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Frequent hemodialysis can alter volume status, blood pressure, and the concentration of osmotically active solutes, each of which might affect residual kidney function (RKF). In the Frequent Hemodialysis Network Daily and Nocturnal Trials, we examined the effects of assignment to six compared with three-times-per-week hemodialysis on follow-up RKF. In both trials, baseline RKF was inversely correlated with number of years since onset of ESRD. In the Nocturnal Trial, 63 participants had non-zero RKF at baseline (mean urine volume 0.76 liter/day, urea clearance 2.3ml/min, and creatinine clearance 4.7ml/min). In those assigned to frequent nocturnal dialysis, these indices were all significantly lower at month 4 and were mostly so at month 12 compared with controls. In the frequent dialysis group, urine volume had declined to zero in 52% and 67% of patients at months 4 and 12, respectively, compared with 18% and 36% in controls. In the Daily Trial, 83 patients had non-zero RKF at baseline (mean urine volume 0.43 liter/day, urea clearance 1.2ml/min, and creatinine clearance 2.7ml/min). Here, treatment assignment did not significantly influence follow-up levels of the measured indices, although the range in baseline RKF was narrower, potentially limiting power to detect differences. Thus, frequent nocturnal hemodialysis appears to promote a more rapid loss of RKF, the mechanism of which remains to be determined. Whether RKF also declines with frequent daily treatment could not be determined.

Objective The study’s purpose is to explore the link of serum albumin on renal progression in patients with chronic kidney disease (CKD). Methods This study was a secondary analysis of a prospective cohort study in which a total of 954 participants were non-selectively and consecutively collected from the research of CKD-ROUTE in Japan between November 2010 and December 2011. We evaluated the association between baseline ALB and renal prognosis (initiation of dialysis or 50% decline in eGFR from baseline) and renal function decline (annual eGFR decline) using the Cox proportional-hazards and linear regression models, respectively. We performed a number of sensitivity analyses to ensure the validity of the results. In addition, we performed subgroup analyses. Results The included patients had a mean age of (66.86 ± 13.41) years, and 522 (69.23%) were male. The mean baseline ALB and eGFR were (3.89 ± 0.59) g/dL and (33.43 ± 17.97) ml/min/1.73 m 2 . The annual decline in eGFR was 2.65 mL/min/1.73 m 2 /year. 218 (28.9%) individuals experienced renal prognosis during a median follow-up period of 36.0 months. The baseline ALB was inversely linked with renal prognosis (HR = 0.61, 95%CI: 0.45, 0.81) and renal function decline (β = -1.41, 95%CI: -2.11, -0.72) after controlling for covariates. The renal prognosis and ALB had a non-linear connection, with ALB’s inflection point occurring at 4.3 g/dL. Effect sizes (HR) were 0.42 (0.32, 0.56) and 6.11 (0.98, 38.22) on the left and right sides of the inflection point, respectively. There was also a non-linear relationship between ALB and renal function decline, and the inflection point of ALB was 4.1 g/dL. The effect sizes(β) on the left and right sides of the inflection point were -2.79(-3.62, -1.96) and 0.02 (-1.97, 1.84), respectively. Conclusion This study shows a negative and non-linear association between ALB and renal function decline as well as renal prognosis in Japanese CKD patients. When ALB is lower than 4.1 g/dL, ALB decline was closely related to poor renal prognosis and renal function decline. From a therapeutic point of view, reducing the decline in ALB makes sense for delaying CKD progression.

