Key result
In rats with combined heart and kidney failure, elevating renal venous pressure exacerbated the reduction in renal blood flow (-6.4 vs -3.7 ml/min, p<0.05) and virtually eliminated GFR.
Why the study?
Increased renal venous pressure is common in combined heart and kidney failure, but whether it impairs cardiovascular stability, renal perfusion, and exacerbates renal dysfunction remained unknown.
p-value: p=<0.05
In a rat model, chronic combined heart and kidney failure exacerbates the reduction in renal blood flow and glomerular filtration rate induced by elevated renal venous pressure.
May identify renal venous pressure as target in experimental cardiorenal failure; leaves open human translation.
Background and Objective Increased renal venous pressure (RVP) is common in combined heart and kidney failure. We previously showed that acute RVP elevation depresses renal blood flow (RBF), glomerular filtration rate (GFR), and induces renal vasoconstriction in the absence of changes in blood pressure in healthy rats. We used our established rodent model of chronic combined heart and kidney failure (H/KF) to test whether RVP elevation would impair cardiovascular stability, renal perfusion and exacerbate renal dysfunction. Methods Male rats were subjected to 5/6 nephrectomy (SN x or Sham) and 6% high salt diet followed 7 weeks later by ligation of the left anterior descending coronary artery (CL or Sham). Experimental groups: CL + SN x ( n = 12), Sham CL + SN x ( n = 9), CL+ Sham SN x ( n = 6), and Sham Control ( n = 6). Six weeks later, anesthetized rats were subjected to an acute experiment whereupon mean arterial pressure (MAP), heart rate (HR), RVP, RBF, and GFR were measured at baseline and during elevation of RVP to 20–25 mmHg for 120 min. Results Baseline MAP, HR, RBF, and renal vascular conductance (RVC) were comparable among groups. Baseline GFR was significantly depressed in CL + SN x and Sham CL + SN x groups compared to Sham Control and CL + Sham SN x groups. Upon RVP increase, MAP and HR fell in all groups. Increased RVP exacerbated the reduction in RBF in CL + SN x (−6.4 ± 0.9 ml/min) compared to Sham Control (−3.7 ± 0.9 ml/min, p < 0.05) with intermediate responses in Sham CL + SN x (−6.8 ± 1.3 ml/min) and CL + Sham SN x (−5.1 ± 0.4 ml/min) groups. RVP increase virtually eliminated GFR in CL + SN x (−99 ± 1%), Sham CL + SN x (−95 ± 5%), and CL + Sham SN x (−100%) groups compared to Sham Control (−84 ± 15% from baseline; p < 0.05). Renal vascular conductance dropped significantly upon RVP increase in rats with HF (CL + SN x : −0.035 ± 0.011; CL + Sham SN x : −0.050 ± 0.005 ml/min·mmHg −1 , p < 0.05) but not Sham CL + SN x (−0.001 ± 0.019 ml/min·mmHg −1 ) or Control (−0.033 ± mL/min·mmHg −1 ). Conclusion Chronic combined heart and kidney failure primarily impairs renal hemodynamic stability in response to elevated RVP compared to healthy rats.
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Hamza et al. (2022) studied Chronic combined heart and kidney failure (n=33). Elevation of renal venous pressure (RVP) vs. Sham Control was evaluated on Changes in renal blood flow (RBF) and glomerular filtration rate (GFR) upon RVP increase (p=<0.05). In rats with combined heart and kidney failure, elevating renal venous pressure exacerbated the reduction in renal blood flow (-6.4 vs -3.7 ml/min, p<0.05) and virtually eliminated GFR.
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