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Genetic basis of adult-onset nephrotic syndrome and focal segmental glomerulosclerosis

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Abstract

Nephrotic syndrome (NS) is one of the most common glomerular diseases with signs of nephrosis, heavy proteinuria, hypoalbuminemia, and edema. Dysfunction of glomerular filtration barrier causes protein loss through the kidneys. Focal segmental glomerulosclerosis (FSGS) accounts for nearly 20% of NS among children and adults. Adult-onset FSGS/NS is often associated with low response to steroid treatment and immunosuppressive medication and poor renal survival. Several genes involved in NS and FSGS have been identified by linkage analysis and next-generation sequencing. Most of these genes encode proteins and are highly expressed in glomerular podocytes, which play crucial roles in slit-diaphragm signaling, regulation of actin cytoskeleton dynamics and maintenance of podocyte integrity, and cell–matrix interactions. In this review, we focus on the recently identified genes in the adult-onset NS and FSGS and discuss clinical significance of screening of these genes.

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Acknowledgments

The study was supported by National Project for the Construction of Clinical Key Specialty and Project of Special Fund for Health-Scientific Research (No. 201002010), National Key Technology R&D Program (No. 2011BAI10B00), Key Projects of National Basic Research Program of China (Nos. 2012CB517700 and 2012CB517604), National Natural Science Foundation of China (Nos. 81270782 and 30771000), Key Discipline Construction Projects Approved by Health Development Planning Commission of Shanghai, and National Project for the Construction of Clinical Key Specialty.

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  1. Institute of Nephrology, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China

    Jian Liu & Weiming Wang

  2. Department of Nephrology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China

    Jian Liu & Weiming Wang

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Liu, J., Wang, W. Genetic basis of adult-onset nephrotic syndrome and focal segmental glomerulosclerosis. Front. Med. 11, 333–339 (2017). https://doi.org/10.1007/s11684-017-0564-1

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