Recent advances in the pathophysiology of ischemic acute renal failure.

By Joseph V. Bonventre, J. Weinberg. Journal of the American Society of Nephrology, 2003

793 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/952aad432232f53abeaa7da7e8f6c62a55a4e053

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In Nephrology

Citations in the corpus

Urinary kidney injury molecule-1: a sensitive quantitative biomarker for early detection of kidney tubular injury. (2006, background): “Acute kidney failure is a common disease and is associated with high mortality rate (6, 38).”
Biomarkers of acute kidney injury. (2008, background): “These include (a) alterations in renal perfusion resulting from loss of autoregulation and increased renal vasoconstriction, (b) tubular dysfunction and cell death by apoptosis and necrosis, (c) desquamation of viable and dead cells contributing to intratubular obstruction, (d ) metabolic alteration”
Pathophysiology of Acute Kidney Injury (2012, neutral): “proximal tubule is considered the most sensitive cellular entity to ischemic, hypoxic or nephrotoxic damage (62, 68).”
Vasculotropic, paracrine actions of infused mesenchymal stem cells are important to the recovery from acute kidney injury. (2007, neutral): “sion, fluid extravasation, and coagulation (7).”
Relationship between Intraoperative Hypotension, Defined by Either Reduction from Baseline or Absolute Thresholds, and Acute Kidney and Myocardial Injury after Noncardiac Surgery: A Retrospective Cohort Analysis (2017, neutral): “001 White 1,530 (87) 48,077 (87) 2,649 (82) 46,958 (87) Black 207 (12) 6,825 (12) 523 (16) 6,509 (12) Other 23 (1) 653 (1) 43 (1) 633 (1) Age, yr 67 ± 13 56 ± 15 < 0.”
A clinical score to predict acute renal failure after cardiac surgery. (2004, background): “The promise indicated by successful interventions in experimental models suggests that the proposed intervention should come early, possibly within 24 to 48 h after inducing renal injury (10,11).”
Acute kidney injury and chronic kidney disease: an integrated clinical syndrome. (2012, background): “Animal models of ATN consistently show an interstitial neutrophil infiltrate during the acute phase of ATN, often followed by monocytic– lymphocytic infiltration in later stages.(32,55,57,58) Monocytes can exacerbate injury and promote fibrosis.”
Update on mechanisms of ischemic acute kidney injury. (2006, neutral): “translational AKI research that has been made since this topic last was reviewed in JASN less than 3 yr ago (208) is chronicled”
Isolation of renal progenitor cells from adult human kidney. (2005, background): “Recovery of renal function after acute renal failure is dependent on the replacement of necrotic tubular cells with functional tubular epithelium.(1) In addition, a pronounced proliferative response of the glomerular and peritubular capillary endothelium(2) is observed after ischemic injury.”