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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] ATN presents with acute kidney injury (AKI) and is one of the most common causes of AKI. [2] Common causes of ATN include low blood pressure and use of nephrotoxic drugs. [2]
Acute kidney injury due to acute tubular necrosis (ATN) was recognized in the 1940s in the United Kingdom, where crush injury victims during the London Blitz developed patchy necrosis of kidney tubules, leading to a sudden decrease in kidney function. [52]
Renal cortical necrosis (RCN) is a rare cause of acute kidney failure. The condition is "usually caused by significantly diminished arterial perfusion of the kidneys due to spasms of the feeding arteries, microvascular injury, or disseminated intravascular coagulation " and is the pathological progression of acute tubular necrosis . [ 1 ]
Characteristics of Some Inherited Tubulopathies [4]; Disorder [OMIM Number] Protein Defect Chromosome Localization Inheritance Clinical Features/Notes Biochemical Features
Acute tubular necrosis due to ischemia is often preceded by prerenal acute kidney injury, since prerenal AKI results in less blood sent to the kidneys. All that secretion and reabsorption in the tubules takes a lot of energy, and so these cells are particularly sensitive to a loss of blood supply, especially the cells in the proximal tubule and ...
Under ideal situations myoglobin will be filtered and excreted with the urine, but if too much myoglobin is released into the circulation or in case of kidney problems, it can occlude the kidneys' filtration system leading to acute tubular necrosis and acute kidney injury. Other causes of myoglobinuria include: McArdle's disease
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.
European guidelines classify a pre-existing decreased kidney function to be a risk factor of contrast-induced nephropathy in the following cases: [5]. Estimated glomerular filtration rate (eGFR) < 45 ml/min/1.73 m 2 of body surface area before intra-arterial administration with first-pass renal exposure (not passing lungs or peripheral circulation before kidneys), or in the intensive care unit