Pathogenesis and clinical manifestations of struvite stones
- Authors
- Glenn M Preminger, MD
Glenn M Preminger, MD
- Section Editor — Renal Ureteral Stones
- Professor of Urologic Surgery
- Duke University Medical Center
- Director of Education
- Endourological Society
- Gary C Curhan, MD, ScD
Gary C Curhan, MD, ScD
- Section Editor — Chronic Kidney Disease
- Professor of Medicine
- Harvard Medical School
- Section Editor
- Stanley Goldfarb, MD
Stanley Goldfarb, MD
- Editor-in-Chief — Nephrology
- Section Editor — Mineral and Bone Metabolism; Renal Ureteral Stones
- Professor of Medicine
- University of Pennsylvania School of Medicine
- Deputy Editor
- Albert Q Lam, MD
Albert Q Lam, MD
- Deputy Editor — Nephrology
- Assistant Professor of Medicine
- Harvard Medical School
INTRODUCTION
Struvite stones may grow rapidly over a period of weeks to months and, if not adequately treated, can develop into a staghorn or branched calculus that fills the entire intrarenal collecting system. A review of the pathogenesis and clinical manifestations of struvite stones will be presented here. The management of these stones is discussed separately. (See "Management of struvite or staghorn calculi".)
PATHOGENESIS
Struvite stones are composed of magnesium ammonium phosphate (struvite) and calcium carbonate-apatite [1]. Normal urine is undersaturated with ammonium phosphate, and struvite stone formation occurs only when ammonia production is increased and the urine pH is elevated, which decreases the solubility of phosphate. The only situation in which this occurs in humans is with an upper urinary tract infection with a urease-producing organism, such as Proteus or Klebsiella. Urease breaks down urinary urea into ammonia plus carbon dioxide:
Urea —> 2NH3 + CO2
The ammonia produced by this reaction then combines with water:
NH3 + H2O —> NH4+ + OH-
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