M
Manjeri A. Venkatachalam
Researcher at University of Texas Health Science Center at San Antonio
Publications - 150
Citations - 13600
Manjeri A. Venkatachalam is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: Apoptosis & Renal function. The author has an hindex of 57, co-authored 147 publications receiving 12528 citations. Previous affiliations of Manjeri A. Venkatachalam include Harvard University & Brigham and Women's Hospital.
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Hyperfiltration in remnant nephrons : A potentially adverse response to renal ablation
TL;DR: In this article, a study was performed in three groups of male Munich-Wistar rats 1 wk after surgery: group I, eight control rats that underwent laparotomy and were fed a normal diet.
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Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression
TL;DR: Experiments using an acute-on-chronic injury model suggest that additional loss of parenchyma caused by failed repair of AKI in kidneys with prior renal mass reduction triggers hemodynamically mediated processes that damage glomeruli to cause progression.
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Ischemic damage and repair in the rat proximal tubule: Differences among the S1, S2, and S3 segments
TL;DR: It is found that S1 and S2 cells alike are only reversibly injured and recover completely to normalcy within 4 hr, whereas S3 cells selectively undergo progressive cell injury and death and are exfoliated into tubular lumina.
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Acute kidney injury: a springboard for progression in chronic kidney disease
Manjeri A. Venkatachalam,Karen A. Griffin,Rongpei Lan,Hui Geng,Pothana Saikumar,Anil K. Bidani +5 more
TL;DR: Considerations based on published and emerging data suggest that a pathology that develops in regenerating tubules after AKI characterized by failure of differentiation and persistently high signaling activity is the proximate cause that drives downstream events in the interstitium: inflammation, capillary rarefaction, and fibroblast proliferation.
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Role of molecular charge in glomerular permeability. Tracer studies with cationized ferritins.
TL;DR: Mouse kidneys were perfused with Krebs-Ringer bicarbonate buffer containing native, anionic horse spleen ferritin or various cationized derivatives, and the glomerular localization of the probe molecules determined by electron microscopy suggested that intrinsic negative charges are present in the GBM and endothelium.