Obesity Increases Renal Cortical Neovascularization in Zucker Rats

Abstract

Growing evidence supports the role of obesity as an independent risk factor for chronic kidney disease. Obesity promotes inflammation. Inflammatory cytokines can induce neovascularization in different organs, including the kidneys. However, whether obesity triggers renal neovascularization and, if so, the physiological significance has never been investigated.Renal microvascular architecture was studied by 3D micro‐computer tomography in lean and obese Zucker rats (LZR and OZR, n=6/group). Mean arterial pressure (MAP), renal blood flow (RBF), and proteinuria were measured in vivo. Systemic inflammation was assessed by measuring levels of interleukin (IL)‐6 and tumornecrosis‐factor (TNF)‐α. In addition, renal histology was studied in cross sections stained with trichrome.Renal microvascular density was significantly elevated in OZR (Figure). Despite mild proteinuria and increased tubulo‐interstitial and glomerular damage in OZR, RBF and MAP were similar in both groups (Figure). Furthermore, OZR showed a substantial elevation in systemic IL‐6 and TNF‐α (3–4 fold), suggesting increased inflammation.The current study shows for the first time increased renal cortical vascularization in an animal model of obesity, which possibly reflects a compensatory mechanism that sustains RBF. However, increased inflammation in obese rats may promote further renal injury, as has been observed in obese humans, as the disease progresses.(Supported by HL‐69194 and Intramural Research Grant Support from the University of Mississippi)