Urinary MCP1 and Microalbumin Increase Prior to Onset of Azotemia in Mice with Polycystic Kidney Disease

摘要

Urinarybiomarkersmayofferamoresensitiveandlessinvasivemeanstomonitorkidneydiseasethantraditionalbloodchemistrybiomarkerssuchascreatinine.CD1suppcy/pcy/sup(pcy)micehaveaslowlyprogressivediseasephenotypethatresembleshumanautosomaldominantpolycystickidneydiseasewithrenalcystformationandinflammation.Previousreportssuggestthatdietaryproteinrestrictionmayslowdiseaseprogressioninmiceandhumanswithpolycystickidneydisease.Accordingly,wefedpcymiceeitherastandardchow(22.5%protein)oraprotein-restricted(11.5%soy-basedprotein)dietfromweaninguntil34wkofage.Every6wkwemeasuredmarkersofkidneydisease,includingserumcreatinine,BUN,andserumalbuminaswellasurinarymonocytechemoattractantprotein1(MCP1),microalbumin,andspecificgravity.Progressionofkidneydiseasewasequivalentforbothdietgroupsdespitedietaryproteinrestriction.Urinarybiomarkersprovedusefulforearlydetectionofdisease,inthaturinarymicroalbuminwaselevatedasearlyas22wkofageandurinaryMCP1wasincreasedby28wkofage,whereasincreasesinserumcreatinineandBUNweredetectedlater(at34wkofage)inbothdietgroups.Thus,urinarymicroalbuminandMCP1analysesprovidedearlier,noninvasiveindicatorsfordetectionofkidneydiseaseanddiseaseprogressioninpcymicethandidserumcreatinineandBUN.