Renal functional decline that is frequently seen during chronic hepatitis B (CHB) treatment can exert adverse effects on overall prognosis. It, however, is difficult to distinguish vulnerable patients who may experience renal dysfunction because most previous CHB studies were conducted in relatively healthy individuals. In this retrospective observational study, renal functional decline in CHB patients receiving oral antiviral agents for more than 6 months was analyzed and risk factors of chronic kidney disease (CKD) progression were determined. Renal functional decline was defined when the estimated glomerular filtration rate (eGFR) decreased by more than 25% from baseline and rapid CKD progression was defined as eGFR decreased by more than 5 mL/min/1.73 m2/y among patients who experienced renal functional decline. A total of 4178 patients were followed up for a median 23 months. Antiviral agents included lamivudine (17.0%), adefovir (3.7%), entecavir (70.4%), telbivudine (0.6%), tenofovir (4.0%), or clevudine (4.3%). Renal functional decline occurred in 706 (16.9%) patients. Based on multivariate Cox regression analysis, age, hypertension, diabetes, history of liver or kidney transplantation, underlying underlying CKD, and simultaneous administration of diuretics increased the hazard ratio for renal functional decline; however, clevudine reduced risk. The eGFR significantly increased over time in patients receiving telbivudine or clevudine compared with lamivudine. Among the 3175 patients followed up for more than 1 year, 407 (12.8%) patients experienced rapid CKD progression. Patients with rapid CKD progression showed lower serum albumin, higher total bilirubin, and prolonged prothrombin time compared with patients with stable renal function, but hepatitis B envelope antigen positivity and hepatitis B virus deoxyribonucleic acid level did not differ between the control and rapid CKD progression groups. Age, diabetes, kidney transplantation, underlying CKD, and simultaneous administration of diuretics were identified as risk factors for rapid CKD progression, and clevudine showed a beneficial effect. Age, hypertension, diabetes, liver or kidney transplantation, underlying CKD, and diuretics were identified as risk factors for renal functional decline. This study suggests that close monitoring of renal function and adequate management are required for CHB patients receiving antiviral agents with these risk factors.

Fluid overload prior to continuous renal replacement therapy (CRRT) is an important prognostic factor. Thus, precise evaluation of fluid status is necessary to treat such patients. In this study, we investigated whether fluid assessment using bioelectrical impedance analysis (BIA) can predict outcomes in critically ill patients requiring CRRT. A prospective observational study was performed in patients who were admitted to the intensive care unit and who required CRRT. BIA was conducted before CRRT; then, the ratio of extracellular water to total body water (ECW/TBW) was derived to estimate volume status. A total of 31 patients treated with CRRT were included. There were 18 men (58.1%), and the median age was 67 years (interquartile range, 51 to 78 years). Fourteen patients (45.2%) died within 28 days after CRRT initiation. Patients were divided into 16 with ECW/TBW ≥0.41 and 15 with ECW/TBW <0.41. Survival rate within 28 days was different between the two groups (P = 0.044). Cox regression analysis revealed a relationship between ECW/TBW ≥0.41 and 28-day mortality, but it was not statistically significant (hazard ratio, 3.0; 95% confidence interval, 0.9 to 9.8; P = 0.061). Lastly, the area under the curve of ECW/TBW for 28-day mortality was analyzed. The area under the curve of ECW/TBW was 0.73 (95% confidence interval, 0.54 to 0.92), and this was significant (P = 0.037). Fluid status can be assessed using BIA in critically ill patients requiring CRRT, and BIA can predict mortality. Further large trials are needed to confirm the usefulness of BIA in critically ill patients.

Hyperuricemia is frequently observed in patients with chronic kidney disease and is recognized as a significant contributor to the progression of renal dysfunction. On the other hand, hypouricemia, although less thoroughly studied, has been implicated in exercise-induced acute kidney injury and urolithiasis. Uric acid (UA), the final product of purine metabolism, is predominantly synthesized in the liver and excreted through both renal and intestinal pathways. The metabolism and excretion of UA are intricately linked to kidney function, underscoring their clinical significance in the context of renal disease. This review provides a comprehensive review of UA metabolism and the key urate transporters, including URAT1, GLUT9, OATs, and ABCG2, which play pivotal roles in maintaining UA homeostasis. Additionally, this review discusses the genetic and environmental factors that influence UA regulation, with a particular focus on the pathological consequences of transporter dysfunction. By elucidating the mechanisms underlying UA handling in the renal and intestinal systems, this review aims to enhance our understanding of UA-related pathophysiology, and to inform the development of targeted therapeutic strategies for modulating UA transport.