2017
Intraperitoneal pyrophosphate treatment reduces renal calcifications in Npt2a null mice
Caballero D, Li Y, Fetene J, Ponsetto J, Chen A, Zhu C, Braddock DT, Bergwitz C. Intraperitoneal pyrophosphate treatment reduces renal calcifications in Npt2a null mice. PLOS ONE 2017, 12: e0180098. PMID: 28704395, PMCID: PMC5509111, DOI: 10.1371/journal.pone.0180098.Peer-Reviewed Original ResearchConceptsRenal calcificationCompared to WT miceElevated urinary excretionRenal stone diseaseNucleotide pyrophosphatase phosphodiesterase 1WT miceDietary calciumUrinary excretionIntraperitoneal administrationStone diseaseNull miceMouse mutationMiceCalcificationNephrocalcinosisNpt2aDisordersUnrecognized factorsContribution of genotypePresent studyPhosphodiesterase 1PPINpt2cPatientsNephrolithiasisResponse of Npt2a knockout mice to dietary calcium and phosphorus
Li Y, Caballero D, Ponsetto J, Chen A, Zhu C, Guo J, Demay M, Jüppner H, Bergwitz C. Response of Npt2a knockout mice to dietary calcium and phosphorus. PLOS ONE 2017, 12: e0176232. PMID: 28448530, PMCID: PMC5407772, DOI: 10.1371/journal.pone.0176232.Peer-Reviewed Original ResearchConceptsCompared to WT miceWT miceDietary calciumDietary phosphateCalcium x phosphorus productUrine phosphate levelsUrinary calcium excretionUrine anion gapDevelopment of novel therapiesWild-typeRenal stone diseaseWild-type miceNpt2a-knockout (KO) miceCalcium excretionFGF23 levelsNovel therapiesPreventing nephrolithiasisPlasma phosphateStone diseaseAnion gapAddition of calciumKnockout micePhosphorus productCalcium phosphate depositionHuman carriers
2016
Impaired urinary osteopontin excretion in Npt2a−/− mice
Caballero D, Li Y, Ponsetto J, Zhu C, Bergwitz C. Impaired urinary osteopontin excretion in Npt2a−/− mice. American Journal Of Physiology. Renal Physiology 2016, 312: f77-f83. PMID: 27784695, PMCID: PMC5283892, DOI: 10.1152/ajprenal.00367.2016.Peer-Reviewed Original ResearchConceptsOPN gene expressionUrinary excretionRenal phosphate wasting disordersHigh-phosphate dietPhosphate wasting disordersOral phosphate supplementationRenal gene expressionRenal stone diseaseGene expressionAdditional risk factorsOPN levelsRole of OPNWasting disordersStone diseaseUrine excretionMouse modelNpt2aRisk factorsMouse mutationPhosphate supplementationRenal phosphateMiceRestored to wild-type levelsExcretionNephrocalcinosis