scholarly journals Rhubarb Anthraquinones Protect Rats against Mercuric Chloride (HgCl2)-Induced Acute Renal Failure

Molecules ◽  
2016 ◽  
Vol 21 (3) ◽  
pp. 298 ◽  
Author(s):  
Dan Gao ◽  
Ling-Na Zeng ◽  
Pin Zhang ◽  
Zhi-Jie Ma ◽  
Rui-Sheng Li ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Mercuric Chloride

Induction of heme oxygenase-1 in toxic renal injury: mercuric chloride-induced acute renal failure in rat

1998 ◽  
Vol 94 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Saburo Horikawa ◽  
Koji Ito ◽  
Satoru Ikeda ◽  
Toshikazu Shibata ◽  
Shino Ishizuka ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Heme Oxygenase ◽  
Mercuric Chloride ◽  
Renal Injury ◽  
Heme Oxygenase 1

scholarly journals Effects of furosemide on low-dose mercuric chloride acute renal failure in the rat

1975 ◽  
Vol 8 (6) ◽  
pp. 362-367 ◽  
Author(s):  
Robert C. Ufferman ◽  
John R. Jaenike ◽  
Richard B. Freeman ◽  
Rufino C. Pabico ◽  
Craig D. Dickstein
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Mercuric Chloride ◽  
Low Dose

Glutathione Monoethyl Ester Moderates Mercuric Chloride-Induced Acute Renal Failure

Nephron ◽  
1992 ◽  
Vol 61 (4) ◽  
pp. 449-455 ◽  
Author(s):  
Mark T. Houser ◽  
Lawrence S. Milner ◽  
Peter C. Kolbeck ◽  
Shu H. Wei ◽  
Sidney J. Stohs
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Mercuric Chloride

scholarly journals Effect of dithiothreitol on mercuric chloride- and uranyl nitrate-induced acute renal failure in the rat.

1977 ◽  
Vol 12 (2) ◽  
pp. 115-121 ◽  
Author(s):  
Jack G. Kleinman ◽  
James S. McNeil ◽  
John H. Schwartz ◽  
Robert J. Hamburger ◽  
Walter Flamenbaum
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Mercuric Chloride ◽  
Uranyl Nitrate

Plasma Mercury during Prolonged Acute Renal Failure after Mercuric Chloride Ingestion

1983 ◽  
Vol 2 (3) ◽  
pp. 535-537 ◽  
Author(s):  
J.A. Newton ◽  
I.M. House ◽  
G.N. Volans ◽  
F.J. Goodwin
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Mercuric Chloride ◽  
Mercury Concentration ◽  
Oliguric Renal Failure ◽  
High Concentrations ◽  
Serial Measurements ◽  
Very High ◽  
Made In

1 Serial measurements of plasma mercury were made in a patient with severe and prolonged acute renal failure due to poisoning with mercuric chloride. 2 An initial mercury concentration in whole blood of 1200 μg/l (6 μmol/l) was recorded, and recovery of renal function coincided with a fall in plasma mercury concentration to below 100 μg/l (0.5 μmol/l). 3 The case demonstrates that survival and recovery of renal function is possible despite very high concentrations of mercury in the blood and oliguric renal failure of nearly six weeks' duration.

scholarly journals Ischemic and nephrotoxic acute renal failure are distinguished by their broad transcriptomic responses

2006 ◽  
Vol 25 (3) ◽  
pp. 375-386 ◽  
Author(s):  
Peter S. T. Yuen ◽  
Sang-Kyung Jo ◽  
Mikaela K. Holly ◽  
Xuzhen Hu ◽  
Robert A. Star
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Mercuric Chloride ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Protein Detection ◽  
Taqman Assay ◽  
Heme Oxygenase 1 ◽  
High Morbidity ◽  
Outer Stripe

Acute renal failure (ARF) has a high morbidity and mortality. In animal ARF models, effective treatments must be administered before or shortly after the insult, limiting their clinical potential. We used microarrays to identify early biomarkers that distinguish ischemic from nephrotoxic ARF or biomarkers that detect both injury types. We compared rat kidney transcriptomes at 2 and 8 h after ischemia/reperfusion and after mercuric chloride. Quality control and statistical analyses were necessary to normalize microarrays from different lots, eliminate outliers, and exclude unaltered genes. Principal component analysis revealed distinct ischemic and nephrotoxic trajectories and clear array groupings. Therefore, we used supervised analysis, t-tests, and fold changes to compile gene lists for each group, exclusive or nonexclusive, alone or in combination. There was little network connectivity, even in the largest group. Some microarray-identified genes were validated by TaqMan assay, ruling out artifacts. Western blotting confirmed that heme oxygenase-1 (HO-1) and activating transcription factor-3 (ATF3) proteins were upregulated; however, unexpectedly, their localization changed within the kidney. HO-1 staining shifted from cortical (early) to outer stripe of the outer medulla (late), primarily in detaching cells, after mercuric chloride but not ischemia/reperfusion. ATF3 staining was similar, but with additional early transient expression in the outer stripe after ischemia/reperfusion. We conclude that microarray-identified genes must be evaluated not only for protein levels but also for anatomical distribution among different zones, nephron segments, or cell types. Although protein detection reagents are limited, microarray data lay a rich foundation to explore biomarkers, therapeutics, and the pathophysiology of ARF.

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