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Kidney ischemia is a loss of blood flow to the kidney cells. Several physical symptoms include shrinkage of one or both kidneys, [19] renovascular hypertension, [20] acute renal failure, [19] progressive azotemia, [19] and acute pulmonary edema. [19] It is a disease with high mortality rate and high morbidity. [21]
Kidney ischemia [1] is a disease with a high morbidity and mortality rate. [2] Blood vessels shrink and undergo apoptosis which results in poor blood flow in the kidneys. More complications happen when failure of the kidney functions result in toxicity in various parts of the body which may cause septic shock, hypovolemia, and a need for surgery. [3]
The renal circulation supplies the blood to the kidneys via the renal arteries, left and right, which branch directly from the abdominal aorta. Despite their relatively small size, the kidneys receive approximately 20% of the cardiac output .
Hemolytic–uremic syndrome (HUS) is a group of blood disorders characterized by low red blood cells, acute kidney injury (previously called acute renal failure), and low platelets. [1] [3] Initial symptoms typically include bloody diarrhea, fever, vomiting, and weakness. [1] [2] Kidney problems and low platelets then occur as the diarrhea ...
In humans, the kidneys together receive roughly 20 - 25% of cardiac output, amounting to 1.2 - 1.3 L/min in a healthy adult. [1] It passes about 94% to the cortex. RBF is closely related to renal plasma flow (RPF), which is the volume of blood plasma delivered to the kidneys per unit time.
Because blood flow to the kidney first reaches the renal cortex (outside) and then the renal medulla (inside), the deeper structures of the kidney are most sensitive to decreased blood flow. Thus the innermost structures of the kidney, known as the renal papillae , are especially dependent on prostaglandin synthesis to maintain adequate blood flow.
When renal blood flow is reduced (indicating hypotension) or there is a decrease in sodium or chloride ion concentration, the macula densa of the distal tubule releases prostaglandins (mainly PGI2 and PGE2) and nitric oxide, which cause the juxtaglomerular cells lining the afferent arterioles to release renin, activating the renin–angiotensin–aldosterone system, to increase blood pressure ...
Acute tubular necrosis (ATN) is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys.Because necrosis is often not present, the term acute tubular injury (ATI) is preferred by pathologists over the older name acute tubular necrosis (ATN). [1]