Oxalate metabolism in renal stone disease with special reference to calcium metabolism and intestinal absorption.
Hyperoxaluria and hypercalciuria are common features of renal calcium stone disease. The purpose of the present investigation was to examine the relationships between the intestinal absorption and the renal handling of oxalate and calcium in patients with idiopathic renal stone disease and in patients with enteric hyperoxaluria following jejunoileal bypass (JIB), in comparison with healthy controls. Hyperoxaluria was associated with a higher frequency of both stone episodes and stone operations than a lower urinary oxalate concentration. Patients with idiopathic stone disease showed increased intestinal uptake of both oxalate and calcium, which was probably of importance for their propensity to form calcium oxalate-containing stones. Hyperoxaluria in patients with JIB was found to be a result of hyperabsorption of oxalate, and these patients displayed altered oxalate kinetics with continued urinary excretion of orally administered 14C-oxalate for more than 48 hours. The prolonged excretion is assumed to be due to a prolonged absorption and/or an increased oxalate pool. Malabsorption of calcium and low fasting urinary calcium excretion in the JIB patients were associated with high tubular reabsorption of calcium, the latter presumably attributable to a compensatory increase in circulating parathyroid hormone (PTH). In most recurrent renal stone formers the urinary calcium concentration was increased, with an inverse relationship to serum PTH, indicating intestinal hyperabsorption of calcium. A subgroup of hypercalciuric patients showed increased urinary calcium due to reduced tubular reabsorption of calcium. It is suggested that this is a renal defect resulting in a compensatory rise in PTH. Two different mechanisms of similar prevalence might explain enhanced secretion of PTH in normocalcaemic stone disease, namely reduced calcium absorption and a renal defect in the form of reduced tubular reabsorption of calcium. Glycosaminoglycans efficiently inhibit calcium oxalate crystal growth by binding to the surface of calcium oxalate crystals. In this study the binding was dependent on ionic strength. Higher affinity to the crystals may be the reason why highly charged glycosaminoglycans were more efficient inhibitors of calcium oxalate crystal growth. A calcium-containing organic marine hydrocolloid with the capacity to bind oxalate in vitro was shown to reduce enteric hyperoxaluria. In addition to biochemical effects considerable improvements in diarrhoeal symptoms were reported.
Lindsjö
M
M
Department of Internal Medicine, University Hospital, Uppsala, Sweden.
D000328:Adult; D000368:Aged; D002118:Calcium / Q000008:administration & dosage / Q000378:metabolism* / Q000627:therapeutic use; D003102:Colloids; D005260:Female; D006025:Glycosaminoglycans / Q000037:antagonists & inhibitors; D006801:Humans; D007408:Intestinal Absorption; D007581:Jejunoileal Bypass; D007669:Kidney Calculi / Q000188:drug therapy / Q000378:metabolism*; D007684:Kidney Tubules / Q000503:physiopathology; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D010070:Oxalates / Q000097:blood / Q000378:metabolism* / Q000652:urine; D019815:Oxalic Acid; D010281:Parathyroid Hormone / Q000097:blood
D003102:Colloids; D006025:Glycosaminoglycans; D010070:Oxalates; D010281:Parathyroid Hormone; D019815:Oxalic Acid; D002118:Calcium