Blog entry by mohammad katout

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During the plenary session of the first day of the 17th International Pediatric Nephrology A ssociation Congress, September 20-24 in Iguacu, Brazil 

Professor Moin A Saleem delivered the keynote talk entitled “Molecular stratification of the nephrotic syndrome”

Being an expert in the field professor Saleem smoothly surfed in the current acumen of exponentially increasing molecular and cell biology updates into the pathogenesis of nephrotic syndrome.

The glomerular podocyte plays a key role in filtration and its loss of function results in loss of protein.  Therefore, the recent advances in molecular genetics and cell biology studies in nephrotic syndrome patients not only revealed the molecular mechanisms of podocytes dysfunction responsible for the disease, but equally importantly provide clues to focus on target molecules on the podocyte to figure out potential circulating factors.

Moreover, those molecules can be utilized as both diagnostic and prognostic biomarkers. This paves the way to personalized therapy to patients with nephrotic syndrome tailored to maximize benefit while minimizing side effects caused by drugs as well as the devastating post-transplantation disease recurrence.

It is quite interesting how whole-exome sequencing revolutionized our understanding through identifying several mutations in families with SSNS, which shed light on new mechanisms of podocyte disruption in minimal change nephrotic syndrome. For instance, epithelial membrane protein 2 (EMP2) is known to regulate the amount of caveolin-1, which contributes to endocytosis and the transcytosis of cholesterol and albumin. Lipopolysaccharide (LPS)-induced caveolin-1 phosphorylation was reported to lead to the increase of transcellular permeability [1,2].

Professor Saleem suggested that there is seemingly an evidence of overlap of SSNS and SRNS. He expects, given the preliminary results of the ongoing research as well, that nephrotic syndrome will be reclassified soon based on pathogenic mechanisms that keep evolving. These would hopefully include the mechanisms of how corticosteroid and immunosuppressives have their effect on single gene mutation nephrotic syndrome.

 

Referrences

Parton RG, del Pozo MA: Caveolae as plasma membrane sensors, protectors and organizers. Nat Rev Mol Cell Biol. 2013; 14(2): 98–112

Wang N, Zhang D, Sun G, et al.: Lipopolysaccharide-induced caveolin-1 phosphorylation-dependent increase in transcellular permeability precedes the increase in paracellular permeability. Drug Des Devel Ther. 2015; 9: 4965–77

[ Modified: Thursday, 1 January 1970, 1:00 AM ]

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