on progression to end-stage renal disease (ESRD) requiring renal replacement therapy (RRT), suggesting that overall medical management was appropriate for all socioeconomic categories. The findings are significant since they come from an ethnically homogeneous population with free access to healthcare; they also relate to a specific aetiology of chronic kidney disease (CKD) expected to be less dependent on unhealthy lifestyles than other more frequent aetiologies that dominate studies of CKD in general, such as diabetic or hypertensive nephropathy. A closer look at the data suggests that living in a high socioeconomic area is associated with lower mortality, rather than the other way round. Furthermore, the differences in mortality were most pronounced during the RRT stage of CKD, providing clues for further research. In this regard, Wilmink et al. and Nee et al. point to access to pre-ESRD nephrology care and to the best kidney transplantation options as modifiable factors to be studied in the realm of T3 translational research to improve CKD patient outcomes.

The Dietary Approaches to Stop Hypertension (DASH) diet lowers blood pressure, an important risk factor for chronic kidney disease (CKD) and end-stage renal disease (ESRD). However, it is unclear whether adherence to a DASH diet confers protection against future ESRD, especially among those with pre-existing CKD and hypertension. We examined whether a DASH diet is associated with lower risk of ESRD among 1,110 adults aged ≥ 20 years with hypertension and CKD (estimated glomerular filtration rate, eGFR 30-59 ml/min/1.73 m2) enrolled in the National Health and Nutrition Examination Survey (1988-1994). Baseline DASH diet accordance score was assessed using a 24-hour dietary recall questionnaire. ESRD was ascertained by linkage to the U.S. Renal Data System registry. We used the Fine-Gray competing risks method to estimate the relative hazard (RH) for ESRD after adjusting for sociodemographics, clinical and nutritional factors, eGFR, and albuminuria. Over a median follow-up of 7.8 years, 18.4% of subjects developed ESRD. Compared to the highest quintile of DASH diet accordance, there was a greater risk of ESRD among subjects in quintiles 1 (RH=1.7; 95% CI 1.1-2.7) and 2 (RH 2.2; 95% CI 1.1-4.1). Significant interactions were observed with diabetes status and race/ethnicity, with the strongest association between DASH diet adherence and ESRD risk observed in individuals with diabetes and in non-Hispanic blacks. Low accordance to a DASH diet is associated with greater risk of ESRD in adults with moderate CKD and hypertension, particularly in non-Hispanic blacks and persons with diabetes.

No abstract available

OBJECTIVE Patients with type 1 diabetes (T1D) with impaired renal function are at increased risk for end-stage renal disease (ESRD). Although the rate of progression varies, determinants and mechanisms of this variation are unknown. RESEARCH DESIGN AND METHODS We examined serum metabolomic profiles associated with variation in renal function decline in participants with T1D (the Joslin Kidney Study prospective cohort). One hundred fifty-eight patients with proteinuria and chronic kidney disease stage 3 were followed for a median of 11 years to determine estimated glomerular filtration rate slopes from serial measurements of serum creatinine and to ascertain time to onset of ESRD. Baseline serum samples were subjected to global metabolomic profiling. RESULTS One hundred ten amino acids and purine and pyrimidine metabolites were detected in at least 80% of participants. Serum levels of seven modified metabolites (C-glycosyltryptophan, pseudouridine, O-sulfotyrosine, N-acetylthreonine, N-acetylserine, N6-carbamoylthreonyladenosine, and N6-acetyllysine) were associated with renal function decline and time to ESRD (P < 0.001) independent of the relevant clinical covariates. The significant metabolites correlated with one another and with the indices of tubular injury. CONCLUSIONS This prospective cohort study in participants with T1D, proteinuria, and impaired renal function at baseline demonstrated that patients with increased circulating levels of certain modified metabolites experience faster renal function decline, leading to ESRD. Whether some of these candidate metabolites are risk factors or just prognostic biomarkers of progression to ESRD in T1D needs to be determined.

Background: Chronic Kidney Disease (CKD) poses a significant global health burden, particularly in low-resource settings. Understanding its etiology is vital for prevention and early intervention. Objective: To assess the underlying causes of CKD among patients presenting to the Nephrology Division of Khyber Teaching Hospital, Peshawar, Pakistan. Methods: This prospective observational study was conducted over four months (November 2024–March 2025) and included 284 CKD patients aged ≥16 years. Data were collected on demographics, comorbidities, CKD etiology, and treatment details. CKD was defined per KDIGO 2012 guidelines. Statistical analysis was performed using SPSS v24. Results: The mean age was 50.61 ± 20.98 years; 63.4% were male. The leading causes of CKD were diabetic nephropathy (30.6%) and hypertensive nephrosclerosis (29.6%), followed by glomerulonephritis (15.8%), polycystic kidney disease (12.0%), and obstructive uropathy (7.4%). The cause remained unknown in 4.6% of patients. Among glomerulonephritis subtypes, focal segmental glomerulosclerosis (FSGS) was most frequent (42.2%). All patients were on hemodialysis: 66.2% via AV fistula, 18.0% via tunneled catheter, and 15.8% via non-tunneled catheter. Conclusion: Diabetes and hypertension are the predominant causes of CKD in our population. Early screening and management of these risk factors are critical to reducing the burden of ESRD.

