Acute kidney injury overview: Difference between revisions
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===Surgery=== | ===Surgery=== | ||
Renal replacement is usually reserved for patients with either severe [[acidosis]], [[Pulmonary edema case study|pulmonary edema]] and [[Uremia|uremic]] [[complications]]. | |||
===Primary Prevention=== | ===Primary Prevention=== | ||
Revision as of 14:31, 25 July 2018
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Acute kidney injury Microchapters |
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Treatment |
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Acute kidney injury overview On the Web |
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American Roentgen Ray Society Images of Acute kidney injury overview |
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Risk calculators and risk factors for Acute kidney injury overview |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]
Overview
Historical Perspective
In 1941, Beall et al described a case of acute kidney injury during world war II. They describe a course of rapidly progressive renal insufficiency with dark urine, edema, elevated potassium levels, and disorientation. In 1946, first hemodialysis was performed by Bywaters et al to treat acute kidney injury.
Classification
Pathophysiology
Acute kidney injury is defined as spontaneous deficit in kidney functions leading to urea retention and electrolyte imabalance. Etiologies of AKI can be divided based on pathophysiologic mechanisms into 3 broad categories: prerenal, intrinsic renal, and postrenal causes. Pre-renal AKI is most common and typically results from hypovolemia. Intrinsic renal is due to damag to renal paranchyma. Post-renal AKI is usually result of an obstruction, may be due to stones or strictures.
Causes
Common causes of acute kidney injury include albendazole, ciprofloxacin, foscarnet sodium, deferasirox, gadoterate and gadoxetate.
Differentiating Acute kidney injury from Other Diseases
Epidemiology and Demographics
The incidence less severe AKI is approximately 200-300 per 100,000 individuals worldwide. The prevalence of acute kidney injury is approximately 400-500 per 100,000 individuals worldwide. Patients of all age groups may develop AKI. The incidence of AKI increases with age; the median age at diagnosis is 76 years. AKI affects men and women equally.
Risk Factors
Common risk factors in the development of acute kidney injury include exposure to contrast, volume depletion, hemodynamic instability, advanced ages, hypertension and diabetes mellitus.
Screening
Several laboratory tests are useful for screening of acute kidney injury among patients with risk factors like BUN, creatinine and urine analysis.
Natural History, Complications, and Prognosis
Certain forms of AKI such as contrast induced nephropathy, usually have a shorter course with creatinine peak in 3-5 days. Common complications of acute kidney injury include anemia, metabolic acidosis, anorexia, nausea and vomiting. In general, the majority of patients that survive the initial insult recover their kidney function within 30 days.
Diagnosis
Diagnostic Study of Choice
Acute kidney injury is diagnosed and staged clinically on the basis of GFR and urinary output. In 2012, the KDIGO AKI guidelines proposed a combined staging scheme that takes into account both criteria and clinical outcome.
History and Symptoms
Physical Examination
Laboratory Findings
In prerenal azotemia, tubular function is preserved and sodium reabsorption increases with the associated renal vasoconstriction. Hence the FENa is usually <1% in prerenal azotemia. A high FENa in the context of prerenal azotemia is possible during diuretic treatment and glycosuria. FEurea is of value in states of reduced effective circulating volume, and in cases where diuretics have been administered. In these situations, a low FEurea (<35%) has a higher sensitivity and specificity than FENa in differentiating between prerenal azotemia and renal AKI.
Electrocardiogram
There are usually no specific ECG findings associated with AKI. However, ECG findings may have various presentations depending on the electrolyte abnormalities presenting in ECG.
X-ray
Echocardiography and Ultrasound
Findings on an ultrasound suggestive of acute kidney injury include obstruction, hydronephrosis, enlarged kidneys, hyperechoic kidneys and thick and echogenic cortices.
CT scan
Findings on CT scan suggestive of acute kidney injury include kidney stones not detected by ultrasonography, hydronephrosis or hydroureter and renal artery stenosis.
MRI
MRI is usually not indicated in acute kidney injury.
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Pharmacologic medical therapies for acute kidney injury include supportive therapy, diuretics, correction of hyperglycemia.
Surgery
Renal replacement is usually reserved for patients with either severe acidosis, pulmonary edema and uremic complications.