Nonsteroidal anti-inflammatory agents and acute renal failure

1996 ◽  
Vol 156 (21) ◽  
pp. 2414-2414 ◽  
Author(s):  
C. F. Gutch
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Anti Inflammatory

Acute renal failure and flank pain after binge drinking and non-steroidal anti-inflammatory drugs.

1997 ◽  
Vol 12 (9) ◽  
pp. 2034-2035 ◽  
Author(s):  
R. EnrA quez ◽  
A. E. Sirvent ◽  
A. AntolA n ◽  
J. B. Cabezuelo ◽  
C. GonzAlez ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Binge Drinking ◽  
Flank Pain ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Acute renal failure: determinants and characteristics of the injury-induced hyperinflammatory response

2006 ◽  
Vol 291 (3) ◽  
pp. F546-F556 ◽  
Author(s):  
Richard A. Zager ◽  
Ali C. M. Johnson ◽  
Steve Lund ◽  
Sherry Hanson
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Lipoteichoic Acid ◽  
Heme Oxygenase 1 ◽  
Inos Mrna ◽  
Chemokine Production ◽  
Tnf Α ◽  
Tlr2 Ligand ◽  
Tlr4 Ligand ◽  
Anti Inflammatory

Acute renal failure (ARF) markedly sensitizes mice to endotoxin (LPS), as evidenced by exaggerated renal cytokine/chemokine production. This study sought to further characterize this state by testing the following: 1) does anti-inflammatory heme oxygenase-1 (HO-1) upregulation in selected ARF models prevent this response? 2) Is the ARF hyperresponsive state specifically triggered by LPS? 3) Does excess iNOS activity/protein nitrosylation participate in this phenomenon? and 4) are upregulated Toll receptors involved? Mice with either 1) rhabdomyolysis-induced ARF (massive HO-1 overexpression), 2) cisplatin nephrotoxicity, 3) or HO-1 inhibition (Sn protoporphyrin) were challenged with either LPS (a TLR4 ligand), lipoteichoic acid (LTA; a TLR2 ligand), or vehicle. Two hours later, renal and plasma TNF-α/mRNA, MCP-1/mRNA, renal nitrotyrosine/iNOS mRNA, and plasma cytokines were assessed. Renal TLR4 was gauged by mRNA and Western blot analysis. Both ARF models markedly hyperresponded to both LPS and LTA, culminating in exaggerated TNF-α, MCP-1, and iNOS/nitrotryosine increments. This was despite the fact that HO-1 exerted anti-inflammatory effects. TLR4 levels were either normal (cisplatin), or markedly depressed (∼50%; rhabdomyolysis) in the ARF kidneys, despite the LPS hyperresponsive state. 1) The ARF kidney can hyperrespond to chemically dissimilar Toll ligands; 2) HO-1 does not prevent this response; 3) excess NO/protein nitrosylation can result; and 4) this hyperresponsiveness can be expressed with either normal or reduced renal TLR4 expression. This suggests that diverse signaling pathways may be involved.

scholarly journals Aggravation of non-steroidal anti-inflammatory drug-induced hepatitis and acute renal failure by slimming drug containing anthraquinones

2004 ◽  
Vol 19 (7) ◽  
pp. 1916-1917 ◽  
Author(s):  
F. K. Li ◽  
C.-K. Lai ◽  
W. T. Poon ◽  
A. Y. W. Chan ◽  
K. W. Chan ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Drug Induced ◽  
Inflammatory Drug ◽  
Anti Inflammatory

scholarly journals Syndrome of flank pain and acute renal failure after binge drinking and nonsteroidal anti-inflammatory drug ingestion.

1995 ◽  
Vol 5 (9) ◽  
pp. 1647-1652
Author(s):  
G R Johnson ◽  
S F Wen
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Binge Drinking ◽  
Acute Tubular Necrosis ◽  
Extracellular Volume ◽  
Renal Perfusion ◽  
Flank Pain ◽  
Inflammatory Drug ◽  
Tubular Necrosis ◽  
Anti Inflammatory

The binge drinking of alcohol combined with the ingestion of a nonsteroidal anti-inflammatory drug (NSAID) is a recently described cause of reversible acute renal failure. The pathogenetic mechanisms leading to acute tubular necrosis in this setting include the initial compromise in renal perfusion due to alcohol-induced extracellular volume contraction and the superimposed renal hemodynamic alterations induced by the NSAID that interfere with the renal autoregulation. Although alcohol may also cause rhabdomyolysis leading to acute tubular necrosis, this is usually not apparent in these cases. Previously, only three such cases have been reported but the incidence is likely to be higher in view of the prevalence of alcohol and NSAID use. Herein is presented another patient in whom the features of flank pain and acute renal failure in association with binge drinking and NSAID ingestion constitute a characteristic syndrome.

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