scholarly journals Alterations in vascular function and morphology in acute ischemic renal failure

1983 ◽  
Vol 23 (5) ◽  
pp. 717-724 ◽  
Author(s):  
Erve Matthys ◽  
Marsha K. Patton ◽  
Richard W. Osgood ◽  
Manjeri A. Venkatachalam ◽  
Jay H. Stein
Keyword(s):  
Renal Failure ◽  
Vascular Function ◽  
Ischemic Renal Failure

Interactions between adenosine and angiotensin II in controlling glomerular filtration

1985 ◽  
Vol 248 (3) ◽  
pp. F340-F346 ◽  
Author(s):  
J. E. Hall ◽  
J. P. Granger ◽  
R. L. Hester
Keyword(s):  
Renal Failure ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Renal Vasoconstriction ◽  
Ischemic Renal Failure ◽  
Constrictor Response

This study examined interactions between adenosine (Ado) and angiotensin II (ANG II) in controlling renal blood flow (RBF) and glomerular filtration rate (GFR). In six normal dogs, intrarenal Ado infusion (1.0 mumol/min) transiently decreased RBF, but during sustained Ado infusion RBF increased to 122 +/- 7% of control, although GFR remained at 75 +/- 6% of control. Blockade of ANG II formation with the converting enzyme inhibitor SQ 14225 (n = 6) almost abolished the transient decrease in RBF but did not prevent the sustained fall in GFR caused by Ado. When circulating ANG II was held constant by intravenous infusion of SQ 14225 and 20 ng . kg-1 . min-1 of ANG II (n = 6), Ado transiently decreased RBF but the return of RBF was much slower than in normal dogs and RBF did not increase above control. Maintenance of constant circulating ANG II did not prevent Ado-mediated decreases in GFR. These observations suggest that Ado-mediated reductions in GFR do not depend entirely on ANG II and may be due to dilation of efferent arterioles by Ado. However, the transient renal vasoconstriction caused by Ado depends on ANG II, and data from this study suggest that part of the waning constrictor response to Ado is due to suppression of renin secretion and endogenous ANG II formation. In circumstances where high ANG II levels are maintained (i.e., ischemic renal failure), Ado may be capable of causing sustained renal vasoconstriction.

Free radical ablation for the prevention of post-ischemic renal failure following renal transplantation

1991 ◽  
Vol 69 (21-23) ◽  
pp. 1083-1094 ◽  
Author(s):  
H. J. Schiller ◽  
K. A. Andreoni ◽  
G. B. Bulkley
Keyword(s):  
Renal Failure ◽  
Renal Transplantation ◽  
Free Radical ◽  
Ischemic Renal Failure

Ischemic Renal Failure

2015 ◽  
pp. 59-66 ◽  
Author(s):  
Pietro Zucchelli ◽  
Alessandro Zuccal�
Keyword(s):  
Renal Failure ◽  
Ischemic Renal Failure

Blood Coagulation Disturbances During Oliguria And Polyuria Of Acute Renal Failure In Man

1981 ◽  
Author(s):  
J Schrader ◽  
H Köstering ◽  
H Kaiser ◽  
P Kramer ◽  
F Scheler
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Blood Coagulation ◽  
Daily Basis ◽  
Coagulation System ◽  
Factor V ◽  
Thrombin Time ◽  
Complex Activity ◽  
Ischemic Renal Failure ◽  
Postrenal Failure

The blood coagulation system makes a significant contribution to renal damage in many disease processes. Intrarenal coagulation appears to occur in a wide variety of diseases as a primary or secondary event. As there is evidence that intraglomerular coagulation is a significant factor in the development and maintenance of oliguria in acute ischemic renal failure, blood coagulation investigations were performed in 20 patients with acute renal failure of varied etiology. The investigations were done on a daily basis from the onset of oliguria (urine flow <20 ml/h)until serum creatinine declined to less than 2,0 mg%. Thus, we were able to detect changes in blood coagulation during oliguria and polyuria. We found an enhanced thrombin generation in both oliguria and polyria. Fibrin monomer complexes were significantly increased in both states, but more predominantly in polyuria. Factor VIII and alpha-1 antitrypsin activities were also elevated. PTT and r- and k-time in TEG were shortened more in polyuria than in oliguria, whereas fibrinogen was elevated more in oliguria than in polyuria. Factor XIII activity and prothrombin complex activity (Quick’s test) were lowered in both states, the lowest values of the former being found in polyuria, the lowest values of the latter in oliguria with a normalizing tendency in the following days. Fibrinolytic activity was also decreased. No significant changes were found in plasminogen, antithrombin III, alpha-2 macroglobulin, factor V and thrombin time. In summary, we found a hypercoagulability in these patients with acute renal failure, which was more predominant during polyuria and which correlated with the tendency to thrombosis and to shorter indwelling periods of i.v. catheters in this state. Consequently, the changes in blood coagulation of 3 patients with acute postrenal failure were not as significant as those found in the other patients. The treatment with anticoagulants in patients with acute renal failure will be discussed.

