Pathophysiology,diagnosis and conservative therapy in calcium kidney calculi

Annual incidences of kidney stones are about 0.1-0.4% of the population, and lifetime prevalences in the USA and Europe range between 8 and 15%. Kidney stones occur more frequently with increasing age and among men. Within ten years, the disease usually recurs in more than 50% of patients. Nowadays, about 85% of all kidney stones contain calcium salts (calcium oxalate and/or calcium phosphate) as their main crystalline components. Because human urine is commonly supersaturated with respect to calcium salts as well as to uric acid, crystalluria is very common, i.e. healthy people excrete up to ten millions of microcrystals every day. Recurrent stone formers appear to excrete lower amounts or structurally defective forms of crystallization inhibitors which allows for the formation of large crystal aggregates as precursors of stones. Alternatively, crystal adhesion to urothelial surfaces may be enhanced in stone formers. Medical treatment of renal colic is based on nonsteroidal antiinflammatory drugs, because prostaglandins appear to play a crucial role in the pathophysiology of pain during ureteral obstruction. In addition, centrally acting analgesics such as pethidine-HCl may be required in many cases. The administration of high amounts (3-4 liters/day) of intravenous fluids should be abandoned, since it may raise intraureteral pressure whereby pain increases and kidney pelvis or fornices may rupture. All first-stone formers should undergo a simple basic evaluation, including stone analysis (x-ray diffraction or infrared spectrometry), serum values of ionized calcium (alternatively: total calcium and albumin) and creatinine, urinalysis and repeated measurements of fasting urine pH in order to detect urinary acidification disorders or low urine pH. In high-risk patients with as first stone episode (i.e. strongly positive family history, inflammatory bowel disease, short-bowel syndrome, nephrocalcinosis, bilateral stones, hypercalcemia, renal tubular acidosis, airline pilots) as well as in all recurrent stone formers, an extended metabolic evaluation should be performed. Two 24-hurines should be collected on free-choice diet not prior to three months after stone passage or urological intervention. Analysis includes measurements of volume, creatinine, calcium, oxalate, uric acid and citrate; sodium and urea as markers of salt and protein consumption are optional but clinically very helpful. Since hypercalciuria is of much less importance than increases in urinary oxalate, therapeutic efforts should primarily focus on lowering urinary oxalate excretion. Sufficient calcium intake, i.e. 1200 mg per day, is crucial, because it allows for binding of oxalate at the intestinal level whereby increases of urinary oxalate (reciprocal hyperoxaluria) can be avoided. Excess intake of flesh protein (meat, fish, poultry) is lithogenic since it increases urinary calcium, oxalate and uric acid, and lower citrate. On the other hand, a diet rich in alkali (vegetables, fruit) is associated with a lower risk of stone formation. A "common sense diet" containing sufficient amounts of fluids, 1200 mg of calcium per day and reduced amounts of flesh protein as well as salt is able to reduce the 5-year stone recurrence rate in calcium stone formers by 50%. The scientific evidence for drug treatment (thiazides, alkali citrate) is rather poor: the most widely quoted randomized thiazide trial included only 42 patients of whom 36% left the protocol prematurely, whereas 36-48% of patients included in three randomized studies with alkali citrate suffered from undesirable side-effects; nevertheless, citrate therapy reduced the stone recurrence rate by 38%, compared with 22% in patients on placebo treatment (p < 0.0005).