[New pathophysiologic aspects of nephrolithiasis].
Urinary supersaturation with stone-forming ions is the driving force of crystallization in renal tubules. Based on concentration measurements of the majority of ions, supersaturation can be calculated by means of a computer program. Assessments of 24-hour urine excretions of lithogenic substances do not necessarily detect intermittent supersaturation which may induce crystallization processes. Even the most elaborate metabolic evaluations fail to detect metabolic abnormalities in 10-30% of unselected patients with nephrolithiasis ("idiopathic" nephrolithiasis). Apart from supersaturation, crystal aggregation seems to be a most important factor in kidney stone formation whose pathophysiologic relevance has so far been underestimated. New studies demonstrate excellent inhibition of calcium oxalate monohydrate crystal aggregation by nephrocalcin and Tamm-Horsfall glycoprotein, 2 glycoproteins produced by the kidneys. In recurrent "idiopathic" calcium oxalate stone formers both proteins are structurally and functionally defective crystal aggregation inhibitors.
Hess
B
B
Nephrologische Station, Medizinische Klinik, Universitätsspital Zürich.
D002129:Calcium Oxalate / Q000037:antagonists & inhibitors / Q000494:pharmacology / Q000652:urine*; D003460:Crystallization; D006023:Glycoproteins / Q000494:pharmacology; D006801:Humans; D007669:Kidney Calculi / Q000503:physiopathology*; D007671:Kidney Concentrating Ability; D007684:Kidney Tubules / Q000503:physiopathology; D009088:Mucoproteins / Q000502:physiology; D058949:Uromodulin
D006023:Glycoproteins; D009088:Mucoproteins; C548612:UMOD protein, human; D058949:Uromodulin; C029490:nephrocalcin; D002129:Calcium Oxalate
Neue pathophysiologische Aspekte der Nephrolithiasis.