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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. [3] The BUN:Cr in renal azotemia is less than 15.
Acute kidney injury was one of the most expensive conditions seen in U.S. hospitals in 2011, with an aggregated cost of nearly $4.7 billion for approximately 498,000 hospital stays. [48] This was a 346% increase in hospitalizations from 1997, when there were 98,000 acute kidney injury stays. [49]
Prerenal acute kidney injury. Acute kidney injury, or AKI, is when the kidney isn’t functioning at 100% and that decrease in function usually over a few days. Actually, AKI used to be known as acute renal failure, or ARF, but AKI is a broader term that also includes subtle decreases in kidney function.
Once the acute phase of the nephritic syndrome is controlled, it is crucial to determine the underlying pathology that caused the onset of the acute nephritic syndrome and to treat that condition. If the underlying cause is not determined and treated appropriately, it increases the risk of a recurrence of nephritic syndrome or chronic kidney ...
Although often reliable at discriminating between prerenal azotemia and acute tubular necrosis, the FE Na has been reported to be <1% occasionally with oliguric and nonoliguric acute tubular necrosis, urinary tract obstruction, acute glomerulonephritis, renal allograft rejection, sepsis, and drug-related alterations in renal hemodynamics. [7]
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]