The present investigation was undertaken to elucidate the mechanisms of renal calcium and magnesium wastage in patients with urinary diversion through intestinal segments. Patients with urinary intestinal diversions demonstrated a hyperchloremic metabolic acidosis, increased serum sulfate and phosphate, and increased urinary excretion of calcium, phosphate, sulfate, and magnesium. A study was conducted in rats utilizing oral or intravenous loads of various solutes to investigate the possible mechanisms of these findings in patients. Ammonium enhances renal sulfate excretion and intestinal sulfate absorption. Increased filtered loads of sulfate inhibit renal tubule sodium and calcium reabsorption. Dietary ammonium and sulfate result in increased serum phosphorous concentrations. Ammonium appears to directly inhibit renal magnesium reabsorption. Renal tubule dysfunction resulting from relieved obstruction appears to enhance the inhibitory effect of sulfate on renal sodium and calcium reabsorption but does not alter the effect of ammonium on renal magnesium excretion. Taken together, these findings suggest that patients with hyperchloremic metabolic acidosis from the chronic reabsorption of ammonium chloride by intestinal urinary diversions may also reabsorb urinary sulfate. This load of ammonium and sulfate inhibits renal calcium and magnesium reabsorption.