Glomerular podocyte dysfunction in inherited renal tubular disease

Author:

Huang Li-Min,Mao Jian-HuaORCID

Abstract

Abstract Background Hereditary renal tubular disease can cause hypercalciuria, acid-base imbalance, hypokalemia, hypomagnesemia, rickets, kidney stones, etc. If these diseases are not diagnosed or treated in time, they can cause kidney damage and electrolyte disturbances, which can be detrimental to the maturation and development of the child. Glomerular involvement in renal tubular disease patients has only been considered recently. Methods We screened 71 papers (including experimental research, clinical research, etc.) about Dent’s disease, Gitelman syndrome, and cystinosis from PubMed, and made reference. Results Glomerular disease was initially underestimated among the clinical signs of renal tubular disease or was treated merely as a consequence of the tubular damage. Renal tubular diseases affect glomerular podocytes through certain mechanisms resulting in functional damage, morphological changes, and glomerular lesions. Conclusions This article focuses on the progress of changes in glomerular podocyte function in Dent disease, Gitelman syndrome, and cystinosis for the purposes of facilitating clinically accurate diagnosis and scientific treatment and improving prognosis.

Publisher

Springer Science and Business Media LLC

Subject

Pediatrics, Perinatology and Child Health

Reference71 articles.

1. Greka A, Mundel P. Cell biology and pathology of podocytes. Annu Rev Physiol. 2012;74:299–323.

2. Mundel P, Kriz W. Structure and function of podocytes: an update. Anat Embryol (Berl). 1995;192:385–97.

3. Somlo S, Mundel P. Getting a foothold in nephrotic syndrome. Nat Genet. 2000;24:333–5.

4. Kerjaschki D. Caught flat-footed: podocyte damage and the molecular bases of focal glomerulosclerosis. J Clin Invest. 2001;108:1583–7.

5. Wrong OM, Norden AG, Feest TG. Dent’s disease; a familial proximal renal tubular syndrome with low-molecular-weight proteinuria, hypercalciuria, nephrocalcinosis, metabolic bone disease, progressive renal failure and a marked male predominance. QJM. 1994;87:473–93.

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