Ischemic Renal Failure

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.

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

Klinische Wochenschrift ◽

10.1007/bf01645163 ◽

1991 ◽

Vol 69 (21-23) ◽

pp. 1083-1094 ◽

Cited By ~ 18

Author(s):

H. J. Schiller ◽

K. A. Andreoni ◽

G. B. Bulkley

Keyword(s):

Renal Failure ◽

Renal Transplantation ◽

Free Radical ◽

Ischemic Renal Failure

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

10.1055/s-0038-1653048 ◽

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.

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N-acetyl cysteine ameliorates ischemic renal failure in the rat

American Journal of Kidney Diseases ◽

10.1016/s0272-6386(96)90191-2 ◽

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

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

AJP Renal Physiology ◽

10.1152/ajprenal.2000.279.3.f426 ◽

2000 ◽

Vol 279 (3) ◽

pp. F426-F439 ◽

Cited By ~ 9

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.

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