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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]
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 ]
There are various forms, [2] and some drugs may affect kidney function in more than one way. Nephrotoxins are substances displaying nephrotoxicity. Nephrotoxicity should not be confused with some medications predominantly excreted by the kidneys needing their dose adjusted for the decreased kidney function (e.g., heparin, lithium).
Acute kidney injuries can be present on top of chronic kidney disease, a condition called acute-on-chronic kidney failure (AoCRF). The acute part of AoCRF may be reversible, and the goal of treatment, as with AKI, is to return the person to baseline kidney function, typically measured by serum creatinine .
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 chemotherapy drug 5-FU can be toxic to some people with cancer. A quick, cheap test can show if chemo is safe for a patient, but few doctors order it.
High potassium levels may lead to potentially fatal disruptions in heart rhythm. Phosphate binds to calcium from the circulation, leading to low calcium levels in the blood. [11] Rhabdomyolysis may cause kidney failure by several mechanisms. The most important is the accumulation of myoglobin in the kidney tubules.
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 ...