Oxalate nephropathy complicating Roux-en-Y Gastric Bypass: an underrecognized cause of irreversible renal failure

Samih H Nasr, Vivette D D'Agati, Samar M Said, Michael B Stokes, Maria V Largoza, Jai Radhakrishnan, Glen S Markowitz, Samih H Nasr, Vivette D D'Agati, Samar M Said, Michael B Stokes, Maria V Largoza, Jai Radhakrishnan, Glen S Markowitz

Abstract

Background and objectives: The most common bariatric surgery is Roux-en-Y gastric bypass (RYGB), which has been associated with hyperoxaluria and nephrolithiasis. We report a novel association of RYGB with renal insufficiency as a result of oxalate nephropathy.

Design, setting, participants, & measurements: Eleven cases of oxalate nephropathy after RYGB were identified from the Renal Pathology Laboratory of Columbia University. The clinical features, pathologic findings, and outcomes are described.

Results: Patients were predominantly white (72.7%) with a mean age of 61.3 yr. Indications for RYGB included morbid obesity (eight patients) and reconstruction after total gastrectomy for gastric cancer (three patients). All 11 patients had a history of hypertension, and 9 were diabetic. Patients presented with acute renal failure, often superimposed on mild chronic renal insufficiency (n = 7), at a median of 12 mo after RYGB. The mean creatinine at baseline, at discovery of acute renal failure, and at biopsy was 1.5, 5.0, and 6.5 mg/dl, respectively. Renal biopsies revealed diffuse tubular degenerative changes, abundant tubular calcium oxalate deposits, and varying degrees of tubulointerstitial scarring. In addition, seven biopsies had underlying diabetic glomerulosclerosis and two had glomerulosclerosis attributable to obesity and hypertension. Eight of 11 patients rapidly progressed to ESRD and required hemodialysis at a mean of 3.2 wk after renal biopsy. The remaining three patients were left with significant chronic kidney disease.

Conclusions: Oxalate nephropathy is an underrecognized complication of RYGB and typically results in rapid progression to ESRD. Patients with pre-existing renal disease may be at higher risk for this complication.

Figures

Figure 1.
Figure 1.
Pathologic findings in oxalate nephropathy. (A) A low-power view shows diffuse tubular degenerative changes with numerous intracellular and intraluminal tubular calcium oxalate deposits. A normal-appearing glomerulus also is present. (hematoxylin and eosin [H&E]). (B) The same field as A is shown under polarized light. The calcium oxalate crystals are more easily identified (H&E). (C) At high magnification, the calcium oxalate deposits form intraluminal translucent crystals (H&E). (D) In this field, the calcium oxalate crystals are smaller and lie within the cytoplasm of tubular epithelium. Tubules exhibit prominent degenerative changes including luminal ectasia, cytoplasmic simplification, and loss of brush border (H&E). Magnifications: ×40 in A and B; ×400 in C and D.

Source: PubMed

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