Prevalence of hyperoxaluria after bariatric surgery.

PURPOSE: Recent investigations have shown increased oxalate excretion in patients in whom kidney stones formed after contemporary bariatric surgery. We determined whether there is an increased prevalence of hyperoxaluria after such procedures performed in nonstone formers. MATERIALS AND METHODS: A total of 58 nonstone forming adults who underwent laparoscopic Roux-en-Y (52) or a biliopancreatic diversion-duodenal switch procedure (6) collected 24-hour urine specimens 6 months or greater after bariatric surgery. Standard stone risk parameters were assessed. Comparisons were made with a group of healthy nonstone forming adults and stone formers in a commercial database. RESULTS: The bariatric group had a significantly higher mean urinary oxalate excretion compared to that in controls and stone formers (67.2 vs 34.1 and 37.0 mg per day, respectively, p <0.001). Mean oxalate excretion of patients who underwent a biliopancreatic diversion-duodenal switch procedure was higher than in the Roux-en-Y group (90 vs 62 mg per day, p <0.05). There was a significant correlation between urine oxalate excretion on the 2 collection days but some patients showed significant variability. Of the patients 74% showed hyperoxaluria in at least 1, 24-hour urine collection and 26% demonstrated profound hyperoxaluria, defined as oxalate excretion more than 100 mg per day, in at least 1 collection. This occurred in 3 of the 6 patients in the biliopancreatic diversion-duodenal switch group and in 12 of the 52 in the Roux-en-Y cohort. Hyperoxaluria was not uniformly expressed. CONCLUSIONS: There is a high prevalence of hyperoxaluria in patients without a history of kidney stones who undergo bariatric surgery. A significant proportion of these patients have profound hyperoxaluria, which is not uniformly expressed.

Crystal-associated nephropathy in patients with brushite nephrolithiasis.

BACKGROUND: We have biopsied the renal cortex and papillae of patients who form brushite renal stones asking if this unusual stone type is associated with specific tissue changes. We contrasted these with biopsies of 15 calcium oxalate stone formers, three stone formers with intestinal bypass, and four normal subjects. METHODS: We studied all ten brushite stone formers treated with percutaneous nephrolithotomy (PNL) during the past 3 years using digital video imaging of renal papillae, and obtained cortical and papillary biopsies. Biopsies were analyzed by light and electron microscopy, microinfrared spectroscopy, and electron diffraction. RESULTS: Apatite crystals plugged scattered terminal collecting ducts whose cells were injured or dead, and surrounding interstitium inflamed and fibrotic. White papillary deposits of interstitial apatite particles, so called Randall's plaque, were also present. Glomerular changes and cortical tubular atrophy and interstitial fibrosis were moderate to severe. CONCLUSION: Brushite stone formers combine the interstitial plaque of calcium oxalate stone formers with the collecting duct apatite plugs found in stone formers with intestinal bypass. Collecting duct injury and interstitial fibrosis are severe. Prominent cortical fibrosis, tubule atrophy, and glomerular pathology seem secondary to the collecting duct plugging. We believe crystallization obstructs and destroys terminal collecting duct segments thereby damaging nephrons, perhaps via intranephronal obstruction, and producing a hitherto unrecognized renal disease.