Update on Oxalate Crystal Disease

The primary goal of this study was to test the hypothesis that Oxalobacter colonization alters colonic oxalate transport thereby reducing urinary oxalate excretion. In addition, we examined the effects of intraluminal calcium on Oxalobacter colonization and tested the hypothesis that endogenously derived colonic oxalate could be degraded by lyophilized Oxalobacter enzymes targeted to this segment of the alimentary tract. Oxalate fluxes were measured across short-circuited, in vitro preparations of proximal and distal colon removed from Sprague-Dawley rats and placed in Ussing chambers. For these studies, rats were colonized with Oxalobacter either artificially or naturally, and urinary oxalate, creatinine and calcium excretions were determined. Colonized rats placed on various dietary treatment regimens were used to evaluate the impact of calcium on Oxalobacter colonization and whether exogenous or endogenous oxalate influenced colonization. Hyperoxaluric rats with some degree of renal insufficiency were also used to determine the effects of administering encapsulated Oxalobacter lysate on colonic oxalate transport and urinary oxalate excretion. We conclude that in addition to its intraluminal oxalate-degrading capacity, Oxalobacter interacts physiologically with colonic mucosa by inducing enteric oxalate secretion/excretion leading to reduced urinary excretion. Whether Oxalobacter, or products of Oxalobacter, can therapeutically reduce urinary oxalate excretion and influence stone disease warrants further investigation in long-term studies in various patient populations.

Hyperoxaluria and increased calcium oxalate stone formation occur after Roux-en-Y gastric bypass (RYGB) surgery for morbid obesity. The etiology of this hyperoxaluria is unknown. We hypothesized that after bariatric surgery, intestinal hyperabsorption of oxalate contributes to increases in plasma oxalate and urinary calcium oxalate supersaturation. We prospectively examined oxalate metabolism in 11 morbidly obese subjects before and 6 and 12 months after RYGB (n = 9) and biliopancreatic diversion-duodenal switch (BPD-DS) (n = 2). We measured 24-hour urinary supersaturations for calcium oxalate, apatite, brushite, uric acid, and sodium urate; fasting plasma oxalate; 72-hour fecal fat; and increases in urine oxalate following an oral oxalate load. Six and 12 months after RYGB, plasma oxalate and urine calcium oxalate supersaturation increased significantly compared with similar measurements obtained before surgery (all P ≤ .02). Fecal fat excretion at 6 and 12 months was increased (P = .026 and .055, 0 vs 6 and 12 months). An increase in urine oxalate excretion after an oral dose of oxalate was observed at 6 and 12 months (all P ≤ .02). Therefore, after bariatric surgery, increases in fecal fat excretion, urinary oxalate excretion after an oral oxalate load, plasma oxalate, and urinary calcium oxalate supersaturation values were observed. Enteric hyperoxaluria is often present in patients after the operations of RYGB and BPD-DS that utilize an element of intestinal malabsorption as a mechanism for weight loss. Copyright © 2011 Mosby, Inc. All rights reserved.

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. 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. 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. 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.