The disorder of the “gut-kidney axis” exacerbates renal function decline in chronic kidney disease (CKD), and current CKD therapy is insufficient to address this issue. Hirudin has a palliative effect on the decline of renal function. However, whether hirudin can delay CKD by regulating the “intestinal renal axis” disorder remains unclear. Unilateral ureteral ligation (UUO) induced CKD rat model, and the rats were treated with bifidobacterium and hirudin for 36 days. After 14 and 36 days of modeling, kidney and colon tissues were collected for pathology, western blot (WB) assay, and quantitative real-time PCR (qPCR) detection. Serum samples were collected for renal function testing. Fecal samples were used for 16S rRNA sequencing and research on fecal bacterial transplantation. Lipopolysaccharide combine with adenosine 5’-triphosphate (LPS + ATP)-induced intestinal epithelial cell injury was treated with a nod-like receptor pyrin domain-associated protein 3 (NLRP3) inhibitor and hirudin. Protein expression was detected using WB and qPCR. The kidneys and colons of the CKD rats exhibited varying degrees of lesions. Creatinine (CRE), blood urea nitrogen (BUN), N-acetyl-β-D-glucosidase (NAG) enzyme, and serum uremic toxins were elevated. The expression of claudin-1 and occludin was decreased, NLRP3 inflammatory-related proteins were increased, and the gut microbiota was disrupted. These pathological changes were more pronounced after 36 days of modeling. Meanwhile, high-dose hirudin treatment significantly improved these lesions and restored the intestinal flora to homeostasis in CKD rats. In vitro, hirudin demonstrated comparable effects to NLRP3 inhibitors by upregulating claudin-1 and occludin expression, and downregulating NLRP3 inflammatory-related proteins expression. The dysbiosis of the gut microbiota and impaired intestinal epithelial barrier function in CKD are associated with renal dysfunction in CKD. Hirudin delays the progression of CKD by regulating the disorder of the “gut-kidney axis” and inhibiting the activation of the NLRP3-ASC-caspase-1 pathway.

Increased serum urate predicts chronic kidney disease independent of other risk factors. The use of xanthine oxidase inhibitors coincides with improved renal function. Whether this is due to reduced serum urate or reduced production of oxidants by xanthine oxidase or another physiological mechanism remains unresolved. Here we applied Mendelian randomization, a statistical genetics approach allowing disentangling of cause and effect in the presence of potential confounding, to determine whether lowering of serum urate by genetic modulation of renal excretion benefits renal function using data from 7979 patients of the Atherosclerosis Risk in Communities and Framingham Heart studies. Mendelian randomization by the two-stage least squares method was done with serum urate as the exposure, a uric acid transporter genetic risk score as instrumental variable, and estimated glomerular filtration rate and serum creatinine as the outcomes. Increased genetic risk score was associated with significantly improved renal function in men but not in women. Analysis of individual genetic variants showed the effect size associated with serum urate did not correlate with that associated with renal function in the Mendelian randomization model. This is consistent with the possibility that the physiological action of these genetic variants in raising serum urate correlates directly with improved renal function. Further studies are required to understand the mechanism of the potential renal function protection mediated by xanthine oxidase inhibitors.

This study aimed to evaluate the association between conventional and unconventional lipid parameters and the risk of future chronic kidney disease (CKD) and progression of renal function decline. Data from 4,542 participants who were free of CKD at baseline were analyzed using information from the China Health and Retirement Longitudinal Study (2011-2015). The follow-up period was four years. The primary endpoints were incident CKD and rapid progression of renal function decline. The associations between lipid parameters and the risk of CKD and rapid progression of renal function decline were assessed using restricted cubic splines (RCS) and logistic regression analysis. Logistic regression analysis showed that high-density lipoprotein cholesterol (HDL-C) was negatively associated with CKD risk, while remnant cholesterol (RC) and the atherogenic index of plasma (AIP) were positively associated. Triglycerides (TG), RC, and AIP were positively correlated with rapid renal function decline, whereas low-density lipoprotein cholesterol (LDL-C) and HDL-C were negatively correlated. Among these parameters, AIP was the most strongly associated with CKD [adjusted odds ratio (OR) (95% CI): 2.091 (1.199, 3.649),  = 0.009] and rapid progression of renal function decline [adjusted OR (95% CI): 3.996 (2.632, 6.068),  < 0.001]. LDL-C and HDL-C were negatively associated with rapid progression of renal function decline, while TG, RC, and AIP were positively associated with this outcome. Among the lipid parameters examined, AIP was the most strongly associated with CKD and rapid progression of renal function decline.

