Kidney stones (nephrolithiasis) will occur in 12% of men and 5% of women during their lifetime. Thus, this is a very common disease. The major types of stones are calcium (70%-80%, oxalate more common than phosphate), uric acid (5%-10%), cystine (<1%), and magnesium ammonium phosphate (struvite) (10%). Combined calcium/urate stones are also often seen. A patient with a calcium-containing stone episode has an overall 50% chance of recurrence within 10 years, which is higher for men than for women. Some patients will have many recurrent stones, leading to substantial morbidity, medical costs, and even mortality. Yet too many nonnephrologists continue to view stone disease as a urologic, that is, surgical, disease rather than a nephrologic, that is, medical, disease. This is very unfortunate, as medical therapy can substantially lower the risk of recurrent stones.
Most kidney stones contain calcium. Idiopathic hypercalciuria is the most common etiology of calcium stones. This is a multigenic autosomal dominant disease. The exact pathogenesis is uncertain, and may have different etiologies in different patients, which include renal phosphorus and/or calcium leak, intestinal hyperabsorption, and increased bone resorption. Risk factors for calcium stones include higher urinary calcium excretion (
Marshall et al., 1972), lower urinary volume, higher urinary oxalate excretion (calcium oxalate stones), higher urinary uric acid excretion (uric acid serves as a nidus for calcium stone formation), lower urinary citrate excretion (citrate is a stone inhibitor), higher urinary pH (calcium phosphate stones form in alkaline urine), and anatomic
abnormalities (medullary sponge kidney, horseshoe kidney). In one study, over 60% of patients with calcium stones had hypercalciuria, over one-third had hyperuricosuria and over one-fourth had hypocitraturia (
Levy et al., 1995) (
Table 20.1).
EVALUATION OF PATIENTS WITH RECURRENT KIDNEY STONES
Patients with recurrent calcium stones require metabolic evaluation to detect biochemical abnormalities, which, if corrected, will lessen the chance of recurrence. Of course, hypercalcemia should be excluded, as such patients are generally also hypercalciuric and treatment of the etiology of hypercalcemia should correct the stone problem. Occasionally, patients may have an underlying distal renal tubular acidosis (RTA), resulting in bone resorption and hypercalciuria. A clue to the presence of RTA is the development of calcium phosphate rather than calcium oxalate stones, which are preferentially formed when the urine pH is elevated. Enteric hyperoxaluria can be seen in malabsorption syndromes such as inflammatory bowel disease and after bariatric surgery. In this disorder, fat malabsorption results in increased binding of calcium to fat and decreased binding of calcium to oxalate in the gut, resulting in more free oxalate available for absorption by the colon; in addition, bile salt-induced increase in colonic oxalate absorption contributes to hyperoxaluria (
Smith et al., 1972;
Chadwick et al., 1973;
Nasr et al., 2008).
Determination of the type of stone and evaluation for biochemical abnormalities or underlying conditions that predispose to stone formation are essential for guiding therapy to prevent recurrent disease. Spontaneously passed or surgically removed stones should undergo stone
analysis. Patients presenting with their first stone require a careful dietary history (
Table 20.2) and a limited laboratory evaluation to exclude hypercalcemia (such as with primary hyperparathyroidism) or hyperchloremic acidosis (such as with distal RTA). A complete metabolic evaluation is indicated in patients with recurrent stones or multiple stones at first presentation (for instance, a stone passage episode accompanied by one or more stones seen in the kidneys on imaging studies). Patients with a strong family history of stones should also undergo a complete metabolic evaluation, as such patients are likely to have idiopathic hypercalciuria. Some have also a recommended a complete metabolic evaluation in patient at high risk for recurrent stone formation (
Preminger, 1989) (
Table 20.3).