Tala Mahmoud1, Elias C Ghandour2,3, Bernard G Jaar4,5,6,7. 1. Faculty of Medicine, University of Balamand, El-Koura, Lebanon. 2. Department of Medicine, Division of Nephrology, Johns Hopkins School of Medicine, Baltimore, MD, USA. 3. Nephrology Center of Maryland, Baltimore, MD, USA. 4. Department of Medicine, Division of Nephrology, Johns Hopkins School of Medicine, Baltimore, MD, USA. bjaar@jhmi.edu. 5. Nephrology Center of Maryland, Baltimore, MD, USA. bjaar@jhmi.edu. 6. Welch Center for Prevention, Epidemiology and Clinical Research, Johns Hopkins University, Baltimore, MD, USA. bjaar@jhmi.edu. 7. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA. bjaar@jhmi.edu.
Abstract
BACKGROUND: Oxalate nephropathy is a rare disorder that can result in acute kidney injury (AKI) and progresses to end-stage kidney disease (ESKD). The causes can be either primary or secondary. Primary hyperoxaluria includes a group of hereditary disorders with enzymatic defects in the glyoxylate pathway, resulting in decreased oxalate metabolism. Secondary hyperoxaluria, often overlooked can result from increased intestinal absorption, nutritional deficiencies, decreased fluid intake, impaired excretion, and increased dietary consumption of oxalate. CASE PRESENTATION: We present a Caucasian case of acute oxalate induced nephropathy associated with consumption of large quantities of green vegetables in a patient with chronic kidney disease (CKD). Imaging study showed no evidence of kidney stone, but a kidney biopsy revealed acute tubular injury, tubular atrophy, interstitial fibrosis, and dense tubular deposition of calcium oxalate crystals. Upon further questioning the patient, we learned that in the months prior to presentation, he had very significantly increased his consumption of green vegetables. Because of no clinical improvement, the patient was initiated and maintained on hemodialysis. CONCLUSION: This report illustrates a case of acute oxalate nephropathy in the setting of very high dietary consumption of oxalate-rich foods in a patient with advanced CKD. Special attention should be given to the secondary causes of hyperoxaluria in patients with predisposing conditions such as CKD.
BACKGROUND:Oxalate nephropathy is a rare disorder that can result in acute kidney injury (AKI) and progresses to end-stage kidney disease (ESKD). The causes can be either primary or secondary. Primary hyperoxaluria includes a group of hereditary disorders with enzymatic defects in the glyoxylate pathway, resulting in decreased oxalate metabolism. Secondary hyperoxaluria, often overlooked can result from increased intestinal absorption, nutritional deficiencies, decreased fluid intake, impaired excretion, and increased dietary consumption of oxalate. CASE PRESENTATION: We present a Caucasian case of acute oxalate induced nephropathy associated with consumption of large quantities of green vegetables in a patient with chronic kidney disease (CKD). Imaging study showed no evidence of kidney stone, but a kidney biopsy revealed acute tubular injury, tubular atrophy, interstitial fibrosis, and dense tubular deposition of calcium oxalate crystals. Upon further questioning the patient, we learned that in the months prior to presentation, he had very significantly increased his consumption of green vegetables. Because of no clinical improvement, the patient was initiated and maintained on hemodialysis. CONCLUSION: This report illustrates a case of acute oxalate nephropathy in the setting of very high dietary consumption of oxalate-rich foods in a patient with advanced CKD. Special attention should be given to the secondary causes of hyperoxaluria in patients with predisposing conditions such as CKD.
Authors: John C Lieske; Carla G Monico; W Scott Holmes; Erik J Bergstralh; Jeffrey M Slezak; Audrey L Rohlinger; Julie B Olson; Dawn S Milliner Journal: Am J Nephrol Date: 2005-06-15 Impact factor: 3.754