Abstract
Increased central venous pressure in congestive heart failure causes renal dysfunction; however, the underlying mechanisms are unclear. We created a rat renal congestion model and investigated the effect of renal congestion on hemodynamics and molecular mechanisms. The inferior vena cava (IVC) between the renal veins was ligated by suture in male Sprague-Dawley rats to increase upstream IVC pressure and induce congestion in the left kidney only. Left kidney congestion reduced renal blood flow, glomerular filtration rate, and increased renal interstitial hydrostatic pressure. Tubulointerstitial and glomerular injury and medullary thick ascending limb hypoxia were observed only in the congestive kidneys. Molecules related to extracellular matrix expansion, tubular injury, and focal adhesion were upregulated in microarray analysis. Renal decapsulation ameliorated the tubulointerstitial injury. Electron microscopy captured pericyte detachment in the congestive kidneys. Transgelin and platelet-derived growth factor receptors, as indicators of pericyte-myofibroblast transition, were upregulated in the pericytes and the adjacent interstitium. With the compression of the peritubular capillaries and tubules, hypoxia and physical stress induce pericyte detachment, which could result in extracellular matrix expansion and tubular injury in renal congestion.
Highlights
The physiological association between the kidney and heart has received significant attention
The catheters were detained for measurement of inferior vena cava (IVC) pressure (IVCP) and urine collection from each kidney
IVC between the renal veins was ligated after the 60-min baseline (Fig. 1a). arterial blood pressure (ABP) and pulse rate (PR) were immediately decreased after ligation
Summary
The physiological association between the kidney and heart has received significant attention. In patients with chronic congestive heart failure (CHF), central venous pressure (CVP) normally measured at the inferior vena cava (IVC) and renal venous pressure (RVP) are higher than in healthy subjects[2]. The underlying mechanisms of renal dysfunction in patients with CHF, are yet unknown. Increased CVP raises RVP, causing renal congestion and renal dysfunction[5,6]. Ligation of the IVC above the renal veins raises RVP10 and induces chronic renal dysfunction[11,12]. Other pathways are involved in tissue fibrosis[18]; little is known about the molecular mechanisms in renal congestion and their roles in CHF-related renal injury. To determine the molecules underlying renal congestion pathophysiology, gene expression arrays of the left and right kidneys were compared within subjects. The functional and structural characteristics of the kidneys were examined using immunohistological analysis and electron microscopy
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