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Sethu M. Madhavan

Researcher at Ohio State University

Publications -  8
Citations -  114

Sethu M. Madhavan is an academic researcher from Ohio State University. The author has contributed to research in topics: Kidney disease & Kidney. The author has an hindex of 2, co-authored 8 publications receiving 13 citations. Previous affiliations of Sethu M. Madhavan include Cleveland Clinic Lerner College of Medicine.

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Acute kidney injury in patients treated with immune checkpoint inhibitors.

Shruti Gupta, +67 more
TL;DR: In this paper, a multivariable logistic regression model was used to identify predictors of ICPi-AKI and its recovery, and the effect of rechallenge versus no re-challenge on survival was estimated.
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APOL1-G0 protects podocytes in a mouse model of HIV-associated nephropathy.

TL;DR: African polymorphisms in the gene for Apolipoprotein L1 (APOL1) confer a survival advantage against lethal trypanosomiasis but also an increased risk for several chronic kidney diseases including HIV-associated nephropathy (HIVAN).
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Cadherin-11, Sparc-related modular calcium binding protein-2, and Pigment epithelium-derived factor are promising non-invasive biomarkers of kidney fibrosis.

Insa M. Schmidt, +247 more
- 01 Sep 2021 - 
TL;DR: In this article, the authors characterize five candidate biomarkers of kidney fibrosis: Cadherin-11 (CDH11), Sparc-related modular calcium binding protein-2 (SMOC2), Pigment epithelium-derived factor (PEDF), Matrix-Gla protein, and Thrombospondin-2 Gene expression profiles in single-cell and single-nucleus RNA-sequencing (sc/snRNA-seq) datasets from rodent models of fibrosis and human chronic kidney disease (CKD) were explored, and Lum
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The relationship between APOL1 structure and function: Clinical implications

TL;DR: Understanding the three-dimensional structure of the protein, with and without the risk variants, can provide insights into the pathogenesis of kidney diseases mediated by APOL1 variants.
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Lack of APOL1 in proximal tubules of normal human kidneys and proteinuric APOL1 transgenic mouse kidneys.

TL;DR: The mechanism of pathogenesis associated with APOL1 polymorphisms and risk for non-diabetic chronic kidney disease (CKD) is not fully understood as mentioned in this paper, and the proximal tubule expression patterns are inconsistent in published reports.