scholarly journals Effect of medial calcification on vascular function in uremia

2011 ◽  
Vol 301 (1) ◽  
pp. F78-F83 ◽  
Author(s):  
Roy L. Sutliff ◽  
Erik R. Walp ◽  
Alexander M. El-Ali ◽  
Stacey Elkhatib ◽  
Koba A. Lomashvili ◽  
...  
Keyword(s):  
Renal Failure ◽  
Vascular Function ◽  
Ex Vivo ◽  
Vascular Dysfunction ◽  
Arterial Compliance ◽  
Calcium Content ◽  
Aortic Compliance ◽  
Maximal Contraction ◽  
Plasma Urea ◽  
Medial Calcification

The contribution of medial calcification to vascular dysfunction in renal failure is unknown. Vascular function was measured ex vivo in control, noncalcified uremic, and calcified uremic aortas from rats with adenine-induced renal failure. Plasma urea was 16 ± 4, 93 ± 14, and 110 ± 25 mg/dl, and aortic calcium content was 27 ± 4, 29 ± 2, and 4,946 ± 1,616 nmol/mg dry wt, respectively, in the three groups. Maximal contraction by phenylephrine (PE) or KCl was reduced 53 and 63% in uremic aortas, and sensitivity to KCl but not PE was increased. Maximal relaxation to acetylcholine was impaired in uremic aortas (30 vs. 65%), and sensitivity to nitroprusside was also reduced, indicating some impairment of endothelium-independent relaxation as well. None of these parameters differed between calcified and noncalcified uremic aortas. However, aortic compliance was reduced in calcified aortas, ranging from 17 to 61% depending on the severity of calcification. We conclude that uremic vascular calcification, even when not severe, significantly reduces arterial compliance. Vascular smooth muscle and endothelial function are altered in renal failure but are not affected by medial calcification, even when severe.

N-acetyl cysteine ameliorates ischemic renal failure in the rat

1996 ◽  
Vol 27 (4) ◽  
pp. A4
Author(s):  
John DiMari ◽  
Judit Megyesi ◽  
Nora Udvarhelyi ◽  
Peter Price ◽  
Roger Davis ◽  
...  
Keyword(s):  
Renal Failure ◽  
Ischemic Renal Failure ◽  
Acetyl Cysteine

Identification of a novel kidney-specific gene downregulated in acute ischemic renal failure

2000 ◽  
Vol 279 (3) ◽  
pp. F426-F439 ◽  
Author(s):  
Erding Hu ◽  
Zunxuan Chen ◽  
Todd Fredrickson ◽  
Miklos Gellai ◽  
Malcolm Jugus ◽  
...  
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Molecular Mechanisms ◽  
Specific Protein ◽  
Kidney Cortex ◽  
Specific Gene ◽  
Mrna Levels ◽  
Ischemic Renal Failure ◽  
New Gene

To gain further insights into the molecular mechanisms involved in acute renal failure, we have isolated a new gene from rat and human, named KSP32 (kidney-specific protein with a molecular mass of 32 kDa). KSP32 encodes a novel gene that shows little homology to other mammalian proteins. It, however, shares extensive homology with several proteins found in the nematode Caenorhabditis elegans and plants. The expression of KSP32 mRNA is highly restricted to kidney. In situ hybidization analysis revealed that the expression of KSP32 mRNA was prominent in the boundary of kidney cortex and outer medulla, exhibiting a raylike formation extending from the medulla into the cortex. Finally, KSP32 mRNA was dramatically downregulated in rat following induction of acute ischemic renal failure. Rapid loss of KSP32 mRNA expression was observed beginning at ∼5 h following renal injury and mRNA levels remained depressed for at least 96 h. Both KSP32 mRNA levels as well as renal function recovered 14 days after injury. Administration of an endothelin receptor antagonist (SB-209670), known to restore renal function, significantly increased KSP32 expression.

