Acute tubular necrosis overview: Difference between revisions
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===Laboratory Findings=== | ===Laboratory Findings=== | ||
[[Complete blood count|CBC]], [[urinalysis]] with sediment [[microscopy]], [[urine]] electrolytes, [[osmolarity]], serum electrolytes, [[blood urea nitrogen]] and [[Creatinine|serum creatinine]], and [[Dipsticks|urine dipstick]] are commonly performed in patients to evaluate acute tubular necrosis and other causes of [[Acute kidney injury|acute renal failure]]. [[Urine]] sediment may show tubular epithelial cells and epithelial cell casts or brown muddy granular [[casts]]. Increased urine [[sodium]] concentration >40 mEq/L, urine [[Fractional sodium excretion|fractional excretion of sodium]] greater than 2 percent along with elevated serum [[creatinine]] concentration at a rate greater than 0.3 mg/dL/day may be found in [[acute tubular necrosis]]. However, these tests may have some limitations. | |||
===Electrocardiogram=== | ===Electrocardiogram=== | ||
Revision as of 19:04, 29 May 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]
Overview
Acute tubular necrosis (ATN) defines a pathologic process rather than a clinical syndrome in which varying degrees of renal tubular injury occur. Clinically, ATN manifests as acute kidney injury although the terms have previously been used interchangeably. ATN is the most common cause of overt AKI. Despite the term, ATN does not necessarily imply cellular necrosis with evidence of non-necrotic injury observed more consistently. Furthermore, clinicopathologic correlation is often irrelevant with severe renal insufficiency sometimes seen with modest pathological findings.[1] ATN can be either ischemic or toxin induced. Classically, ischemic ATN follows hypotension or hypovolemia with patchy involvement usually observed. On the other hand, toxic ATN is usually a dose-dependent injury seen with medications, diagnostic agents, and heavy metals with proximal tubule damage involving almost all nephrons.[2]
Historical Perspective
Classification
Acute tubular necrosis may be classified based on mechanisms of tubular injury into three categories ischemic, toxin-induced, and mixed.
Pathophysiology
Causes
Acute tubular necrosis is commonly caused by renal ischemia resulting from conditions such as volume depletion, hypotension, septic shock, cirrhosis, and DIC. It is also caused by exposure to various nephrotoxic medications including aminoglycosides, amphotericin B, ACE inhibitors, NSAIDs, antiviral drugs, cytotoxic therapy,and also exposure to radio contrast substances.
Differentiating Xyz from Other Diseases
Epidemiology and Demographics
Incidence of acute tubular necrosis is approximately 88 per 100,000 individuals worldwide. The mean age at diagnosis of acute tubular necrosis was 59.5 years. Mortality rate is high with acute tubular necrosis among hospitalized and ICU patients. Acute tubular necrosis affects men and women equally.
Risk Factors
Common risk factors in the development of acute tubular necrosis include any condition that lead to decreased renal perfusion such as recent abdominal and cardiac surgery, marked hypovolemia, sepsis, hemorrhagic shock, severe pancreatitis, and diabetes mellitus. Nephrotoxic medications ( eg, ACE inhibitors, NSAIDs, aminoglycosides, radio contrast media) can also be a risk for developing acute tubular necrosis.
Screening
Screening for acute tubular necrosis is usually not recommended for asymptomatic individuals. Screening is usually recommended for patients who are at high risk for developing acute tubular necrosis. Screening evaluation includes measurement of serum creatinine, urine output, blood urea nitrogen, urinary and serum electrolytes.
Natural History, Complications, and Prognosis
Acute tubular necrosis may usually develop through 3 phases, initiation, maintenance and recovery. Common complications of acute tubular necrosis include electrolyte imbalance(eg, hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis), platelet dysfunction and altered consciousness or coma. Prognosis depends on the underlying etiology and severity of kidney damage. When compared to ischemic acute tubular necrosis, nephrotoxic and mixed acute tubular necrosis have the good prognosis.
Diagnosis
Diagnostic Study of Choice
History and Symptoms
History taking is an important aspect in making a diagnosis of acute tubular necrosis. It provides clues to precipitating factors, causes and associated comorbid conditions leading to decreased renal perfusion and kidney injury. Most common symptoms of acute tubular necrosis include decreased or absent urinary output, postural dizziness, edema, excess thirst, tachycardia, altered mental status and easy fatiguability.
Physical Examination
On physical examination, patients with acute tubular necrosis may show the findings of volume depletion. They usually appear ill, dehydrated, and lethargic. Common physical examinationfindings of acute tubular necrosis include orthostatic hypotension and other signs of hypovolemia (dry mucous membranes, sunken eyes, poor skin turgor and delayed capillary refill, and decreased jugular venous pressure).
Laboratory Findings
CBC, urinalysis with sediment microscopy, urine electrolytes, osmolarity, serum electrolytes, blood urea nitrogen and serum creatinine, and urine dipstick are commonly performed in patients to evaluate acute tubular necrosis and other causes of acute renal failure. Urine sediment may show tubular epithelial cells and epithelial cell casts or brown muddy granular casts. Increased urine sodium concentration >40 mEq/L, urine fractional excretion of sodium greater than 2 percent along with elevated serum creatinine concentration at a rate greater than 0.3 mg/dL/day may be found in acute tubular necrosis. However, these tests may have some limitations.
Electrocardiogram
X-ray
Echocardiography and Ultrasound
CT scan
MRI
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
References
- ↑ Rosen S, Stillman IE (2008). "Acute tubular necrosis is a syndrome of physiologic and pathologic dissociation". J Am Soc Nephrol. 19 (5): 871–5. doi:10.1681/ASN.2007080913. PMID 18235086.
- ↑ Fogo A, Cohen AH, Colvin RB et al. Fundamentals of Renal Pathology. Springer 2013. Acute Tubular Necrosis. http://dx.doi.org/10.1007/978-3-642-39080-7_15