Benign Familial Haematuria

Overview of Benign Familial Haematuria

Most recent studies have shown that Benign Familial Haematuria shares some biological mechanisms with alport-syndrome-x-linked, complete-hearing-loss, familial-hematuria, focal-glomerulosclerosis, glioblastoma, glomerulonephritis, glomerulosclerosis-(disorder), hereditary-nephritis, iga-glomerulonephritis, kidney-diseases, kidney-failure, kidney-failure-chronic, lipoid-nephrosis, microscopic-hematuria, nephritis, nephrotic-syndrome, proteinuria-of-undiagnosed-cause, sclerosis, segmental-glomerulosclerosis, thin-basement-membrane-disease.

Among the many pathways, these few ones have gauged particular interests from scientists studying Benign Familial Haematuria, and have been seen in publications frequently: Pathogenesis

Quite a number of genes have been found to play important roles in Benign Familial Haematuria, such as ABO, ACTN4, APP, ATP6V0A4, C1QL1, C3, COL4A3, COL4A4, COL4A5, CRH, FMN1, FOXC2, FUT2, LYZ, MUC5AC, NEFH, PLP2, SGCG, SLC2A10, 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.

Benign Familial Haematuria Related Genes

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Pathways Related to Benign Familial Haematuria

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

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