Aim: The influence of serum urate on kidney disease is attracting attention, but the effects of uric acid (UA) on nephrosclerosis have not been elucidated.Methods: We reviewed data from 45 patients diagnosed with arterial/arteriolar nephrosclerosis. The renal outcomes of the arterial/arteriolar nephrosclerosis patients were assessed by performing logistic and Cox regression analyses. A Kaplan-Meier analysis was used to evaluate the impact of hyperuricemia (HU) on kidney survival. The renal outcomes of patients with and without HU were compared by using a propensity score-matched cohort.Results: The logistic regression models showed no significant differences in renal outcomes, according to baseline parameters or follow-up parameters, except the serum UA value and body mass index (BMI). Baseline serum UA level had the highest odds ratio (OR) for estimated glomerular filtration rate (eGFR) decline (OR, 1.86; 95% confidence interval (CI), 1.12 to 3.45), among the parameters assessed. In the multivariate Cox regression analysis, HU (UA ≥ 8.0 mg/dL) (P = 0.01) and BMI (P = 0.03) were significantly associated with a ≥ 50% eGFR decline or ESRD. The Kaplan-Meier analysis in the propensity score-matched cohort indicated that the renal survival rate of the group of arterial/arteriolar nephrosclerosis patients with HU was significantly lower than that of the group without HU (log rank, P = 0.03).Conclusion: The results of this study suggest that the baseline serum UA value can serve as a renal outcome predictor in arterial/arteriolar nephrosclerosis patients.

Increased non-HDL-C levels are a risk factor for renal function decline in HIV-infected patients.

Background: Stem cell transplantation (SCT) places a heavy burden on the kidneys, often resulting in renal dysfunction or nephrotic syndrome. This study attempted to show that early-onset proteinuria predicts the development of overt nephropathy. Methods: A total of 831 patients who received allogeneic SCT were surveyed. Excluding those with prior kidney disease and those lacking in an observation period ≥1 year after SCT, 251 patients were eligible for the study. Dipstick proteinuria ≥1+ within 1 year after SCT was defined as ‘incident proteinuria', and subsequent persistence of an estimated glomerular filtration rate of <60 ml/min/1.73 m² at 1 year or longer after SCT was defined as ‘incident chronic kidney disease (CKD)'. Between-group differences were analyzed using the chi-square or Mann-Whitney U test. Factors associated with the incidence of CKD were investigated by multivariate Cox proportional regression analysis. Kidney-biopsied tissue was examined in all nephrotic syndrome patients. Results: The mean duration of follow-up was 4 years. Thirty-four (13.5%) and 66 (26.3%) patients developed incident proteinuria and incident CKD, respectively. Nine (3.6%) patients developed nephrotic syndrome mainly due to membranous nephropathy. The incidence of CKD was significantly greater in patients with incident proteinuria than those without (61.8 vs. 20.7%, p < 0.0001), and incident dipstick proteinuria was a significant risk for incident CKD (hazard ratio 4.39, 95% CI 2.44-7.73, p < 0.0001). Conclusion: SCT patients who manifest dipstick proteinuria are predisposed to overt nephropathy. Routine monitoring of the urine dipstick test is strongly recommended, as it facilitates early nephrology care for post-SCT patients.

DMN and cART-induced TIN was noted in the biopsy cases. In the autopsy cases, renal arteriosclerosis, global glomerulosclerosis, and tubulointerstitial atrophy were remarkable. Early diagnosis of kidney diseases should be crucial to introduce optimal management, including controlling rigorous comorbidities and appropriate use of cART, to prevent further progression of CKD.