Urolithiasis in patients with inflammatory bowel disease – possibilities of prevention and metabolic influence

Inflammatory bowel diseases (IBD) are typically accompanied by diarrhoea and frequently by malabsorption, both of which are predisposing factors for the formation of renal calculi. In patients who have not undergone bowel surgery the prevalence of urolithiasis has ranged from 1.5 to 5%, but after surgery, stone prevalence can increase to up to 16%. Enteric hyperoxaluria is a frequent complication of inflammatory bowel diseases after ileal-coecal resection, ileostomy, colostomy resection and bariatric surgery. The excess of oxalate is primarily excreted by the kidneys. Increased urinary excretion of oxalate results in urinary calcium oxalate supersaturation, leading to crystal aggregation, urolithiasis, and/or nephrocalcinosis. Prevention of oxalate lithiasis includes high fluid intake, nutritionally balanced low-oxalate, low-fat, low-salt diet, prescription of oral citrate and magnesium, calcium supplement, and also biological manipulation of intestinal flora (microbiota). In IBD patients, urolithiasis can be associated with serious urinary tract infection – in some cases asymptomatic – which can lead to chronic renal insufficiency and failure. New therapeutic approaches to patients with inflammatory bowel diseases have completely changed the natural history of these diseases with reduced number of bowel surgery. Whether this has changed the prevalence and risk factors for urinary calculi in patients with inflammatory bowel diseases is still unknown.