AMINO ACIDS' PROTECTIVE EFFECTS ON EXPERIMENTAL ACUTE RENAL FAILURE

2000 ◽  
Vol 1 (2) ◽  
pp. 212
Author(s):  
Li-ping XIE
Keyword(s):  
Amino Acids ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Protective Effects

Oestrogen protects against ischaemic acute renal failure in rats by suppressing renal endothelin-1 overproduction

2002 ◽  
Vol 103 (s2002) ◽  
pp. 434S-437S ◽  
Author(s):  
Masanori TAKAOKA ◽  
Mikihiro YUBA ◽  
Toshihide FUJII ◽  
Mamoru OHKITA ◽  
Yasuo MATSUMURA
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Acute Renal Failure ◽  
Renal Dysfunction ◽  
Tissue Injury ◽  
Male Rats ◽  
Left Renal Artery ◽  
Protective Effects ◽  
Endothelin 1 ◽  
Ischaemia Reperfusion

We investigated whether the treatment with 17β-oestradiol has renal protective effects in male rats with ischaemic acute renal failure (ARF). We also examined if the effect of 17β-oestradiol is accompanied by suppression of enhanced endothelin-1 production in postischaemic kidneys. Ischaemic ARF was induced by clamping the left renal artery and vein for 45min followed by reperfusion, 2 weeks after contralateral nephrectomy. Renal function parameters such as blood urea nitrogen, plasma creatinine and creatinine clearance were measured to test the effectiveness of the steroid hormone. Renal function in ARF rats markedly decreased 24h after reperfusion. The ischaemia/reperfusion-induced renal dysfunction was dose-dependently improved by pretreatment with 17β-oestradiol (20 or 100µg/kg, intravenously). Histopathological examination of the kidney of untreated ARF rats revealed severe lesions, such as tubular necrosis, proteinaceous casts in tubuli and medullary congestion, all of which were markedly improved by the higher dose of 17β-oestradiol. In addition, endothelin-1 content in the kidney after the ischaemia/reperfusion increased significantly by approx. 2-fold over sham-operated rats, and this elevation was dose-dependently suppressed by the 17β-oestradiol treatment. These results suggest that oestrogen exhibits protective effects against renal dysfunction and tissue injury induced by ischaemia/reperfusion, possibly through the suppression of endothelin-1 overproduction in postischaemic kidneys.

Evidence suggesting a role for hydroxyl radical in glycerol-induced acute renal failure

1988 ◽  
Vol 255 (3) ◽  
pp. F438-F443 ◽  
Author(s):  
S. V. Shah ◽  
P. D. Walker
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Hydroxyl Radical ◽  
Tissue Injury ◽  
Iron Chelator ◽  
Radical Scavenger ◽  
Reactive Oxygen Metabolites ◽  
Protective Effects ◽  
Hydroxyl Radical Scavenger ◽  
Hydroxyl Radical Scavengers

Reactive oxygen metabolites, in particular hydroxyl radical, have been shown to be important mediators of tissue injury in several models of acute renal failure. The aim of the present study was to examine the role of hydroxyl radical in glycerol-induced acute renal failure, a model for myoglobinuric renal injury. Rats injected with glycerol alone (8 mg/kg im following dehydration for 24 h) developed significant renal failure compared with dehydrated controls. Rats treated with glycerol and a hydroxyl radical scavenger, dimethylthiourea (DMTU), had significantly lower blood urea nitrogen (BUN) and creatinine. In contrast, urea, which is chemically similar to DMTU but is not a hydroxyl radical scavenger, provided no protection. In addition, DMTU prevented the glycerol-induced rise in renal cortical malondialdehyde content (a measure of lipid peroxidation that serves as a marker of free radical-mediated tissue injury). A second hydroxyl radical scavenger, sodium benzoate, had a similar protective effect on renal function (as measured by both BUN and creatinine). Because the generation of hydroxyl radical in biological systems requires the presence of a trace metal such as iron, we also examined the effect of the iron chelator, deferoxamine on glycerol-induced renal failure. Deferoxamine was also protective. The interventional agents were also associated with a marked reduction in histological evidence of renal damage. The protective effects of two hydroxyl radical scavengers as well as an iron chelator implicate a role for hydroxyl radical in glycerol-induced acute renal failure.

scholarly journals Amniotic fluid stem cells ameliorate cisplatin-induced acute renal failure through induction of autophagy and inhibition of apoptosis

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Ekta Minocha ◽  
Rohit Anthony Sinha ◽  
Manali Jain ◽  
Chandra Prakash Chaturvedi ◽  
Soniya Nityanand
Keyword(s):  
Stem Cells ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Amniotic Fluid ◽  
Cell Types ◽  
Treated Group ◽  
Protective Role ◽  
Protective Effects ◽  
Amniotic Fluid Stem Cells

