Epidemiology: The annual incidence of urolithiasis in the population is at least 0.1%. In rural areas, there are remarkably less actual stone formers than in urban districts, and also vegetarians show less stone diseases. Calcium carbonate as a urinary calculus compound is not in the strict sense impossible, but often an artifact. About 10% of homocygotic cystinuria patients never suffer an actual stone disease. Pathogenesis: It is obvious that for stone formation urinary supersaturation alone is not sufficient. Besides the well-known inhibitors like citrate, magnesium and pyrophosphate there have to be other important urinary constituents. Risk factors are high protein or glucose intakes and, in general, hyperalimentation, simply because any food has to be deplenished somehow and increases the urine concentration. A special cause may be found in alterations of the renal tubuli. Diagnostic: For the quite difficult oxalate analysis, an enzymatic test is commercially available. Up to now, the most important analytical task in urolithiasis is still the correct analysis of urinary calculi. Qualitative chemical analysis shows up to 50% erroneous results, leading to false therapies. To determine the calculus compounds the best appropriate method is by far the X-ray diffraction analysis. Therapy: The results with adsorption medicines are contradictory. Satisfactory therapies are given for uricosuria with allopurinol and for oxaluria with pyridoxine. A new therapy for cystinuria may be the combined application of ascorbic acid and sodium hydrogen carbonate.

Keywords:
Epidemiology, Pathogenesis, Diagnostic, Therapy
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© 1981 S. Karger AG, Basel
1981
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