Hyperoxaluria and renal calculi.

Many Western countries are experiencing an epidemic of renal calculi, causing immediate problems with acute pain and morbidity together with worries for the future because of the likelihood of recurrent stone formation. Renal or ureteric colic is the commonest surgical admission diagnosis in this country and it has been suggested that up to 12 million Americans will suffer a stone episode during their lifetime.' Because of the scale of the clinical problem presented by renal colic, immediate and short-term management dominates the discussion with rather less attention paid to analysis of the factors involved in stone formation and prevention of recurrence. In view of the substantial costs of the treatment of kidney stones ($2 billion in 1986 in the USA alone2), this focus may not be altogether appropriate. Most upper tract stones are composed ofcalcium oxalate and the definition of 'idiopathic hypercalciuria' some 60 years ago has tended to emphasize the importance of increased urinary calcium excretion in their aetiology. However, in the last 10-15 years, it has become clear that quite small changes in urinary oxalate levels may have profound effects on the likelihood ofcalcium oxalate crystal formation and subsequent urolithiasis.3 The current interest in hyperoxaluria and its pathophysiology results from the development of accurate methods of measuring oxalate in blood and urine4'5 and advances in our understanding of the physical processes involved in urinary crystal formation.6 We review some current thinking on oxalate and renal calculi; a number of excellent recent reviews on the broader aspects of urolithiasis are also available.' 7-9