BMC Nephrology最新文献

Background: Dysuricemia, encompassing both hyperuricemia (serum uric acid: SUA > 7 mg/dl) and hypouricemia (SUA ≤ 3 mg/dL), has been linked to cardio-renal risks, but it remains unclear whether consistent or transient dysuricemia contributes to the risk of chronic kidney disease (CKD).

Purpose: To investigate whether consistent and transient dysuricemia influences annual changes in the estimated glomerular filtration rate (eGFR) in healthy participants.

Methods: We retrospectively analyzed 1142 healthy participants who underwent health checkups with at least four consecutive annual measurements of eGFR and SUA. Participants with consistently hyperuricemia, hypouricemia, or normouricemia (7 mg/dL ≥ SUA > 3 mg/dL) throughout follow-up were categorized as consistent hyperuricemia (n = 36), consistent hypouricemia (n = 8) and normouricemia (n = 759), respectively. Others were classified as transient hyperuricemia (n = 282) and transient hypouricemia (n = 57). Annualized eGFR decline was compared using ANOVA, and incident CKD stage 3 events were evaluated using χ² or Fisher's exact tests. Multivariable analyses were performed to examine the association between baseline SUA and subsequent renal outcomes.

Results: Hyperuricemia was positively associated with obesity, liver dysfunction, dyslipidemia, and higher baseline eGFR compared with normouricemia, whereas hypouricemia showed negative associations with obesity and liver dysfunction. Transient hyperuricemia was significantly associated with obesity, liver dysfunction, and dyslipidemia relative to consistent normouricemia, while transient hypouricemia was negatively associated with obesity and liver dysfunction. Transient hyperuricemia exhibited significantly faster annual eGFR decline than normouricemia, while transient hypouricemia showed no significant difference. Baseline SUA ≥ 7 mg/dL was associated with higher baseline eGFR but predicted a significantly faster subsequent eGFR decline. In multivariable linear regression, baseline SUA level was independently associated with eGFR change, whereas baseline SUA status did not independently predict incident CKD stage 3.

Conclusion: Transient hyperuricemia, rather than transient hypouricemia, is associated with accelerated eGFR decline in healthy individuals. Baseline SUA provides prognostic information regarding renal function trajectory, but does not independently predict CKD stage 3, suggesting that SUA should be interpreted as a clinically useful marker of renal vulnerability rather than a proven causal factor.

Background: Abnormal circadian pattern of urinary sodium excretion was associated with high blood pressure and target-organ injury. However, whether urinary circadian pattern of sodium excretion is associated with chronic kidney disease (CKD) progression has not been elucidated.

Methods: We evaluated 1604 participants with CKD in this retrospective cohort study. We studied the association between clinical outcomes and day: night ratio of urinary sodium excretion, using urine collected separately during daytime and nighttime. The primary outcome was defined as a decrease of ≥ 30% in eGFR from baseline or initiation of renal-replacement therapy. The secondary outcome was a decrease of ≥ 50% in eGFR from baseline or initiation of renal-replacement therapy.

Results: The primary and secondary outcome occurred in 319 and 247 patients during 5710.2 person-years of follow-up, respectively. The Kaplan-Meier (KM) analysis showed an association between lower day: night ratio of urinary sodium excretion and primary and secondary outcome (both P < 0.05). In multivariate analysis, fully adjusted hazard ratios (95% confidence intervals) for patients with day: night ratio of urinary sodium excretion in the lowest quartile were 2.29 (1.55-3.39) for the primary outcome and 2.42 (1.53-3.85) for the secondary outcome, compared to the highest quartile.

Conclusion: Abnormal circadian pattern of urinary sodium excretion, characterized by a lower day: night ratio of urinary sodium excretion, is associated with CKD progression in CKD patients. These findings suggest day: night ratio of urinary sodium excretion may serve as a marker to recognize CKD progression.

Clinical trial number: Not applicable.

Background: Acute kidney injury (AKI) is defined by an increase in serum creatinine according to the Kidney Disease: Improving Global Outcomes criteria. In contrast, pseudo-renal failure is a rare condition characterized by azotemia and electrolyte imbalance that mimic AKI, while the actual renal function remains preserved. Because of its rarity and nonspecific presentation, pseudo-renal failure is often misdiagnosed as true AKI. We report a rare case of pseudo-renal failure caused by intraperitoneal bladder rupture following gynecologic surgery. This case is unique in that pseudo-renal failure was accompanied by severe hyponatremia and nephrotic-range proteinuria despite the absence of significant glomerular pathology, highlighting an important diagnostic pitfall.

Case presentation: A 49-year-old woman presented with progressive renal dysfunction and persistent mild lower abdominal discomfort two weeks after total laparoscopic hysterectomy with bilateral salpingo-oophorectomy for uterine leiomyoma. Laboratory tests revealed markedly elevated blood urea nitrogen (68.2 mg/dL) and creatinine (4.48 mg/dL), with relatively preserved cystatin C (1.34 mg/L), severe hyponatremia (123 mmol/L), and nephrotic-range proteinuria (7.9 g/day). A kidney biopsy was performed to evaluate for an underlying glomerular disease; however, it revealed only minor glomerular changes with no significant pathological abnormalities. Abdominal ultrasonography revealed moderate ascites without other remarkable findings. To investigate the cause of the ascites, diagnostic paracentesis was performed, which revealed an ascitic creatinine level higher than the serum creatinine level, suggesting urinary ascites. Consequently, computed tomography (CT) cystography confirmed urinary leakage caused by intraperitoneal bladder rupture. The patient underwent the surgical repair following Foley catheter placement. Her renal function normalized postoperatively, with resolution of hyponatremia and a reduction in proteinuria.

Conclusions: This case highlights the importance of recognizing pseudo-renal failure as a differential diagnosis of unexplained azotemia, particularly in patients with recent pelvic surgery. The coexistence of elevated serum creatinine with relatively preserved cystatin C, ascites, hyponatremia, and nephrotic-range proteinuria should raise suspicion for urinary tract injury. Measurement of ascitic fluid creatinine and CT cystography are key diagnostic tools for genitourinary trauma that can prevent unnecessary invasive procedures and guide timely therapeutic interventions. Ultimately, awareness of this entity enables prompt diagnosis and favorable clinical outcomes for patients.