title: [Pathophysiology, diagnosis and conservative therapy of non-calcium kidney calculi].
abstract: While calcium oxalate and calcium phosphate make up at least 80% of all kidney stones, infection-induced and uric acid stones occur in 10% and 8%, respectively. Although any type of stone may become infected, the term "infection stones" means that stone formation exclusively depends on urease-producing bacteria. The splitting of urea leads to a rise in urinary pH which may induce crystallization of struvite (magnesium-ammonium-phosphate), the major constituent of infection stones, or carbonate apatite. Struvite stones account for the majority of staghorn calculi. They can grow quite large and may fill the entire collecting system. Patients with struvite stones may present with acute flank pain or remain completely asymptomatic. The cure of infection stones requires complete removal of the stone material. For uric acid crystallization and stone formation, low urine pH (below 5.5) is a more important risk factor than increased urinary uric acid excretion. Main causes of low urine pH are tubular disorders (including gout), chronic diarrheal states or severe dehydration. Accordingly, the treatment of uric acid stones consists not only of hydration (urine volume above 2000 ml per day), but mainly of urine alkalinization to pH values between 6.2 and 6.8. Urinary uric acid excretion can be reduced by a low-purine diet as well as--in case of recurrent uric acid stones and/or gout--by allopurinol. Cystinuria is a rare hereditary gene disorders with impaired tubular reabsorption of cystine. Stone formation occurs as a consequence of cystine's relatively low solubility at urine pH levels below 8. Only symptomatic diet and drug treatments are currently available, with urine dilution and urine alkalinization being the most efficient ones. Cystine stones respond poorly to shockwave lithotripsy, so that invasive procedures may regularly be necessary. 2,8-dihydroxy-adenine stones occur as a consequence of an enzyme deficiency that involves purine metabolism. These resulting stones are not visible by fluoroscopy and are therefore often misinterpreted as uric acid stones. Low-purine diet and allopurinol reduce the frequency of stone formation.
authors.affiliation: Urologische Universitätsklinik, Inselspital, Bern.
authors.forename: W
authors.initials: W
authors.lastname: Hochreiter
authors.forename: Th
authors.initials: T
authors.lastname: Knoll
authors.forename: B
authors.initials: B
authors.lastname: Hess
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology; D001419:Bacteria / Q000201:enzymology; D017610:Calcium Compounds / Q000652:urine*; D003553:Cystine / Q000378:metabolism*; D003555:Cystinuria / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology; D006801:Humans; D007669:Kidney Calculi / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D012307:Risk Factors; D014510:Urease / Q000502:physiology; D014527:Uric Acid / Q000652:urine*; D014552:Urinary Tract Infections / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*
chemical_list: D017610:Calcium Compounds; D014527:Uric Acid; D003553:Cystine; D014510:Urease