Abstract Background We have recently demonstrated that amniotic fluid stem cells (AFSC) express renal progenitor markers and can be differentiated in vitro into renal lineage cell types, viz, juxtaglomerular and renal proximal tubular epithelial-like cells. Here, we have evaluated the therapeutic efficacy of AFSC in a cisplatin-induced rat model of acute renal failure (ARF) and investigated the underlying mechanisms responsible for their renoprotective effects. Methods ARF was induced in Wistar rats by intra-peritoneal injection of cisplatin (7 mg/kg). Five days after cisplatin injection, rats were randomized into two groups and injected with either AFSC or normal saline intravenously. On days 8 and 12 after cisplatin injection, the blood biochemical parameters, histopathological changes, apoptosis and expression of pro-apoptotic, anti-apoptotic, and autophagy-related proteins in renal tissues were studied in both groups of rats. To further confirm whether the protective effects of AFSC on cisplatin-induced apoptosis were dependent on autophagy, chloroquine, an autophagy inhibitor, was administered by the intra-peritoneal route. Results Administration of AFSC in ARF rats resulted in improvement of renal function and attenuation of renal damage as reflected by significant decrease in blood urea nitrogen, serum creatinine levels, tubular cell apoptosis as assessed by Bax/Bcl2 ratio, and expression of the pro-apoptotic proteins, viz, PUMA, Bax, cleaved caspase-3, and cleaved caspase-9, as compared to the saline-treated group. Furthermore, in the AFSC-treated group as compared to the saline-treated group, there was a significant increase in the activation of autophagy as evident by increased expression of LC3-II, ATG5, ATG7, Beclin1, and phospho-AMPK levels with a concomitant decrease in phospho-p70S6K and p62 expression levels. Chloroquine administration led to significant reduction in the anti-apoptotic effects of the AFSC therapy and further deterioration in the renal structure and function caused by cisplatin. Conclusion AFSC led to amelioration of cisplatin-induced ARF which was mediated by inhibition of apoptosis and activation of autophagy. The protective effects of AFSC were blunted by chloroquine, an inhibitor of autophagy, highlighting that activation of autophagy is an important mechanism of action for the protective role of AFSC in cisplatin-induced renal injury.

Theophylline-induced protection in myoglobinuric acute renal failure: further characterization

1987 ◽  
Vol 65 (1) ◽  
pp. 42-45 ◽  
Author(s):  
A. K. Bidani ◽  
P. C. Churchill ◽  
W. Packer
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Serum Creatinine ◽  
Biological Fluids ◽  
Peak Serum ◽  
Tubuloglomerular Feedback ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Adenosine Receptor Antagonist ◽  
Myoglobinuric Acute Renal Failure

We have reported previously that aminophylline has an ameliorating effect on the course and severity of glycerol-induced myoglobinuric acute renal failure in rats. Since aminophylline dissociates into theophylline in biological fluids and since theophylline is an adenosine receptor antagonist, we attributed the ameliorating effects to antagonism of the hemodynamic effects of endogenous adenosine. However, theophylline blocks tubuloglomerular feedback and produces natriuresis, and either of these effects might have accounted for the beneficial effects in acute renal failure. Therefore, this study was designed to further characterize the effects of theophylline in glycerol-induced acute renal failure in rats. Aminophylline had dose-dependent beneficial effects, as judged by the peak serum creatinine during the 3 days following induction of acute renal failure, by the number of animals with peak serum creatinine >1 mg/dL, and by the mortality rate. Both furosemide and theophylline block tubuloglomerular feedback and produce natriuresis, but aminophylline had protective effects, whereas furosemide actually increased mortality, compared with aminophylline, following induction of myoglobinuric acute renal failure. Therefore, aminophylline's protective effects are independent of tubuloglomerular feedback and natriuresis. These results offer further support for the hypothesis that adenosine-induced hemodynamic changes play a pathogenic role in glycerol-induced acute renal failure in rats.

Acute renal failure: biochemical evaluation of total parenteral nutrition with essential l-amino acids

Resuscitation ◽  
1978 ◽  
Vol 6 (3) ◽  
pp. 191-196 ◽  
Author(s):  
R. Proietti ◽  
G. Pelosi ◽  
E. Scrascia ◽  
S.I. Magalini ◽  
A. Bondoli
Keyword(s):  
Amino Acids ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Biochemical Evaluation

Parenteral essential amino acids in acute renal failure

Urology ◽  
1975 ◽  
Vol 6 (2) ◽  
pp. 154-157 ◽  
Author(s):  
Charles D. Leonard ◽  
Robert G. Luke ◽  
Robert R. Siegel
Keyword(s):  
Amino Acids ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Essential Amino Acids
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