Treatment of acute renal failure caused by renal artery occlusion with renal artery angioplasty

2002 ◽  
Vol 40 (1) ◽  
pp. 189-194 ◽  
Author(s):  
Karen M. Dwyer ◽  
John I. Vrazas ◽  
Robert S. Lodge ◽  
Timothy J. Humphery ◽  
Stephen M. Schlicht ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Artery ◽  
Artery Occlusion ◽  
Renal Artery Occlusion

scholarly journals Restoration of renal function by a novel prostaglandin EP4 receptor-derived peptide in models of acute renal failure

2013 ◽  
Vol 304 (1) ◽  
pp. R10-R22 ◽  
Author(s):  
Martin Leduc ◽  
Xin Hou ◽  
David Hamel ◽  
Melanie Sanchez ◽  
Christiane Quiniou ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Renal Artery ◽  
Artery Occlusion ◽  
Hek293 Cells ◽  
Heme Oxygenase 1 ◽  
Histological Changes ◽  
Ep4 Receptor ◽  
Renal Artery Occlusion

Acute renal failure (ARF) is a serious medical complication characterized by an abrupt and sustained decline in renal function. Despite significant advances in supportive care, there is currently no effective treatment to restore renal function. PGE2 is a lipid hormone mediator abundantly produced in the kidney, where it acts locally to regulate renal function; several studies suggest that modulating EP4 receptor activity could improve renal function following kidney injury. An optimized peptidomimetic ligand of EP4 receptor, THG213.29, was tested for its efficacy to improve renal function (glomerular filtration rate, renal plasma flow, and urine output) and histological changes in a model of ARF induced by either cisplatin or renal artery occlusion in Sprague-Dawley rats. THG213.29 modulated PGE2-binding dissociation kinetics, indicative of an allosteric binding mode. Consistently, THG213.29 antagonized EP4-mediated relaxation of piglet saphenous vein rings, partially inhibited EP4-mediated cAMP production, but did not affect Gαi activation or β-arrestin recruitment. In vivo, THG213.29 significantly improved renal function and histological changes in cisplatin- and renal artery occlusion-induced ARF models. THG213.29 increased mRNA expression of heme-oxygenase 1, Bcl2, and FGF-2 in renal cortex; correspondingly, in EP4-transfected HEK293 cells, THG213.29 augmented FGF-2 and abrogated EP4-dependent overexpression of inflammatory IL-6 and of apoptotic death domain-associated protein and BCL2-associated agonist of cell death. Our results demonstrate that THG213.29 represents a novel class of diuretic agent with noncompetitive allosteric modulator effects on EP4 receptor, resulting in improved renal function and integrity following acute renal failure.

Complete Resolution of Acute Renal Failure after Left Renal Artery Angioplasty and Stent Placement for Total Renal Artery Occlusion

Cardiology ◽  
2006 ◽  
Vol 108 (1) ◽  
pp. 51-54 ◽  
Author(s):  
Arshad Rehan ◽  
Yassar Almanaseer ◽  
Devang M. Desai ◽  
Arshad Ali ◽  
Hiroshi Yamasaki
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Renal Artery ◽  
Stent Placement ◽  
Complete Resolution ◽  
Artery Occlusion ◽  
Left Renal Artery ◽  
Renal Artery Occlusion

scholarly journals Successful revascularization of the kidney: Case reports

2004 ◽  
Vol 132 (9-10) ◽  
pp. 323-326
Author(s):  
Lazar Davidovic ◽  
Radomir Sindjelic ◽  
Mirjana Stanojevic ◽  
Ilija Kuzmanovic ◽  
Momcilo Colic ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Renal Function ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Medical Therapy ◽  
Case Reports ◽  
Artery Occlusion ◽  
First Case ◽  
Renal Artery Occlusion

Three cases of successful kidney revascularization and recovery of renal function are presented in this study. In all three cases, renal failure and renovascular hypertension were caused by renal artery occlusion associated with aortic aneurysm (two abdominal and one thoracoabdominal). Prior to operation, one patient required dialysis 4 months, one 25 days and one 2 days. After kidney revascularization, renal function recovered immediately in the first case, in the second case after three months, and in the third case after 10 days. In one case, blood pressure restored to normal without medical therapy, while in two other cases blood pressure decreased nearly to normal with minimal medical therapy. In appropriately selected cases, revascularization of the occluded renal artery is recommended for treatment of both renal failure and renovascular hypertension. In such cases, collateral circulation is crucial to enable the preservation of dysfunctional kidney.

scholarly journals Restoration of end stage renal failure with spleno-renal bypass in a patient with renal artery occlusion due to AAA.

