Hyperoxalaemia

Overview of Hyperoxalaemia

Most recent studies have shown that Hyperoxalaemia shares some biological mechanisms with acute-intermittent-porphyria, ascorbic-acid-deficiency, glomerulonephritis, hereditary-diseases, hyperoxaluria, hyperoxaluria-primary, kidney-calculi, kidney-diseases, kidney-failure, kidney-failure-chronic, nephrocalcinosis, nephrolithiasis-calcium-oxalate, primary-hyperoxaluria-type-i, renal-insufficiency, secondary-oxalosis, uremia, uremia-syndrome, urolithiasis, vitamin-b-6-deficiency.

Among the many pathways, these few ones have gauged particular interests from scientists studying Hyperoxalaemia, and have been seen in publications frequently: Anion Transport, Diuresis, Excretion, Glomerular Filtration, Intestinal Absorption, Localization, Oxalate Transport, Pathogenesis, Secretion, Transepithelial Transport, Transport

Quite a number of genes have been found to play important roles in Hyperoxalaemia, such as AGT, AGXT, C1QL1, CRH, EPO, FUT2, HCRT, HTT, PDXP, PHC1, PLP1, PRDX5, SAT1, SLC13A1, SLC26A1, SLC26A6, SLC38A1, SMARCB1, SQLE. 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.

Hyperoxalaemia Related Genes

click to see detail information for each gene

Pathways Related to Hyperoxalaemia

This information is being compiled and will come in a future update

Related Diseases