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.