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

dc.contributor.authorEvan, Andrew P.
dc.contributor.authorCoe, Fredric L.
dc.contributor.authorConnors, Bret A.
dc.contributor.authorHanda, Rajash K.
dc.contributor.authorLingeman, James E.
dc.contributor.authorWorcester, Elaine M.
dc.contributor.departmentDepartment of Anatomy & Cell Biology, IU School of Medicineen_US
dc.date.accessioned2016-08-18T15:58:03Z
dc.date.available2016-08-18T15:58:03Z
dc.date.issued2015-04-15
dc.description.abstractHuman 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.en_US
dc.identifier.citationEvan, A. P., Coe, F. L., Connors, B. A., Handa, R. K., Lingeman, J. E., & Worcester, E. M. (2015). Mechanism by which shock wave lithotripsy can promote formation of human calcium phosphate stones. American Journal of Physiology - Renal Physiology, 308(8), F938–F949. http://doi.org/10.1152/ajprenal.00655.2014en_US
dc.identifier.issn1522-1466en_US
dc.identifier.urihttps://hdl.handle.net/1805/10728
dc.language.isoen_USen_US
dc.publisherAmerican Physiological Societyen_US
dc.relation.isversionof10.1152/ajprenal.00655.2014en_US
dc.relation.journalAmerican Journal of Physiology. Renal Physiologyen_US
dc.rightsPublisher Policyen_US
dc.sourcePMCen_US
dc.subjectCalcium Phosphatesen_US
dc.subjectUrineen_US
dc.subjectKidney Tubulesen_US
dc.subjectmetabolismen_US
dc.subjectLithotripsyen_US
dc.subjectadverse effectsen_US
dc.subjectNephrolithiasisen_US
dc.subjectRenal Eliminationen_US
dc.titleMechanism by which shock wave lithotripsy can promote formation of human calcium phosphate stonesen_US
dc.typeArticleen_US
ul.alternative.fulltexthttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398833/en_US
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