Increased severity of renal ischemia-reperfusion injury with venous clamping compared to arterial clamping in a rat model
ABSTRACT Arterial inflow occlusion is a well-known mechanism of renal injury during major vascular surgery. In contrast, renal injury from venous outflow obstruction is poorly understood. The goal of this study was to examine the injury pattern of renal venous outflow obstruction, compare this with the traditional model of arterial occlusion, and examine possible mechanisms.
Male Fisher rats were used for the renal warm ischemia model. Twenty-five minutes of renal ischemia was induced by selectively occluding either the renal artery or vein. After 24 h of reperfusion, whole blood and kidney tissue were collected for further analysis.
Serum creatinine (SCr) concentrations taken 24 h after reperfusion were significantly greater in the venous occlusion group (V) when compared to the arterial group (A). While histology did not demonstrate significant differences in extent of necrosis between both groups, a stronger inflammatory response resulted from venous occlusion. Specifically, significantly greater MCP-1 mRNA and significantly greater MCP-1, TNF-alpha, and HO-1 protein levels were found in the venous group, while no differences in MIP-2, ICAM-1, and VCAM-1 mRNA expression existed between A and V. Further analysis demonstrated presence of increased cleaved caspase-3 protein in the artery group than in the venous group.
Venous renal outflow obstruction results in more severe functional renal injury when compared to arterial inflow occlusion. Macrophage activation and neutrophilic infiltration appear to be exaggerated during venous occlusion.
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- "Although resuscitation targeting the forward determinants of renal blood flow (MAP and CO) is common, little is known about backward determinants (renal venous pressure). In experimental studies, renal venous congestion has been shown to be important in promoting renal injury [8,15,16]. Uncoupling CO and AKI has also been observed in experimental septic models [17,18]. In patients with acute heart failure, the increase in CVP, but not CO, has been found to be strongly associated with AKI [19,20]. "
ABSTRACT: The role of systemic hemodynamics in the pathogenesis of septic acute kidney injury (AKI) has received little attention. The purpose of this study was to investigate the association between systemic hemodynamics and new or persistent of AKI in severe sepsis. A retrospective study between 2006 and 2010 was performed in a surgical ICU in a teaching hospital. AKI was defined as development (new AKI) or persistent AKI during the five days following admission based on the acute kidney injury network (AKIN) criteria. We studied the association between the following hemodynamic targets within 24 hours of admission and AKI: central venous pressure (CVP), cardiac output (CO), mean arterial pressure (MAP), diastolic arterial pressure (DAP), central venous oxygen saturation (ScvO2) or mixed venous oxygen saturation (SvO2). This study included 137 ICU septic patients. Of these, 69 had new or persistent AKI. AKI patients had a higher simplified acute physiology score (SAPS) (57 (46 to 67) versus 45 (33 to 52), P <0.001) and a higher mortality (38% versus 15%, P = 0.003) than those with no AKI or improving AKI. MAP, ScvO2 and CO were not significantly different between groups. Patients with AKI had lower DAP and higher CVP (P = 0.0003). The CVP value was associated with the risk of developing new or persistent AKI even after adjustment for fluid balance and positive end expiratory pressure (PEEP) level (OR = 1.22 (1.08 to 1.39), P = 0.002). A linear relationship between CVP and the risk of new or persistent AKI was observed. We observed no association between most systemic hemodynamic parameters and AKI in septic patients. Association between elevated CVP and AKI suggests a role of venous congestion in the development of AKI. The paradigm that targeting high CVP may reduce occurrence of AKI should probably be revised. Furthermore, DAP should be considered as a potential important hemodynamic target for the kidney.Critical care (London, England) 11/2013; 17(6):R278. DOI:10.1186/cc13133 · 4.48 Impact Factor
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- "IL-6 and TNF-a will trigger leukocyte–endothelium interactions and microcirculatory dysfunction, and alter renal microvascular O2 distribution and promote organ damage [25,38]. In addition, the venous warm ischemia from suprarenal IVC occlusion can also activate inflammatory response in renal tissue and aggravate kidney injury . Macrophage activation and neutrophilic infiltration appear to be exaggerated during venous occlusion and increase severity of renal injury . "
ABSTRACT: Background Acute kidney injury (AKI) is a common complication after liver transplantation (LT) and associated with a high mortality. The renal resistive index (RI) is used to assess early renal function impairment in critical care patients. However, limited data are available concerning changes of renal RI and the development of AKI early after reperfusion. We approached to investigate the changes of renal RI and AKI after reperfusion in a rat liver transplantation model. Methods Rats were randomly divided into sham group or LT group. Ten rats in each group were used for the hemodynamic study and twenty for Doppler measurements during the procedure. Ten rats were sacrificed 30 min or 2 h after the reperfusion. We harvested kidneys, serum and urine for further analysis of the renal function. Results The intrarenal RI increased significantly in the anhepatic stage and decreased significantly after the reperfusion in the LT group compared with sham group (P < 0.05). AKI was seen after the reperfusion in the LT group. No correlation was noted between the RI and renal function parameters 30 min after reperfusion. Conclusions The intrarenal RI increased significantly during the anhepatic stage, and decreased significantly early after the reperfusion. Intrarenal RI was unable to assess renal function in a rat liver transplantation model.BMC Nephrology 03/2013; 14(1):55. DOI:10.1186/1471-2369-14-55 · 1.69 Impact Factor
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ABSTRACT: The purpose of this study was to investigate the effect of iloprost, a cytoprotective prostacyclin analog, on renal injury during unilateral renal I/R in rats and to determine whether the levels of serum cystatin C (CyC) and beta2-microglobulin (B2M), as markers of glomerular function, might denote this injury. Thirty-two Wistar rats were randomized into four groups (n = 8) as follows: control (sham laparotomy), renal I/R (60-min left renal ischemia and 120-min reperfusion), renal I/R + iloprost (20 ng kg(-1) min(-1) infusion during renal I/R period, i.v.), and control + iloprost. Blood and kidney tissue samples were obtained for biochemical and histological analysis from all rats. Serum urea, creatinine, CyC, and B2M levels were evaluated for biochemical analysis. Histopathological changes in renal structure were examined for histological analysis. Serum urea, creatinine, and CyC levels were significantly increased in the renal I/R group. Iloprost treatment decreased these three markers in the renal I/R + iloprost group. beta2-Microglobulin levels were not significantly changed in any group. Histological analyses showed that renal I/R elicited significant renal injury, whereas iloprost significantly decreased I/R-induced renal injury. Serum CyC level is one of the good indicators of acute renal damage due to I/R produced by renal artery occlusion. In contrast, we have shown that there are no significant changes in the levels of serum B2M levels that would make it an accurate diagnostic tool for detecting acute changes in renal injury subject to renal I/R in rats.Shock (Augusta, Ga.) 04/2009; 32(5):498-502. DOI:10.1097/SHK.0b013e3181a1ba54 · 3.05 Impact Factor