Classically, a single renal artery supplies, and a single renal vein drains each kidney. The morphology and variations in the renal vascular structures are of great importance when performing any type of renal surgery. The present case describes a rare combination of renal vasculature variation in a formalin-fixed, Chinese male cadaver. In this case, the left kidney is drained by a main renal vein (MRV) and an inferior renal vein (IRV), the latter might be the remnant of the left dorsal renal vein during the embryonic period. Two sets of renal arteries are present in this case, possibly due to persistent mesonephric arteries during embryonic development. Describing such anatomical variations is not only of academic interest but also important to help radiologists with the correct interpretation of image examinations and for surgeons to be prepared in advance.

This work describes a comprehensive study of the vascular tree and perfusion characteristics of normal kidney and renal cell carcinoma. Methods: Nephrectomy specimens were perfused ex-vivo, and the regional blood flow was determined by infusion of radioactive microspheres. The vascular architecture was characterized by micronized barium sulphate infusion. Kidneys were subsequently sagitally sectioned, and autoradiograms were obtained to show the perfusate flow in relation to adjacent contact X-ray angiograms. Vascular resistance in defined tissue compartments was quantified, and finally, the tumor vasculature was 3D reconstructed via the micro-CT technique. Results show that the vascular tree of the kidney could be distinctly defined, and autoradiograms disclosed a high cortical flow. The peripheral resistance unit of the whole perfused specimen was 0.78 ± 0.40 (n = 26), while that of the renal cortex was 0.17 ± 0.07 (n = 15 with 114 samples). Micro-CT images from both cortex and medulla defined the vascular architecture. Angiograms from the renal tumors demonstrated a significant vascular heterogeneity within and between different tumors. A dense and irregular capillary network characterized peripheral tumor areas, whereas central parts of the tumors were less vascularized. Despite the dense capillarity, low perfusion through vessels with a diameter below 15 µm was seen on the autoradiograms. We conclude that micronized barium sulphate infusion may be used to demonstrate the vascular architecture in a complex organ. The vascular resistance was low, with little variation in the cortex of the normal kidney. Tumor tissue showed a considerable vascular structural heterogeneity with low perfusion through the peripheral nutritive capillaries and very poor perfusion of the central tumor, indicating intratumoral pressure exceeding the perfusion pressure. The merits and shortcomings of the various techniques used are discussed.

Renal vasculature, which is highly innervated by sympathetic fibers, contributes to cardiovascular homeostasis. This renal sympathetic outflow is inhibited by 5-HT in normoglycaemic rats. Considering that diabetes induces cardiovascular complications, we aimed to determine whether diabetic state modifies noradrenergic input at renal level and its serotonergic modulation in rats. Alloxan diabetic rats were anaesthetized (pentobarbital; 60 mg/kg i.p.) and prepared for in situ autoperfusion of the left kidney to continuously measure systemic blood pressure (SBP), heart rate (HR), and renal perfusion pressure (RPP). Electrical stimulation of renal sympathetic outflow induces frequency-dependent increases (Δ) in RPP (23.9 ± 2.1, 59.5 ± 1.9, and 80.5 ± 3.5 mm Hg at 2, 4, and 6 Hz, respectively), which were higher than in normoglycaemic rats, without modifying HR or SBP. Intraarterial bolus of 5-HT and 5-CT (5-HT1/5/7 agonist) reduced electrically induced ΔRPP. Only L-694,247 (5-HT1D agonist) reproduced 5-CT inhibition on sympathetic-induced vasoconstrictions, whereas it did not modify exogenous noradrenaline-induced ΔRPP. 5-CT inhibition was exclusively abolished by i.v. bolus of LY310762 (5-HT1D antagonist). An inhibitor of guanylyl cyclase, ODQ (i.v.), completely reversed the L-694,247 inhibitory effect. In conclusion, diabetes induces an enhancement in sympathetic-induced vasopressor responses at the renal level. Prejunctional 5-HT1D receptors, via the nitric oxide pathway, inhibit noradrenergic-induced vasoconstrictions in diabetic rats.

