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Published byMarcia Hampton Modified over 8 years ago
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Presentation by JoAnn Czech RN/CDS St. Cloud Hospital
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Acute tubular necrosis is kidney injury characterized by acute tubular cell injury and dysfunction. Common causes are hypotension causing renal hypoperfusion and nephrotoxic drugs. The condition is asymptomatic unless it causes renal failure The diagnosis is suspected when azotemia develops after a hypotensive event, severe sepsis, or drug exposure and is distinguished from prerenal azotemia by laboratory testing and response to volume expansion.
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Hypotension (ischemic ATN, common) Nephrotoxins (common) Sepsis (common) Major surgery Third-degree burns covering > 15% of BSA Disorders resulting in other endogenous toxins, such as tumor lysis or multiple myeloma (uncommon)
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Massive volume loss, particularly in patients with septic or hemorrhagic shock or pancreatitis or in patients who have had serious surgery, increases the risk of ischemic ATN. ATN is more likely to develop in patients with the following: Baseline creatinine clearance < 47 mL/min Diabetes mellitus Preexisting hypovolemia or poor renal perfusion
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ATN is usually asymptomatic but may cause symptoms or signs of acute renal failure, typically oliguria. Differentiation from prerenal azotemia, based mainly on laboratory findings and, in the case of blood or fluid loss, response to volume expansion. ATN is suspected when serum creatinine rises ≥ 0.5 mg/dL/day above baseline after an apparent trigger. It may occur days after exposure to some nephrotoxins. ATN must be differentiated from prerenal azotemia because treatment differs. In prerenal azotemia, renal perfusion is decreased enough to elevate serum BUN out of proportion to creatinine, but not enough to cause ischemic damage to tubular cells.
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Prerenal azotemia can be caused by direct intravascular fluid loss (eg, from hemorrhage, GI tract or urinary losses) or by a relative decrease in effective circulating volume without loss of total body fluid (eg, in heart failure or portal hypertension with ascites). If fluid loss is the cause, volume expansion using IV normal saline solution normalizes serum creatinine level. If ATN is the cause, IV saline typically causes no rapid change in serum creatinine.
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Renal (kidney) cortical necrosis is death of the tissue in the outer part of kidney (cortex) that results from blockage of the small arteries that supply blood to the cortex and that causes acute kidney failure. Usually the cause is a major, catastrophic disorder that decreases blood pressure. Symptoms may include dark urine, decreased urine volume, fever, and pain in the side of the body. Sometimes an imaging test or tissue analysis (biopsy) is done to confirm the diagnosis.
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Renal cortical necrosis can occur at any age. About 10% of the cases occur in infants and children.. The next most common cause is a bacterial infection of the bloodstream (sepsis). In children, renal cortical necrosis may follow severe infection, severe dehydration, shock, or the hemolytic-uremic syndrome.
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In adults, sepsis causes one third of all cases of renal cortical necrosis. Other causes in adults include rejection of a transplanted kidney, burns, inflammation of the pancreas, injury, use of certain drugs, and poisoning from certain chemicals. The diagnosis is often confirmed with an imaging test such as computed tomography (CT) angiography. Kidney biopsy can give doctors the most accurate diagnostic information, but a biopsy involves removing kidney tissue and may be unnecessary if the diagnosis is evident.
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Renal papillary necrosis is a disorder of the kidneys in which all or part of renal papillae die. The renal papillae is the area where the openings of the collecting ducts enter the kidney. Necrosis (tissue death) of the renal papillae may make the kidney unable to concentrate the urine
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Conditions causing this condition: Diabetic Nephropathy Kidney infection Kidney transplant rejection Urinary tract obstruction Sickle cell anemia is a common cause of renal papillary necrosis.
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Symptoms may include: Back pain or flank pain Bloody urine Cloudy urine Dark, rust-colored, or brown urine Tissue in the urine Chills Incontinence Increased urinary frequency or urgency
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An examination may reveal tenderness when touching the body over the affected kidney. There may be a history of chronic or recurrent urinary tract infections. There may be signs of obstructive uropathy or renal failure. A urinalysis may show dead tissue in the urine. An IVP may show obstruction or tissue. There is no specific treatment for renal papillary necrosis. Treatment depends on the underlying cause. If the underlying cause can be controlled, it may go away on its own.
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