Background/Aims: There is a paucity of literature that investigates a biomarker associated with successful renal recovery following continuous renal replacement therapy (CRRT). Our study aimed to identify potential renal biomarkers or clinical indicators that could predict the successful weaning from CRRT. Methods: We conducted a prospective, observational study of 110 patients who had received CRRT and were weaned after renal recovery. Patients were considered to have successfully weaned from CRRT once there was no need for renal replacement therapy (RRT) for at least 14 days. For patients who had to restart dialysis within 14 days were considered unsuccessful. Results: Of the 110 patients evaluated, 89 (80.9%) were successfully weaned from CRRT. These patients had lower serum cystatin C (CysC) levels and higher urine output than the group that restarted RRT at the time of CRRT cessation. However, the levels of serum creatinine and neutrophil gelatinase-associated lipocalin were not significantly lower in the successful group compared to the restart-RRT group. A multivariable logistic regression showed that serum CysC was an independent predictor for the successful weaning from CRRT. Furthermore, in a multivariable Cox proportional hazards analysis, the group that was successfully weaned from CRRT had a lower in-hospital mortality compared to the restarted RRT group. Conclusion: Serum CysC, at the time of CRRT cessation, is an independent predictor of the successful weaning from CRRT in critically ill patients with acute kidney injury.
Rationale:Povidone-iodine is a broad-spectrum antiseptic applied topically to treat wounds and prevent their infection. There have been several case reports of acute kidney injury (AKI) in burn patients after povidone-iodine irrigation and in patients receiving the substance as a sclerotherapy agent for management of lymphocele after renal transplantation. However, biopsy-confirmed AKI after ingestion of povidone-iodine has not previously been described.Patient concerns:A 47-year-old man who had apparently ingested povidone-iodine solution and presented with nausea, vomiting, and reduced urine output. Laboratory data revealed blood urea nitrogen of 124 mg/dL, serum creatinine of 6.3 mg/dL, impaired liver function, and leukocytosis. Urine iodine/creatinine ratio was markedly elevated.Diagnoses:Acute tubular necrosis and interstitial nephritis secondary to povidone-iodine ingestion.Interventions:The patient was admitted to the intensive care unit and underwent continuous venovenous hemodiafiltration. Kidney biopsy showed acute tubular necrosis and interstitial nephritis. Unstained sections showed tan objects in the tubular lumina that were suspected to be povidone-iodine casts. Corticosteroid therapy (1 mg/kg/day) was started after kidney biopsy.Outcomes:Renal function recovered after hemodialysis and corticosteroid medication, but not completely.Lessons:We have reported the first case of biopsy-confirmed AKI accompanied by increased urine iodine concentration following povidone-iodine ingestion.
Background: The present study was designed to investigate the role of the local renin-angiotensin-aldosterone system (RAAS), endothelin (ET) and the natriuretic peptide system (NPS) for the development of renal fibrosis and progressive renal disease in experimental unilateral ureteral obstructed (UUO) rats. Methods: Male Sprague-Dawley rats (180–200 g) were unilaterally obstructed by ligation of the proximal ureters for 14 days. Control rats were treated in the same way, except that no ligature was made. The mRNA expressions of local renin-angiotensin system, aldosterone synthase (CYP11B2), ET-1 and NPS was determined in the cortex by real-time polymerase chain reaction. Results: Following the unilateral ureteral obstruction, the mRNA expressions of angiotensin-converting enzyme 1, ET-1 and transforming growth factor-β1 (TGF-β1) were increased, while angiotensin-converting enzyme 2 was decreased in the obstructed kidney compared with the controls. Angiotensin II type 1 receptor was decreased and TGF-β1 was not changed in contralateral kidney compared with the controls. Atrial natriuretic peptide, brain natriuretic peptide, and C-type natri- uretic peptide expressions were increased in UUO kidneys compared with the controls, while natriuretic peptide receptor-A was decreased in UUO kidneys. Conclusion: The local RAAS and ET-1 was upregulated which may play a role in the progressive renal fibrosis in obstructed kidneys in rats with UUO. The enhanced activity of NPS in UUO kidney may play a role to compensate against progressive renal fibrosis in chronic obstructive uropathy.
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