BACKGROUND: Diabetes mellitus (DM) induces cardiac and cerebral microvascular dysfunction via increased glycation, oxidative stress and endothelial activation. Liraglutide, a glucagon-like peptide-1 analogue, inhibited NOX2 and adhesion molecules in isolated endothelial cells. Here, we have studied how Liraglutide affects advanced glycation, NOX expression and inflammation of the cardiac, cerebral and renal microvasculature in diabetic rats.
METHODS: DM was induced in Sprague-Dawley rats (n = 15) via intraperitoneal streptozotocin (STZ) injection (60 mg/kg bodyweight). Ten control rats remained nondiabetic. From day 9 post-STZ injection, Liraglutide (200 μg/kg bodyweight; n = 7) or vehicle (n = 8) was injected subcutaneously daily until termination on day 29. The advanced glycation endproduct N-ε-(carboxymethyl)lysine (CML), NOX2, NOX4, ICAM-1 and VCAM-1 were subsequently immunohistochemically analysed and quantified to compare Liraglutide treatment with placebo.
RESULTS: In the heart, Liraglutide treatment significantly reduced the DM-increased scores/cm2 for CML in both ventricles (from 253 ± 53 to 72 ± 12; p = .003) and atria (343 ± 29 to 122 ± 8; p = .0001) and for NOX2, ICAM-1 and VCAM-1, but not for NOX4. Also in the cerebrum and cerebellum of the brain, Liraglutide significantly reduced the scores/cm2 for CML (to 60 ± 7 (p = .0005) and 47 ± 13 (p = .02), respectively), and for NOX2 and NOX4. In the kidney, the DM-induced expression of ICAM-1 and VCAM-1 was decreased in the blood vessels and glomeruli by Liraglutide treatment. Liraglutide did not affect blood glucose levels or bodyweight.
CONCLUSIONS: Our study implies that Liraglutide protects the cardiac, cerebral and renal microvasculature against diabetes-induced dysfunction, independent of lowering blood glucose in a type 1 diabetes rat model.

Three-dimensional (3D) printed model of the renal vasculature shows a high level of accuracy of subsequent divisions of both the arterial and the venous tree. However, minor artifacts appeared in the form of oval endings to the terminal branches of the vascular tree, contrary to the anticipated sharply pointed segments. Unfortunately, selective laser sintering process does not currently permit to present the arterial, venous and urinary systems in distinct colors, hence topographic relationship between the vascular and the pelvicalyceal systems is difficult to attain. Nonetheless, the 3D printed model can be used for educational purposes to demonstrate the vast renal vasculature and may also serve as a reference model whilst evaluating morphological anomalies of the intrarenal vasculature in a surgical setting.

Given the relevance of the inextricable coupling between microcirculation and physiology, and the relation to organ function and disease progression, the construction of synthetic vascular networks for mathematical modelling and computer simulation is becoming an increasingly broad field of research. Building vascular networks that mimic in vivo morphometry is feasible through algorithms such as constrained constructive optimization (CCO) and variations. Nevertheless, these methods are limited by the maximum number of vessels to be generated due to the whole network update required at each vessel addition. In this work, we propose a CCO-based approach endowed with a domain decomposition strategy to concurrently create vascular networks. The performance of this approach is evaluated by analysing the agreement with the sequentially generated networks and studying the scalability when building vascular networks up to 200 000 vascular segments. Finally, we apply our method to vascularize a highly complex geometry corresponding to the cortex of a prototypical human kidney. The technique presented in this work enables the automatic generation of extensive vascular networks, removing the limitation from previous works. Thus, we can extend vascular networks (e.g. obtained from medical images) to pre-arteriolar level, yielding patient-specific whole-organ vascular models with an unprecedented level of detail.

