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The venous drainage of the kidney large mirrors its arterial supply, except that there are no segmental veins. [4] The stellate veins arise from the capillaries, then drain successively through interlobular veins and interlobar veins until these converge from across the kidney to form the renal vein for that kidney.
The renal veins in the renal circulation, are large-calibre [1] veins that drain blood filtered by the kidneys into the inferior vena cava. There is one renal vein draining each kidney. [citation needed] Each renal vein is formed by the convergence of the interlobar veins of one kidney. [2]
The mechanism behind RVT is no different from other types of blood clots in other parts of the body. Rudolf Virchow, was the first to describe the physiological mechanism behind venous thrombosis (blood clots) using three related factors, known as Virchow's Triad; damage to the blood vessel (endothelial damage), decrease in blood flow (stasis) and increased coagulability of the blood ...
Renal artery stenosis (RAS) is the narrowing of one or both of the renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia.This narrowing of the renal artery can impede blood flow to the target kidney, resulting in renovascular hypertension – a secondary type of high blood pressure.
Due to the anatomical position of the aorta, the inferior vena cava, and the kidneys, the right renal artery is normally longer than the left renal artery. [1] [6] The right passes behind the inferior vena cava, the right renal vein, the head of the pancreas, and the descending part of the duodenum. It’s somewhat lower than the left one.
Angiotension converting enzyme. The pathogenesis of renovascular hypertension involves the narrowing of the arteries supplying the kidneys which causes a low perfusion pressure that is detected by the juxtaglomerular apparatus (via the macula densa cells, which act as baroreceptors; located on the afferent arteriole wall). [6]
Renal infarction is a medical condition caused by an abrupt disruption of the renal blood flow in either one of the segmental branches or the major ipsilateral renal artery. [3] Patients who have experienced an acute renal infarction usually report sudden onset flank pain , which is often accompanied by fever , nausea , and vomiting .
From anterior to posterior, the renal vein exits, the renal artery enters, and the renal pelvis exits the kidney. On the left hand side the hilum is located at the L1 vertebral level and the right kidney at level L1-2. The lower border of the kidneys is usually alongside L3.