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Abstract

A class of genetic diseases known as polycystic kidney disease (PKD) includes renal cyst formation and expansion, gradual renal function loss, and a variety of extrarenal symptoms. Autosomal-dominant PKD, the most prevalent kind, is brought on by mutations in either of the two PKD1 or PKD2 genes. Recent advances in genomic and proteomic science have led to the identification of novel genes involved in a wide range of recessive, less common PKD disorders. Polycystic kidney disease caused by autosomal dominant mutation-based, molecular, diagnosis. (ADPKD)Is complicated by genetic and allelic heterogeneity, large multi exongenes, duplication of PKD1, and a high level of unclassified variants (UCV). Present mutation detection levels are 60 to 70%, and PKD1 and PKD2 UCV have not been systematically classified.

Keywords

Rapamycin, PKD, APKD, cAMP, tolvaptan

Reference

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Seema Kashyap
Corresponding author

Rungta Institute of Pharmaceutical Sciences (C G)

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Eshu Sahu
Co-author

Rungta Institute of Pharmaceutical Sciences (C G)

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Bignesh Pradhan
Co-author

Rungta Institute of Pharmaceutical Sciences (C G)

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Dali Kanwar
Co-author

Rungta Institute of Pharmaceutical Sciences (C G)

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Chhabi Lal
Co-author

Rungta Institute of Pharmaceutical Sciences (C G)

Seema Kashyap*, Eshu Sahu, Bignesh Pradhan, Dali Kanwar, Chhabi Lal, Aryan Nath Yogi, Rajesh Kumar Nema, Harish Sharma, Gyanesh Kumar Sahu, Review on “Polycystic kidney disease pathophysiology and prognosis”, Int. J. in Pharm. Sci., 2023, Vol 1, Issue 5, 219-225. https://doi.org/10.5281/zenodo.7928776

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