Pathologic kidney specimen showing marked pallor of acute kidney injury pathophysiology pdf cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury.
AKI is diagnosed on the basis of characteristic laboratory findings, such as elevated blood urea nitrogen and creatinine, or inability of the kidneys to produce sufficient amounts of urine. AKI may lead to a number of complications, including metabolic acidosis, high potassium levels, uremia, changes in body fluid balance, and effects on other organ systems, including death. People who have experienced AKI may have an increased risk of chronic kidney disease in the future.
Management includes treatment of the underlying cause and supportive care, such as renal replacement therapy. The clinical picture is often dominated by the underlying cause. The symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue, loss of appetite, headache, nausea and vomiting.
Marked increases in the potassium level can lead to abnormal heart rhythms, which can be severe and life-threatening. Fluid balance is frequently affected, though blood pressure can be high, low or normal.
If the kidney injury is the result of dehydration, there may be thirst as well as evidence of fluid depletion on physical examination. Acute kidney injury is diagnosed on the basis of clinical history and laboratory data. AKI often occurs due to multiple processes. The most common cause is dehydration and sepsis combined with nephrotoxic drugs, especially following surgery or contrast agents.