Literature DB >> 25656372

Mechanism by which shock wave lithotripsy can promote formation of human calcium phosphate stones.

Andrew P Evan1, Fredric L Coe2, Bret A Connors3, Rajash K Handa3, James E Lingeman4, Elaine M Worcester5.   

Abstract

Human stone calcium phosphate (CaP) content correlates with higher urine CaP supersaturation (SS) and urine pH as well as with the number of shock wave lithotripsy (SWL) treatments. SWL does damage medullary collecting ducts and vasa recta, sites for urine pH regulation. We tested the hypothesis that SWL raises urine pH and therefore Cap SS, resulting in CaP nucleation and tubular plugging. The left kidney (T) of nine farm pigs was treated with SWL, and metabolic studies were performed using bilateral ureteral catheters for up to 70 days post-SWL. Some animals were given an NH4Cl load to sort out effects on urine pH of CD injury vs. increased HCO3 (-) delivery. Histopathological studies were performed at the end of the functional studies. The mean pH of the T kidneys exceeded that of the control (C) kidneys by 0.18 units in 14 experiments on 9 pigs. Increased HCO3 (-) delivery to CD is at least partly responsible for the pH difference because NH4Cl acidosis abolished it. The T kidneys excreted more Na, K, HCO3 (-), water, Ca, Mg, and Cl than C kidneys. A single nephron site that could produce losses of all of these is the thick ascending limb. Extensive injury was noted in medullary thick ascending limbs and collecting ducts. Linear bands showing nephron loss and fibrosis were found in the cortex and extended into the medulla. Thus SWL produces tubule cell injury easily observed histopathologically that leads to functional disturbances across a wide range of electrolyte metabolism including higher than control urine pH.
Copyright © 2015 the American Physiological Society.

Entities:  

Keywords:  histopathology; pH regulation; renal function; thick ascending limb

Mesh:

Substances:

Year:  2015        PMID: 25656372      PMCID: PMC4398833          DOI: 10.1152/ajprenal.00655.2014

Source DB:  PubMed          Journal:  Am J Physiol Renal Physiol        ISSN: 1522-1466


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