80-85% of all urinary stones are calcium containing. The majority are either calcium oxalate or calcium phosphate calculi but mixed stones are also common. Calcifications within the renal parenchyma (nephrocalcinosis) rarely cause symptoms and are associated with a number of pathological processes (i.e. renal tubular acidosis and hyperparathyroidism). Often nephrocalcinosis coexists with nephrolithiasis, although the converse is very uncommon. A number of metabolic abnormalities can predispose to calcium calculi and these are outlined below.
An excess of urinary calcium can arise from increased absorption from the small bowel (absorptive hypercalcuria), increased resorption of calcium from bones (resorptive hypercalcuria), from an intrinsic renal tubular defect (renal hypercalcuria), or it can also be idiopathic. For absorptive hypercalcuria cellulose, phosphate can be used, although this can result in a secondary hyperoxaluria, thus limiting its value. Alternatively, thiazide diuretics may be used but their effect is often not maintained over the long term. In type 2 disease, a reduction in calcium intake can prove beneficial. The treatment of renal hypercalcuria is uncertain but interest has developed around the role of prostaglandins in its aetiology. The use of NSAID’s and other agents that inhibit prostaglandin production (i.e. fish oil and evening primrose oil) may help reduce the urinary calcium concentration. Resorptive hypercalcuria is usually secondary to hyperparathyroidism, which should be looked for and treated if found. Other causes of hypercalcaemia (commonly malignancy) should also be excluded.
Hyperoxaluria is associated with calcium oxalate stone formation in three different circumstances. Primary oxaluria is a rare genetic disorder, enteric oxaluria follows increased absorption from malabsorption or short bowel syndrome and, finally, idiopathic stone formers often have mild hyperoxaluria. Primary oxaluria can be treated with pryidoxine and thiazide diuretics. Treatment of enteric disease is aimed at improving the predisposing condition, attempting to reduce absorption by decreasing intake, increasing binding of oxalate in the bowel (adding calcium carbonate, cholestyramine) and finally increasing fluid intake. Idiopathic hyperoxaluria can be treated with thiazide diuretics and pyridoxine and reduced oxalate intake.
Uric acid can promote calcium stone formation by facilitating the formation of nuclei. Treatment of hyperuricosuria is aimed at reducing purine intake (red meat, fish and poultry) but allopurinol is often used due to the poor compliance with this particular dietary restriction.