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Helmut G. Rennke

Researcher at Brigham and Women's Hospital

Publications -  267
Citations -  35414

Helmut G. Rennke is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Renal function & Kidney. The author has an hindex of 77, co-authored 256 publications receiving 33959 citations. Previous affiliations of Helmut G. Rennke include Boston Medical Center & Mayo Clinic.

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Role of abnormally high transmural pressure in the permselectivity defect of glomerular capillary wall: a study in early passive Heymann nephritis.

TL;DR: Results indicate that the permselectivity defect in passive Heymann nephritis is attributable, at least in part, to impaired size selectivity of the glomerular capillary wall caused by a prevailing abnormally high transcapillary hydraulic pressure difference.
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Pharmacological GLI2 inhibition prevents myofibroblast cell-cycle progression and reduces kidney fibrosis

TL;DR: It is demonstrated that GLI2, but not GLI1, drives myofibroblast cell-cycle progression in cultured mesenchymal stem cell-like progenitors, and pharmacologic targeting of this pathway with darinaparsin reduced fibrosis through reduction ofGLI2 protein levels and subsequent cell- cycle arrest in myofIBroblasts.
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Evaluation of the nonneoplastic pathology in tumor nephrectomy specimens : Predicting the risk of progressive renal failure

TL;DR: It is concluded that adequate examination of nonneoplastic renal parenchyma is an important tool in recognizing patients at risk for progressive renal disease after neph rectomy and could be an essential step in providing early preventive and treatment measures and better medical care of patients undergoing nephrectomy for neoplastic processes.
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Fibrin(ogen) is internalized and degraded by activated human monocytoid cells via Mac-1 (CD11b/CD18): a nonplasmin fibrinolytic pathway

TL;DR: FGN is internalized and degraded by activated human monocytoid cells via Mac-1 in the absence of plasmin, thereby providing an alternative fibrinolytic pathway, and in addition to the function of cell adhesion, integrins may also act as receptors that mediate the internalization and degradation of bound ligands.
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How does glomerular epithelial cell injury contribute to progressive glomerular damage

TL;DR: This work has shown that large plasma proteins are retained in the subendothelium by the size-restrictive water-filled channels of the lamina densa and accumulate upstream in the form of hyaline which eventually occludes individual loops.