The study investigates the prognostic impact of the severity and etiology of chronic kidney disease (CKD) in patients with heart failure with mildly reduced ejection fraction (HFmrEF). Data regarding the outcomes in patients with CKD in HFmrEF is scarce. Consecutive patients with HFmrEF were retrospectively included at one institution from 2016 to 2022. Prognosis of patients with different stages and etiologies of CKD was investigated with regard to the primary endpoint of all-cause mortality at 30 months. A total of 2155 consecutive patients with HFmrEF were included with an overall prevalence of CKD of 31%. Even milder stages of CKD (i.e., KDIGO stage 3a) were associated with an increased risk of 30-months all-cause mortality (HR = 1.242; 95% CI 1.147–1.346; p = 0.001). However, long-term prognosis did not differ in patients with KDIGO stage 5 compared to patients with stage 4 (HR = 0.886; 95% CI 0.616–1.275; p = 0.515). Furthermore, the highest risk of HF-related rehospitalization was observed in patients with KDIGO stages 3b and 4 (log rank p ≤ 0.015), whereas patients with KDIGO stage 5 had a lower risk of HF-related rehospitalization compared to patients with KDIGO stage 4 (HR = 0.440; 95% CI 0.228–0.849; p = 0.014). In contrast, the etiology of CKD was not associated with the risk of 30-month all-cause mortality (log rank p ≥ 0.347) and HF-related rehospitalization (log rank p ≥ 0.149). In patients with HFmrEF, even milder stages of CKD were independently associated with increased risk of 30-months all-cause mortality.

The causes of chronic kidney disease (CKD) affects its outcomes. However, the relative risks for adverse outcomes according to specific causes of CKD is not well established. In a prospective cohort study from KNOW-CKD, a cohort was analyzed using overlap propensity score weighting methods. Patients were grouped into four categories according to the cause of CKD: glomerulonephritis (GN), diabetic nephropathy (DN), hypertensive nephropathy (HTN), or polycystic kidney disease (PKD). From a total of 2070 patients, the hazard ratio of kidney failure, the composite of cardiovascular disease (CVD) and mortality, and the slope of the estimated glomerular filtration rate (eGFR) decline according to the cause of CKD were compared between causative groups in a pairwise manner. There were 565 cases of kidney failure and 259 cases of composite CVD and death over 6.0 years of follow-up. Patients with PKD had a significantly increased risk for kidney failure compared to those with GN [Hazard ratio (HR) 1.82], HTN (HR 2.23), and DN (HR 1.73). For the composite outcome of CVD and death, the DN group had increased risks compared to the GN (HR 2.07), and HTN (HR 1.73) groups but not to the PKD group. The adjusted annual eGFR change for the DN and PKD groups were − 3.07 and − 3.37 mL/min/1.73 m^2 per year, respectively, and all of these values were significantly different than those of the GN and HTN groups (− 2.16 and − 1.42 mL/min/1.73 m^2 per year, respectively). In summary, the risk of kidney disease progression was relatively higher in patients with PKD compared to other causes of CKD. However, the composite of CVD and death was relatively higher in patients with DN-related CKD than in those with GN- and HTN-related CKD.