Ultra-processed food (UPF) consumption has been associated with increased risk of cardiovascular risk factors and mortality. However, little is known on the UPF effect on renal function. The aim of this study is to assess prospectively the association between consumption of UPF and renal function decline. This is a prospective cohort study of 1312 community-dwelling individuals aged 60 and older recruited during 2008–2010 and followed up to December 2015. At baseline, a validated dietary history was obtained. UPF was identified according to NOVA classification. At baseline and at follow-up, serum creatinine (SCr) and estimated glomerular filtration rate (eGFR) levels were ascertained and changes were calculated. A combined end-point of renal decline was considered: SCr increase or eGFR decreased beyond that expected for age. Logistic regression with adjustment for potential confounders was performed. During follow-up, 183 cases of renal function decline occurred. The fully adjusted odds ratios (95% CI) of renal function decline across terciles of percentage of total energy intake from UPF were 1.56 (1.02–2.38) for the second tercile, and 1.74 (1.14–2.66) for the highest tercile; p-trend was 0.026. High UPF consumption is independently associated with an increase higher than 50% in the risk of renal function decline in Spanish older adults.

PurposeTo externally validate the Palacios’ equation estimating the new baseline glomerular filtration rate (NB-GFR) after partial or radical-nephrectomy (PN, RN) for Renal cancer carcinoma (RCC).Materials and methodsOur research group recently published two studies that investigated the association between renal function and cancer-specific survival in RCC. The first one included 3457 patients undergone RN or PN for a cT1-2 RCC coming from five high-volume centers; the second one considered 1767 patients undergone RN or PN for a cT1-4 RCC in a single high-volume center. From such datasets, available complete patients’ data were used to calculate the predicted NB-GFR through the Palacios’ equation: predicted NB-GFR = 35.03 + 0.65 ∙ preoperative GFR – 18.19 ∙ (if radical nephrectomy) – 0.25 ∙ age + 2.83 ∙ (if tumor size > 7 cm) – 2.09 ∙ (if diabetes). The observed NB-GFR was calculated by the CKD-EPI equation on serum creatinine at 3–12 months after surgery. Concordance between observed and predicted NB-GFR was evaluated by Lin’s concordance correlation coefficient and Bland-Altman analysis.Results2419 patients were included (1210, cohort #1; 1219, cohort #2). The median observed NB-GFR value in cohorts #1 and #2 was 73.0 ml/min/1.73 m2 (IQR 56.1–90.1) and 64.2 ml/min/1.73 m2 (IQR 49.6–83); the median predicted NB-GFR was 71.1 ml/min/1.73 m2 (IQR 58–81.5) and 62.6 ml/min/1.73m2 (IQR 47.9–75.9). The concordance line showed a slope of 0.80 and 0.86, and an intercept at 11.02 and 5.41 ml/min/1.73 m2 in the cohort#1 and #2, respectively. The Palacio’s equation moderately over-estimated and under-estimated NB-GFR, for values below and above the cut-off of 50 ml/min/1.73 m2 and 35 ml/min/1.73m2 in cohort#1 and #2. The Lin’s concordance correlation coefficient was 0.79 (95% CI 0.77–0.81) and 0.83 (95% CI 0.82–0.85).ConclusionsWe confirm the predictive performances of Palacios’ equation, supporting its utilization in clinical practice.

Background Keto-analogues administration plays an important role in clinical chronic kidney disease (CKD) adjunctive therapy, however previous studies on their reno-protective effect mainly focused on kidney pathological changes induced by nephrectomy. This study was designed to explore the currently understudied alternative mechanisms by which compound α-ketoacid tablets (KA) influenced ischemia–reperfusion (IR) induced murine renal injury, and to probe the current status of KA administration on staving CKD progression in Chinese CKD patients at different stages. Methods In animal experiment, IR surgery was performed to mimic progressive chronic kidney injury, while KA was administrated orally. For clinical research, a retrospective cohort study was conducted to delineate the usage and effects of KA on attenuating CKD exacerbation. End-point CKD event was defined as 50% reduction of initial estimated glomerular filtration rate (eGFR). Kaplan–Meier analysis and COX proportional hazard regression model were adopted to calculate the cumulative probability to reach the end-point and hazard ratio of renal function deterioration. Results In animal study, KA presented a protective effect on IR induced renal injury and fibrosis by attenuating inflammatory infiltration and apoptosis via inhibition of nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. In clinical research, after adjusting basic demographic factors, patients at stages 4 and 5 in KA group presented a much delayed and slower incidence of eGFR decrease compared to those in No-KA group (hazard ratio (HR) = 0.115, 95% confidence interval (CI) 0.021–0.639, p  = 0.0134), demonstrating a positive effect of KA on staving CKD progression. Conclusion KA improved IR induced chronic renal injury and fibrosis, and seemed to be a prospective protective factor in end stage renal disease.

