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Acute kidney injury (AKI) is a clinical syndrome characterized by a rapid decline of renal function in a short period of time. In recent years, the incidence of AKI has been increasing gradually. Once the AKI occurs in a patient whose mortality in hospital may be increased significantly, the length of stay in hospital will be prolonged and the hospitalization costs increased in a short term, the long-term consequences include AKI recurrence, development into chronic kidney disease (CKD) or end-stage kidney disease (ESRD), cardiovascular events and death, etc. Ischemia/reperfusion (I/R) injury and contrast agents are common causes of AKI. The nephropathy induced by I/R and contrast agent is associated with intracellular calcium overload caused by Na+-Ca2+ exchanger (NCX). In this article, a systematic review of the relationship between NCX and AKI was conducted, aiming to provide a reference for further recognizing the prevention, treatment and prognosis of AKI.
ABSTRACT
Objective To evaluate the effects of autophagy on contrast-induced acute kidney injury (CI-AKI) in rat models.Methods Eighteen male rats were divided into control group (Con),CI-AKI group (CI-AKI) and rapamycin-pretreated group (Rapa).In the CI-AKI group,CI-AKI was induced by intraperitoneal injection of iohexol (12.25 g/kg I).In the Rapa group,rapamycin was given by intraperitoneal injection with a dose of 5 mg/(kg ·d) for consecutive 7 days,and then injected with iohexol (12.25 g/kg I).Rats in the Con group were injected by the same dose of saline.The renal function,renal histopathology,and the levels of LC3 Ⅱ / Ⅰ and Beclin-1 as well as catalase (CAT) in the kidneys of rats were evaluated one day after the injection.Results Compared with the Con group,serum creatinine in the CI-AKI group was significantly increased ((239.93±27.00)μmol/L) vs (51.70±10.59) μmol/L,P＜0.05),and the content of CAT was significantly decreased ((14.86 ± 0.32) U/mg vs (18.72±1.46) U/mg,P＜0.05).In the CI-AKI group,renal tubules were severely injured,and the expression of autophagy-related proteins LC3 Ⅲ / Ⅰ and Beclin-1 in renal tissue was increased.Compared with the CI-AKI group,the pretreatment of rapamycin (Rapa group) increased the expression of LC3 Ⅱ / Ⅰ and Beclin-1 as well as the content of CAT in renal tissue ((17.62±1.86) U/mg vs (14.86±0.32) U/mg,P＜0.05),and inhibited the increase of contrast-induced serum creatinine ((187.62± 47.76) μmol/L vs (239.93±27.00) μmol/L,P＜0.05) and renal tubule injury.Conclusions The results showed that contrast administration can induce autophagy activation in kidneys,while enhancing autophagy can attenuate contrast-induced oxidative stress injury and related renal injury.
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Objective To evaluate the effects of autophagy on oxidative stress induced by contrast media in podocytes.Methods The differentiated mouse podocytes were exposed to contrast media (Iopromide,50 mg/L)、rapamycin (Rap,autophagy enhancer,1 ng/L),3-methyladenine (3-MA,autophagy inhibitor,2 mmol/L) for 2 hours.The expression of autophagy protein LC3-Ⅱ and Beclin-1 as well as oxidative stress-related proteins Catalase,MnSOD were detected by Western blot.The formations of autophagy were observed by MDC staining,and the levels of reactive oxygen species (ROS) by CM-H2DCFDA staining.Cell activity was evaluated by CCK8 assay.Results Both the levels of oxidative stress and autophagy in podocytes increased when stimulated by contrast media,the expression of LC3-Ⅱ and Beclin-1 were enhanced,Catalase and MnSOD were inhibited (all P ＜ 0.05).Rapamycin increased the expression of Catalase,MnSOD and cell activity of podocytes,reduced the generation of ROS (all P ＜ 0.05),but in Rap group,cell activity showed no significant difference (P ＞ 0.05).3-MA decreased the expression of Catalase 、MnSOD and inhibited the cell activity of podocyte,increased the generation of ROS (all P ＜ 0.05).Conclusion Autophagy protects podocyte from contrast media by the means of reducing oxidative stress.
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This report presented a case of 75-year-old woman who had received drug treatments two months earlier for nephrotic syndrome and was admitted to our hospital for inferior wall myocardial infarction with elevated creatinine and anemia.Kidney pathology after myocardial infarction showed allergic acute interstitial nephritis which induced acute renal failure.We stopped tripterygium glycosides and used cortical hormone,consequently.Thereafter,the symptoms of renal failure and anemia were improved and we considered tripterygium glycosides resulted in above allergic acute interstitial nephritis and anemia.Therefore,we had to carry out renal needle biopsy in the patient with the elderly nephrotic syndrome before confirmatory treatment to avoid blind use of tripterygium glycosides.
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Objective To investigate the renoprotective effects of KB-R7943 on renal injury induced bycontrast media. Method Tubular epithelial cells were trested with varions cencentration of KB-B7943 (10-5,10-6 mol/L) for 12 hours before contrast media was used. After cells we, re incubated with contrast media (CM)(110 mgI/L) for 1 hour, cells injury was assessed by using LDH, and cell morphologic changes and cells apopto-sis were evaluated with inverted microscope and flow cytometry, respoelively. Intracellular Ca2+ and reactive oxy-gen species (ROS) were analyzed by using confocal microscope. The expression of Na+/Ca2+exchanger mRNAwas evaluated by RT-PCR. Mannitol with same osmolarity (20% mannitol, 770 mOsm/L) of CM was used as con-trol. One-way analysis of variance and q-test were used for comparison between groups. The simple linear correla-tion was employed to analyze the correlation. P < 0.05 was considered significant. Results Contrast media sig-nificantly induced tubular cells damage significantly and apoptosis at 1 hour after incubation, meanwhile, intracel-lular Ca2+ and ROS were inoreased progressively in CM group. KB-R7943 significantly attenuated cells damage andapoptosis in dose-dependent in association with decreased intracellular Ca2+ and ROS. Expression of Na+/Ca2+exchanger mRNA was not changed. Conclusions KB-R7943 has renoprotective effects on the contrast-media-in-duced renal tubular cyotoxicity