Abstract

Calcium oxalate renal stones (RS) and hyperoxaluria are common in patients with inflammatory bowel disease (IBD). The absence of intestinal oxalate degrading bacteria, Oxalobacter formigenes, may cause hyperoxaluria in IBD. The aim of the present study was to examine: (i) the colonization of O. formigenes in patients with IBD and controls and to correlate its presence with urinary oxalate excretion; and (ii) urinary analytes contributing to RS in IBD. Stool samples were studied for O. formigenes using polymerase chain reaction and Southern blotting in patients with IBD (n = 48: ulcerative colitis, 37; Crohn's disease, 11), RS (n = 87) and healthy subjects that were used as controls (n = 48). Levels of urinary oxalate, citrate, calcium, magnesium, creatinine and uric acid were estimated spectrophotometrically in each patient and in 13 controls for 24 h. Five of the 48 (10.4%) patients with IBD had RS. Five of the 48 (10.4%) patients with IBD, 25 of the 87 (29%) with RS and 27 of the 48 (56%) controls were colonized with O. formigenes (P < 0.001 for RS vs controls and P = 0.01 for RS vs IBD). Patients without O. formigenes had higher urinary oxalate than those with it (IBD, median 0.48 [range 0.11-2.09]vs 0.43 [range 0.16-1.10] mmol/24 h, P = NS; RS, median 0.59 mmol/24 h, range 0.14-1.90 vs 0.44 mmol/24 h, range 0.23-0.97; P = 0.008, Mann-Whitney U-test). Median excretion of oxalate was higher in IBD and RS than in controls (0.47 [0.11-2.09], 0.56 [0.14-1.9] and 0.41 [0.21-0.62] mmol/24 h; P < 0.01), respectively. Median calcium was also higher in IBD and RS than in controls (6.50 [1.38-21.00], 6.78 [1.55-20.30] and 4.99 [1.47-9.60] mmol/24 h; P < 0.05, Kruskal-Wallis H-test), respectively. Median urinary magnesium was higher in IBD than in RS and controls (4.57 [1.50-12.30], 3.60 [0.90-6.35] and 2.49 [0.74-4.80]; P < 0.001, Kruskal-Wallis H-test), respectively. Urinary citrate excretion was comparable in IBD, RS and controls. Patients with IBD and RS rarely have O. formigenes in their stools as compared with controls; this may contribute to hyperoxaluria in IBD. Hyperoxaluria and hypercalciuria may contribute to RS in patients with IBD. Hypermagnesuria in patients with IBD may protect them from RS.

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