Hypertension impairs the function of the kidney and its vasculature. Adrenergic activation is involved in these processes by promoting oxidative stress and mitochondrial dysfunction. Thus, the targeting of mitochondrial function and mitochondrial oxidative stress may be an approach to alleviate hypertensive kidney damage. Avocado oil, a source of oleic acid and antioxidants, improves mitochondrial dysfunction, decreases mitochondrial oxidative stress, and enhances vascular function in hypertensive rats. However, whether avocado oil improves the function of renal vasculature during the adrenergic stimulation, and if this is related to improvement in renal damage and enhancement of mitochondrial activity is unknown. Thus, the effects of avocado oil on renal vascular responses to adrenergic stimulation, mitochondrial dysfunction, oxidative stress, and renal damage were compared with prazosin, an antagonist of α1-adrenoceptors, in hypertensive rats induced by L-NAME. Avocado oil or prazosin decreased blood pressure, improved endothelium-dependent renal vasodilation, prevented mitochondrial dysfunction and kidney damage in hypertensive rats. However, avocado oil, but not prazosin, decreased mitochondrial ROS generation and improved the redox state of mitochondrial glutathione. These results suggest that avocado oil and prazosin prevented hypertensive renal damage due to the improvement in mitochondrial function.

The GLP-1 receptor (GLP-1R) in the kidney is expressed exclusively in vascular smooth muscle cells in arteries and arterioles. Downstream effects of the activation of the renal vascular GLP-1R are elusive but may involve regulation of the renin-angiotensin-aldosterone system (RAAS). The expression of Ren1 in the mouse renal vasculature was investigated by in situ hybridization after a single subcutaneous dose of liraglutide, semaglutide and after repeated injections of liraglutide. Single and repeated exposure to GLP-1R agonists induced expression of Ren1 in the renal vascular smooth muscle cell compartment compared with vehicle injected controls (p < .0001) for both semaglutide and liraglutide. The present data show a robust induction of Ren1 expression in the vascular smooth muscle cells of the kidney after single and repeated GLP-1R activation and this renin recruitment may be involved in the effects of GLP-1R agonist treatment on kidney disease.

Members of the transient receptor potential (TRP) channels that are expressed in the kidney have gained prominence in recent years following discoveries of their role in maintaining the integrity of the filtration barrier, regulating tubular reabsorption of Ca2+ and Mg2+, and sensing osmotic stimuli. Furthermore, evidence has linked mutations in TRP channels to kidney disease pathophysiological mechanisms, including focal segmental glomerulosclerosis, disturbances in Mg2+ homeostasis, and polycystic kidney disease. Several subtypes of TRP channels are expressed in the renal vasculature, from preglomerular arteries and arterioles to the descending vasa recta. Although investigations on the physiological and pathological significance of renal vascular TRP channels are sparse, studies on isolated vessels and cells have suggested their involvement in renal vasoregulation. Renal blood flow (RBF) is an essential determinant of kidney function, including glomerular filtration, water and solute reabsorption, and waste product excretion. Functional alterations in ion channels that are expressed in the endothelium and smooth muscle of renal vessels can modulate renal vascular resistance, arterial pressure, and RBF. Hence, renal vascular TRP channels are potential therapeutic targets for the treatment of kidney disease. This review summarizes the current knowledge of TRP channel expression in renal vasculature and their role in controlling kidney function in health and disease.

Variation in the number of renal arteries is rare and is the most frequent and clinically important variation in the renal vascular system. Typically, this variant represents an immature form of complicated development of the renal arteries resulting from the persistence of more than one mesonephric artery during the transition period from mesonephros to metanephros in embryogenesis. The knowledge of this anatomical variation will allow the best healthcare to be provided for patients undergoing kidney surgical procedures and may reduce or eliminate avoidable postoperative complications. Although a double renal artery consists of a common anatomical variation, three or more arteries in a single kidney is less common. Herein, we report a case of a 42-year-old healthy cadaveric donor whose left kidney was found to have three renal arteries.