title: Two cases of nephrotic syndrome (NS)-induced acute kidney injury (AKI) associated with renal hypouricemia.
abstract: Renal hypouricemia is a clinical disorder attributed to an increased renal urate excretion rate and is well known to involve a high risk of urolithiasis and exercise-induced acute kidney injury (AKI). This report concerns two interesting cases of nephrotic syndrome (NS)-induced AKI associated with renal hypouricemia. A 64-year-old female (Case 1) and a 37-year-old male (Case 2) were hospitalized because of AKI (serum creatinine: 2.07 mg/dl and 3.3 mg/dl, respectively), oliguria and NS. They were treated with prednisolone and temporary hemodialysis. Renal function improved, but hypouricemia persisted during hospitalization. Histological findings in both cases led to a diagnosis of minimal change nephrotic syndrome and identification of the diuretic phase of tubulointerstitial damage because of findings such as acute tubular necrosis. Furthermore, distal tubules of Case 2 showed an amorphous mass, possibly a uric acid crystal. Analysis of the two cases with the URAT1 gene, encoded by SLC22A12, found a homozygous mutation in exon 4 (W258stop) of each one. Our cases show that patients with renal hypouricemia may be susceptible to AKI without involvement of exercise if they possess some facilitators. Renal hypouricemic patients should therefore be carefully examined for all complications from renal hypouricemia because of high risk of AKI.
authors: Division of Nephrology and Kidney Center, Kobe University School of Medicine, Hyogo, Matsudo, Japan.
authors: Y
authors: Y
authors: Takeda
authors: A
authors: A
authors: Abe
authors: S
authors: S
authors: Nakanishi
authors: M
authors: M
authors: Umezu
authors: K
authors: K
authors: Hirano
authors: H
authors: H
authors: Hayakawa
authors: I
authors: I
authors: Ohno
authors: K
authors: K
authors: Ichida
authors: Y
authors: Y
authors: Yamaguchi
authors: T
authors: T
authors: Hosoya
authors: M
authors: M
authors: Fukagawa
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology* / Q000473:pathology; D000328:Adult; D001706:Biopsy; D005260:Female; D006801:Humans; D007668:Kidney / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009404:Nephrotic Syndrome / Q000150:complications* / Q000473:pathology; D027361:Organic Anion Transporters / Q000235:genetics; D027701:Organic Cation Transport Proteins / Q000235:genetics; D015499:Renal Tubular Transport, Inborn Errors / Q000209:etiology / Q000235:genetics / Q000473:pathology; D014545:Urinary Calculi / Q000209:etiology / Q000235:genetics / Q000473:pathology
chemical_list: D027361:Organic Anion Transporters; D027701:Organic Cation Transport Proteins; C491241:SLC22A12 protein, human