Background/Objectives: The Prognostic Nutritional Index (PNI), which integrates serum albumin and lymphocyte count, reflects both nutritional and inflammatory status. However, its role in early renal function decline among patients with type 2 diabetes (T2D), particularly in relation to glycemic control, remains unclear. This study aimed to: (1) characterize the dose–response relationship between PNI and early renal function decline in type 2 diabetes using restricted cubic splines; (2) identify whether glycemic control (HbA1c) modifies the PNI–renal decline association; and (3) evaluate the clinical utility of combining PNI and HbA1c for risk stratification. Methods: We analyzed data from 1711 community-based participants with T2D who had preserved renal function at baseline. The PNI was calculated as serum albumin (g/L) + 5 × lymphocyte count (×109/L). The primary outcome was a composite of rapid estimated glomerular filtration rate (eGFR) decline (>3 mL/min/1.73 m2 per year) or incident chronic kidney disease (CKD) stage 3. Restricted cubic spline models, multivariable regression, and Johnson–Neyman analyses were used to examine non-linearity and effect modification by glycated hemoglobin (HbA1c). Results: A consistent inverse linear association was observed between PNI and the rate of eGFR decline (P for non-linearity > 0.05). Johnson–Neyman analysis further demonstrated that the protective association of PNI was statistically significant within an HbA1c range of 7.24% to 8.71%. Stratification by clinical cut-offs revealed a significant effect modification by glycemic status. The inverse linear association between PNI and renal risk was most pronounced under hyperglycemic stress, as evidenced by the markedly elevated incidence (50.0%) among individuals with both poor glycemic control (HbA1c ≥ 8%) and low PNI (<50). Conversely, under good glycemic control (HbA1c < 8%), this inverse association was substantially attenuated, with a lower incidence observed in the low-PNI subgroup (6.7%) than in the high-PNI subgroup (15.9%). These findings indicate that the protective role of PNI is conditional upon the glycemic milieu. Conclusions: The PNI demonstrates a stable linear association with early renal function decline in T2D, with its protective effect most pronounced at suboptimal HbA1c levels. Combining PNI and HbA1c effectively identifies a high-risk subgroup characterized by synergistic risk, underscoring the need for integrated nutritional and glycemic management.

The Japan Diabetes Complications Study (JDCS), a nation-wide, multicenter, prospective study of patients with type 2 diabetes, reported that hemoglobin A1c (HbA1c), systolic blood pressure, and smoking were risk factors for the onset of macroalbuminuria. This study explored the risk factors for glomerular filtration rate (GFR) decline in the JDCS patients. We examined the 1407 JDCS patients (667 women, mean age 59years, 974 normoalbuminuria, 433 microalbuminuria) whose urinary albumin-to-creatinine ratio (UACR) and estimated GFR (eGFR) were determined at baseline with an 8-year follow-up. We divided all the patients into four groups according to baseline eGFR: G1 (120≤eGFR), G2 (90≤eGFR<120), G3 (60≤eGFR<90), G4 (eGFR<60). The eGFRs in groups G1 and G2 decreased at follow-up compared to those at the baseline. The risk of annual eGFR decline rate≥3ml/min/1.73m2 (rapid decliners) increased as the baseline eGFR increased. Advanced age, high HbA1c, and UACR, or diabetic retinopathy at baseline were risk factors for the rapid decliners. Especially the G1 group had a significant risk for the rapid decliners. The frequency of the patients with GFR<60ml/min/1.73m2 at the follow-up amounted to 31.1% in the rapid decliners, which was higher than 12% in the non-rapid decliners. In normo- and microalbuminuric patients with type 2 diabetes, extra careful attention should be paid to patients with eGFR ≥120ml/min/1.73m2 to detect cases with rapidly decreased GFR under the normal range.