Health Human Disease Blog

Renal stone formation and its significant mor­bidity are common, affecting up to 5 per cent of the general population at least once during a life­time. Calcium, usually as calcium oxalate or cal­cium phosphate, is the most common constituent of renal calculi. Calcium is present in some form in almost 90 per cent of all renal stones. Uric acid, cystine, and magnesium are the other major stone constituents. Up to 75 per cent of all stones, com­posed predominantly of calcium oxalate, occur in the syndrome of idiopathic urolithiasis. About 5 per cent of calcium stone formation is attributable to hyperparathyroidism. Some degree of uric acid lithiasis is contributory to about 20 per cent of all renal calculi.

Urinary stone formation depends on a number of factors. The saturation of urine with a mineral is governed by the amount excreted and the vol­ume of urine in which it is contained. Urine is frequently supersaturated with respect to cal­cium. Crystallization from solution requires a nidus, or “seed,” upon which to grow, and crystal precipitation may be inhibited by certain com­pounds. Each of these elements is thought to be of importance in formation of renal calculi, but other mechanisms contribute to the process of urolithiasis.

Idiopathic urolithiasis, in which no underlying metabolic or infectious etiology is evident, ac­counts for the majority of cases of renal stone for­mation. Hypercalciuria, defined as the excretion of greater than 4 mg calcium/kg/24 hours, is seen in the absence of hypercalcemia in about 80 per cent of these cases. At least two subtypes of hy­percalciuria appear to exist: in “renal” hypercal­ciuria, a deficiency in renal calcium reabsorption appears to drive increased intestinal calcium ab­sorption, whereas in “absorptive” hypercalciuria, there is a primary increase in intestinal calcium absorption necessitating an increase in urinary calcium excretion. In both circumstances, serum calcium and phosphate levels are normal. Stone formation in idiopathic hypercalciuria is believed to depend heavily on the constant supersaturation of urine with calcium.

The cause of stone formation in patients with normal levels of urinary calcium excretion is less certain. However, hyperuricosuria has been ob­served in a large number of patients with idi­opathic urolithiasis and may coexist with hyper­calciuria in up to 20 per cent of patients. The finding of uric acid in calculi composed predom­inantly of calcium salts has led to the notion that uric acid crystals may serve as a nidus for calcium stone growth.

Secondary hypercalciuria, in which the serum calcium concentration may be found to be ele­vated, occurs in only 5 to 7 per cent of recurrent stone formers. Hyperparathyroidism, distal RTA, sarcoidosis, and hypervitaminosis D account for a large number of these cases.

Chronic urinary tract infection with urea-split­ting organisms (i.e., Proteus species] is associated with struvite (triple phosphate] stones containing magnesium and calcium. These frequently form as “staghorn” calculi, outlining the renal calyces. A vicious dependency develops in which urinary tract infection cannot be cleared owing to the presence of the foreign body (calculus] and stone formation continues as long as the urine is in­fected.

Passage of a renal stone is often the initial man­ifestation of renal stone disease and presents as ureteral colic, sharp unilateral flank pain that ra­diates to the groin. Hematuria is characteristically present in the urinalysis and crystalluria may be obvious. A plain abdominal radiograph will dem­onstrate the densely opaque calcium stones and the faintly opaque, sulfur-containing cystine stones. Only pure uric acid stones are radiolucent. An excretory urogram (IVP] may be required to demonstrate small stones or the site along the uri­nary tract at which a stone has lodged.

The workup for renal calculus is indicated in . Serial plain abdominal radiographs identify changes in stone size and number, serum calcium determinations identify hypercalcemic disorders associated with stone formation, and urine cultures identify etiological (urea-splitting] and complicating bacterial involvement. Hyper­calciuria and hyperuricosuria are identified by appropriate 24-hour urine collections. Any stone passed in the urine should be subjected to anal­ysis to determine its mineral composition.

Treatment of urolithiasis may be as simple as the promotion of a brisk diuresis to enhance spon­taneous passage of a stone. Surgical removal of stones may be required, especially when the urine is chronically infected or when renal compromise secondary to obstruction is evident. The major ef­fort of medical management is directed toward re­ducing the likelihood of stone growth and recur­rent formation.

In all cases, prevention of urolithiasis includes forced hydration with water to produce a dilute urine. This suffices to prevent recurrence in some individuals, especially in hot climates. If hyper­calcemia is present, parathyroidectomy for hy­perparathyroidism or specific therapy for the el­evation in serum calcium is indicated. In cases of idiopathic hypercalciuria, dramatic reductions in urinary calcium excretion and stone formation can be achieved with thiazide diuretics and salt-restricted diet. Thiazide therapy should reduce the 24-hour urinary calcium excretion by almost half. If hyperuricosuria coexists, the addition of allopurinol to reduce the uric acid load is advan­tageous. In fact, allopurinol may reduce calcium stone formation even in the absence of clear hy­peruricosuria. Successful treatment of struvite stones may require specific, long-term antibiotic therapy in combination with surgical lithotomy.