Abstract: PUB384
Crystalline Nephropathy: A Hidden Complication of Bariatric Surgery
Session Information
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Padodara, Aakash, University of Miami Health System, Miami, Florida, United States
- Kaufman, Katelyn, University of Miami Health System, Miami, Florida, United States
- Fernandez Bojanini, Carlos A., University of Miami Health System, Miami, Florida, United States
- Valle, Gabriel A., University of Miami Health System, Miami, Florida, United States
Introduction
Oxalate nephropathy (ON) is an uncommon etiology of kidney disease characterized by the accumulation of calcium oxalate crystals in the renal parenchyma. It is a pleomorphic disorder which can present as Acute or Chronic Kidney injury and frequently progresses to end stage renal disease. Although the exact prevalence of this condition is unknown, ON was identified in 1% of 2265 consecutive kidney biopsies and it is often associated with specific conditions such as primary and enteric hyperoxalurias or ethylene glycol toxicity.
Case Description
A 74-year-old male with type 2 diabetes, heart failure with preserved exection fraction, atrial fibrillation, CVA, and chronic kidney disease 3b and morbid obesity s/p remote Roux-en-Y gastric bypass (RNYGB) was noted to develop rapidly progressive deterioration of his kidney function following an episode of Herpes Zoster infection treated with Valacyclovir . After 6 weeks of conservative management his eGFR declined to 8 mL/min/1.73m2 and was associated with insidious uremic symptoms necessitating hospitalization for initiation of dialysis. A kidney biopsy showed diffuse severe epithelial cell injury with features consistent with ON, diabetic glomerulosclerosis, Class IIa, moderate interstitial fibrosis, 18% global glomerular sclerosis and arteriosclerosis.
Discussion
The mechanism of ON in gastric bypass surgery, specifically jejunoileal bypass and RYGB surgery, encompasses increased dietary oxalate availability as undigested fatty acids bind to intraluminal calcium in the small intestine leaving a large load of unbound oxalate to be absorbed in the colon. Subsequent hyperoxaluria and the formation of calcium oxalate crystals within the tubules and renal parenchyma cause tubular obstruction, interstitial inflammation and scarring. ON remains largely an unsuspected diagnosis, is progressive in nature and has a poor prognosis. Clinicians should recognize the potential risks of this hyper absorptive complication of RYGB in patients who develop renal dysfunction and institute measures to forestall the progression of this disorder.