Chronic kidney disease (CKD) is a significant global public health issue. However, the burden of CKD by etiology and trends over time remains inadequately studied. Data from the Global Burden of Disease Study 2021 (GBD 2021) were analyzed, including cases by region, etiology, age, and sex. Metrics included age-standardized incidence rate (ASIR), age-standardized mortality rate (ASMR), age-standardized prevalence rate (ASPR), disability-adjusted life years (DALYs), and age-standardized DALYs rate (ASDR) between 1990 and 2021. The Joinpoint regression analysis was used to calculate the average annual percentage change (AAPC), and age-period-cohort (APC) analysis was performed to assess trends. In 2021, CKD posed a substantial global burden, with 673,722,703 cases and 19,935,038 new cases. The incidence rate was 233.6 with an AAPC of 0.634. CKD caused 1,527,639 deaths, corresponding to a mortality rate of 18.5 and an AAPC of 0.745. DALYs associated with CKD totaled 44,453,684, with an AAPC of 0.322. CKD burden was primarily attributed to diabetes mellitus type 2 (DMT2), hypertension, and unspecified causes, affecting individuals aged 50 years and older. ASIR and ASPR were higher among females, while males had higher ASMR and ASDR. At regional and national levels, the incidence of CKD was positively correlated with the socio-demographic index (SDI), while mortality, DALYs, and prevalence negatively correlated with SDI. APC analysis revealed an elevated mortality risk (Net Drift = 0.3), increasing with age and over successive periods. Birth cohort analysis indicated higher mortality risks among individuals born after 1992. The global burden of CKD continued to rise due to aging populations, increasing risk factors, and improved detection. While some regions showed success in reducing CKD mortality, widening disparities demanded urgent attention. Early-stage disease and modifiable risks offered prevention opportunities, but realizing this required sustained healthcare investment, especially in resource-limited settings. Therefore, coordinated efforts addressing both risk factors and disease management would be essential to reduce its growing burden.

Background Chronic kidney disease (CKD) poses a significant global health challenge; however, its burden on pediatric populations remains underexplored. This study assesses the incidence, prevalence, mortality, and disability-adjusted life years (DALYs) of pediatric CKD attributable to type 1 diabetes mellitus, type 2 diabetes mellitus, hypertension, glomerulonephritis, and congenital anomalies of the kidney and urinary tract from 1990 to 2021. Methods Data were extracted from the Global Burden of Disease (GBD) 2021 database. CKD burden was stratified by etiology, age, sex, sociodemographic index (SDI), and geography. Average annual percentage changes (AAPCs) in incidence, prevalence, mortality, and DALYs were calculated. Results Globally, CKD-related mortality and DALYs decreased for type 1 diabetes mellitus (-2.176% AAPC), type 2 diabetes mellitus (-1.556%), glomerulonephritis (-0.854%), hypertension (-0.800%), and congenital anomalies of the kidney and urinary tract (-2.143%). The incidence of hypertension incidence increased (+1.299%). Boys experienced higher incidence and prevalence rates for all etiologies, while girls had more significant reductions in mortality and DALYs. High-SDI regions showed the steepest declines in CKD burden, while low-SDI regions experienced limited reductions and increasing hypertension prevalence. Conclusions Pediatric CKD burden reflects disparities by etiology, geography, and SDI. Interventions to improve early diagnosis, healthcare access, and targeted management strategies, particularly in low-SDI regions, are essential. Addressing obesity and improving treatment for glomerulonephritis are priorities. Standardized diagnostic criteria and broader global efforts are needed to mitigate the burden of pediatric CKD.

ABSTRACT Background Diabetes mellitus (DM) and chronic kidney disease (CKD) are well-known cardiovascular and mortality risk factors. To what extent they act in an additive manner and whether the etiology of CKD modifies the risk is uncertain. Methods The multicenter, prospective, observational German Chronic Kidney Disease study comprises 5217 participants (1868 with DM) with a baseline mean estimated glomerular filtration rate of 30–60 mL/min/1.73 m2 and/or proteinuria >0.5 g/day. We categorized patients whose CKD was caused by cardiovascular or metabolic diseases (CKDcvm) with and without DM, as opposed to genuine CKD (CKDgen) with and without DM. Recorded outcomes were first events of non-cardiovascular and cardiovascular death, 4-point major adverse cardiovascular events (4-point MACE) and hospitalization for heart failure (HHF). Results During the 6.5-year follow-up 603 (12%) non-cardiovascular and 209 (4%) cardiovascular deaths, 645 (12%) 4-point MACE, and 398 (8%) HHF were observed, most frequently in patients with DM having CKDcvm. DM increased the risk of non-cardiovascular [hazard ratio (HR) 1.92; 95% confidence interval (CI) 1.59–2.32] and cardiovascular (HR 2.25; 95% CI 1.62–3.12) deaths, 4-point MACE (HR 1.93; 95% CI 1.62–2.31) and HHF (HR 1.87; 95% CI 1.48–2.36). Mortality risks were elevated by DM to a similar extent in CKDcvm and CKDgen, but for HHF in CKDcvm only (HR 2.07; 95% CI 1.55–2.77). In patients with DM, CKDcvm (versus CKDgen) only increased the risk for HHF (HR 1.93; 95% CI 1.15–3.22). Conclusions DM contributes to cardiovascular and mortality excess risk in patients with moderate to severe CKD in both, CKDcvm and CKDgen. Patients with DM and CKDcvm are particularly susceptible to HHF.