1999 ◽  
Vol 32 (6) ◽  
pp. 1029-1033
Author(s):  
Hiroyuki Amano ◽  
Tamotsu Tojinbara ◽  
Noriko Kondou ◽  
Tooru Uehara ◽  
Shouhei Fuchinoue ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Artery ◽  
Artery Occlusion ◽  
End Stage Renal Failure ◽  
Renal Artery Occlusion ◽  
End Stage

Fluids and renals

2014 ◽  
Author(s):  
Tim Raine ◽  
James Dawson ◽  
Stephan Sanders ◽  
Simon Eccles
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Artery ◽  
Kidney Injury ◽  
Artery Occlusion ◽  
Electrolyte Imbalance ◽  
Serum Urea ◽  
Renal Artery Occlusion ◽  
Urological Disorders

Acute kidney injuryChronic renal failureHaematuriaProteinuriaGlomerular diseaseUrological disordersLow urine outputIV fluidsPotassium emergenciesElectrolyte imbalanceAcute rise from baseline of serum urea and creatinine ±oliguria ( Table 12.1);1there are three basic mechanisms:•Prerenal hypoperfusion of kidney due to eg ↓BP, hypovolaemia, renal artery occlusion (mass, emboli)...

scholarly journals Reversible renal failure with renal artery occlusion.

BMJ ◽  
1972 ◽  
Vol 2 (5804) ◽  
pp. 27-28 ◽  
Author(s):  
O P Quantock ◽  
G N Thatcher
Keyword(s):  
Renal Failure ◽  
Renal Artery ◽  
Artery Occlusion ◽  
Renal Artery Occlusion

Evidence against oxidant injury as a critical mediator of postischemic acute renal failure

1988 ◽  
Vol 255 (3) ◽  
pp. F450-F460 ◽  
Author(s):  
L. M. Gamelin ◽  
R. A. Zager
Keyword(s):  
Lipid Peroxidation ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Artery Occlusion ◽  
Significant Rise ◽  
Oxidant Injury ◽  
Vascular Congestion ◽  
Renal Artery Occlusion ◽  
Proximal Tubular

The purpose of this study is to confirm previous evidence for reactive oxygen species (ROS) as critical mediators of postischemic renal injury by documenting lipid peroxidation after ischemic-hypoxic insults and by demonstrating that antioxidants confer protection. Renal malondialdehyde (MDA) concentrations, an index of lipid peroxidation, were measured using uncorrected and tissue-chromagen-corrected methods in 1) cortical (C), outer medullary stripe (OMS), inner medullary (IM) whole renal tissues, and C and OMS mitochondria obtained 15 min after in vivo renal artery occlusion (RAO; x 45 min); 2) C, OMS, and IM whole tissues obtained 15 min after completing 45 min of ischemia in an isolated perfused kidney; and 3) isolated proximal tubular cell (PTC) suspensions after 45 min of hypoxia with 15 min of reoxygenation. Despite significant oxygen deprivation-induced injury in each of these systems, no significant rise in MDA concentrations could be documented, with the sole exception of the in vivo IM region (by uncorrected MDA assay only). The latter rise could be attributed to medullary vascular congestion causing a hemoglobin-induced artifact in the MDA assay. Sixty-minute in vivo RAO plus reflow also did not raise MDA. To validate the MDA assay 4.2 mM H2O2 was added to PTC. An abrupt fourfold rise in MDA resulted. Pretreatment of 30- and 45-min RAO rats with two antioxidants (allopurinol or superoxide dismutase) failed to confer functional or morphological protection. We conclude that ROS may not be critical consistent mediators of in vivo postischemic acute renal failure.

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