THE DUFFY ANTIGEN RECEPTOR FOR CHEMOKINES (DARC) IN ACUTE POST-ISCHEMIC RENAL FAILURE (APRF) - A CONDUCTOR OF RENAL CHEMOKINE PRESENTATION.

2005 ◽  
Vol 33 ◽  
pp. A139
Author(s):  
Kai Singbartl ◽  
Alexander Zarbock ◽  
Mirco Schmolke ◽  
Marion Scharte ◽  
Hugo Van Aken
Keyword(s):  
Renal Failure ◽  
Antigen Receptor ◽  
Duffy Antigen ◽  
Ischemic Renal Failure

scholarly journals Vascular function in rats with adenine-induced chronic renal failure

2012 ◽  
Vol 302 (12) ◽  
pp. R1426-R1435 ◽  
Author(s):  
Lisa Nguy ◽  
Holger Nilsson ◽  
Jaana Lundgren ◽  
Maria E. Johansson ◽  
Tom Teerlink ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Vascular Function ◽  
Ex Vivo ◽  
Mesenteric Arteries ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Resistance Arteries ◽  
Severe Renal Failure ◽  
Stress Markers

The aim of the present study was to characterize the function of resistance arteries, and the aorta, in rats with adenine-induced chronic renal failure (A-CRF). Sprague-Dawley rats were randomized to chow with or without adenine supplementation. After 6–10 wk, mesenteric arteries and thoracic aortas were analyzed ex vivo by wire myography. Plasma creatinine concentrations were elevated twofold at 2 wk, and eight-fold at the time of death in A-CRF animals. Ambulatory systolic and diastolic blood pressures measured by radiotelemetry were significantly elevated in A-CRF animals from week 3 and onward. At death, A-CRF animals had anemia, hyperphosphatemia, hyperparathyroidism, and elevated plasma levels of asymmetric dimethylarginine and oxidative stress markers. There were no significant differences between groups in the sensitivity, or maximal response, to ACh, sodium nitroprusside (SNP), norepinephrine, or phenylephrine in either mesenteric arteries or aortas. However, in A-CRF animals, the rate of aortic relaxation was significantly reduced following washout of KCl (both in intact and endothelium-denuded aorta) and in response to ACh and SNP. Also the rate of contraction in response to KCl was significantly reduced in A-CRF animals both in mesenteric arteries and aortas. The media of A-CRF aortas was thickened and showed focal areas of fragmented elastic lamellae and disorganized smooth muscle cells. No vascular calcifications could be detected. These results indicate that severe renal failure for a duration of less than 10 wk in this model primarily affects the aorta and mainly slows the rate of relaxation.

Eicosanoids and renal vascular function in diseases

2006 ◽  
Vol 111 (1) ◽  
pp. 21-34 ◽  
Author(s):  
John D. Imig
Keyword(s):  
Metabolic Syndrome ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Arachidonic Acid ◽  
Renal Disease ◽  
Vascular Function ◽  
Renal Vasculature ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites ◽  
Renal Vascular

Arachidonic acid metabolites are vital for the proper control of renal haemodynamics and, when not properly controlled, can contribute to renal vascular injury and end-stage renal disease. Three major enzymatic pathways, COX (cyclo-oxygenase), CYP450 (cytochrome P450) and LOX (lipoxygenase), are responsible for the metabolism of arachidonic acid metabolites to bioactive eicosanoids. These eicosanoids can dilate or constrict the renal vasculature and maintain vascular resistance in the face of changing vasoactive hormones. Renal vascular generation of eicosanoids is altered in pathophysiological conditions such as hypertension, diabetes, metabolic syndrome and acute renal failure. Experimental evidence supports the concept that altered eicosanoid metabolism contributes to renal haemodynamic alterations and the development and progression of nephropathy. The possible beneficial renal vascular actions of enzymatic inhibitors, eicosanoid analogues and receptor antagonists have been examined in hypertension, diabetes and metabolic syndrome. This review highlights the roles of renal vascular eicosanoids in the pathogenesis of nephropathy and therapeutic targets for renal disease related to hypertension, diabetes, metabolic syndrome and acute renal failure.

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