This generally leads to a BUN:Cr ratio > 20 and a fractional excretion of Na of < 1% and an elevated urine osmolarity. Primary renal azotemia
Renal azotemia (acute kidney failure) typically leads to uremia. It is an intrinsic disease of the kidney, generally the result of kidney parenchymal damage. Causes include kidney failure, glomerulonephritis, acute tubular necrosis, or other kidney disease.The BUN:Cr in renal azotemia is less than 15. In cases of kidney disease, glomerular filtration rate decreases, so nothing gets filtered as well as it normally would. However, in addition to not being normally filtered, what urea does get filtered is not reabsorbed by the proximal tubule as it normally would be. This results in lower levels of urea in the blood and higher levels of urea in the urine as compared to creatinine. Creatinine filtration decreases, leading to a higher amount of creatinine in the blood. Third spacing of fluids such as peritonitis, osmotic diuresis, or low aldosterone states such as Addisons disease all elevate urea. Postrenal azotemia
Blockage of urine flow in an area below the kidneys results in postrenal azotemia. It can be caused by congenital abnormalities such as vesicoureteral reflux, blockage of the ureters by kidney stones, pregnancy, compression of the ureters by cancer, prostatic hyperplasia, or blockage of the urethra by kidney or bladder stones. Like in prerenal azotemia, there is no inherent renal disease. The increased resistance to urine flow can cause back up into the kidneys, leading to hydronephrosis.The BUN:Cr in postrenal azotemia is initially >15.
Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction. The resulting lesion is referred to as an infarct
(from the Latin infarctus, "stuffed into"). Causes
Infarction occurs as a result of prolonged ischemia, which is the insufficient supply of oxygen and nutrition to an area of tissue due to a disruption in blood supply. The blood vessel supplying the affected area of tissue may be blocked due to an obstruction in the vessel (e.g., an arterial embolus, thrombus, or atherosclerotic plaque), compressed by something outside of the vessel causing it to narrow (e.g., tumor, volvulus, or hernia), ruptured by trauma causing a loss of blood pressure downstream of the rupture, or vasoconstricted, which is the narrowing of the blood vessel by contraction of the muscle wall rather than an external force (e.g., cocaine vasoconstriction leading to myocardial infarction). Hypertension and atherosclerosis are risk factors for both atherosclerotic plaques and thromboembolism. In atherosclerotic formations, a plaque develops under a fibrous cap. When the fibrous cap is degraded by metalloproteinases released from macrophages or by intravascular shear force from blood flow, subendothelial thrombogenic material (extracellular matrix) is exposed to circulating platelets and thrombus formation occurs on the vessel wall occluding blood flow.