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Disease Info Card
Hypercalciuria
Information about Hypercalciuria: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Hypercalciuria
Most recent studies have shown that Hypercalciuria shares some biological mechanisms with acidosis, calcium-metabolism-disorders, fracture, hypercalcemia, hyperoxaluria, hyperparathyroidism-primary, hypophosphatemia, kidney-calculi, kidney-diseases, kidney-failure, lithiasis, nephrocalcinosis, nephrolithiasis, osteopenia, osteoporosis, proteinuria-of-undiagnosed-cause, renal-tubular-acidosis, urolithiasis.
Among the many pathways, these few ones have gauged particular interests from scientists studying Hypercalciuria, and have been seen in publications frequently: Bone Mineralization, Bone Remodeling, Bone Resorption, Cell Proliferation, Diuresis, Endocytosis, Excretion, Flight, Glomerular Filtration, Hormone Secretion, Intestinal Absorption, Ion Transport, Lactation, Localization, Menopause, Natriuresis, Pathogenesis, Secretion, Translation, Transport
Quite a number of genes have been found to play important roles in Hypercalciuria, such as ALB, BEST1, BGLAP, CALB2, CALCA, CASR, CD55, CLCN5, CLDN16, CR2, DHRS4, DMD, INS, PTH, PTRH1, RAPGEF5, SLC34A3, TDGF1, TRPV5. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.