SummaryAcute kidney injury (AKI) is a sudden loss of renal function with a subsequent rise in creatinine and blood urea nitrogen (BUN). It is most frequently caused by decreased renal perfusion (prerenal) but may also be due to direct damage to the kidneys (intrarenal or intrinsic) or inadequate urine drainage (postrenal). In AKI, the acid-base, fluid, and electrolyte balances are disturbed and the urinary excretion of substances such as drugs is impaired. AKI may be asymptomatic or manifest with oliguria or anuria and, when kidney dysfunction is severe, it may manifest with symptoms and signs of uremia; in some cases, polyuria may occur as a result of impaired tubular reabsorption. A diagnosis of AKI can be made based on an increase in serum creatinine concentration and/or decrease in urine output. Initial evaluation includes blood and urine studies, which may help identify the mechanism of kidney injury and any metabolic complications of AKI. Additional specific investigations are guided by the suspected cause. Rapid evaluation, diagnosis, and treatment are necessary to prevent irreversible loss of renal function. Management is based on the mechanism of kidney injury and the underlying causes. Treatment is primarily supportive and aims to ensure adequate kidney perfusion and prevent complications and further kidney damage. Show
EtiologyPrerenal acute kidney injury [1][2][3]Prerenal causes include any condition that leads to decreased renal perfusion(∼ 60% of cases of AKI). [1][2][3]
Prolonged prerenal injury leads to intrinsic injury, as decreased renal perfusion causes tubular necrosis. Intrinsic acute kidney injuryIntrinsic causes include any condition that leads to severe direct kidney damage (∼ 35% of cases of AKI). [1][2][3]
Postrenal acute kidney injuryPostrenal causes include any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra (∼ 5% of cases of AKI). [1][2][3]
As long as the contralateral kidney remains intact, patients with unilateral ureteral obstruction typically maintain normal serum creatinine levels. Overview of nephrotoxic medicationsPathophysiologyPrerenal
Intrinsic
Postrenal
Four phases of AKI
References:[2][4] Clinical features
Subtypes and variantsAcute tubular necrosis
Contrast-induced nephropathy
References:[2][3][6] DiagnosticsA diagnosis of AKI can be made based on an acute increase in serum creatinine and/or decrease in urine output in accordance with the definition of AKI. In the absence of previously documented creatinine levels, stable creatinine levels with findings such as chronic anemia and small hyperechoic kidneys on ultrasound suggest CKD rather than AKI. Clinical presentation, laboratory tests, imaging, response to initial therapy, and, in some cases, histopathology are required to determine the underlying cause of AKI. Initial evaluationLaboratory studiesOverview of diagnostic findingsDespite the common use of BUN:creatinine ratio and urinary fractional excretions (i.e., FENa, FEUrea) in clinical practice, observational data suggest that they do not reliably distinguish prerenal AKI from intrinsic AKI. [10][11] The most likely mechanism of AKI is primarily determined based on clinical presentation and response to therapy. Evaluating patients' response to initial interventions is key to confirming the mechanism of AKI and guiding further workup and management steps. Prerenal AKI [8][9]
Patients with prerenal AKI receiving diuretic therapy may have a falsely elevated FENa. Therefore, FEUrea may be more informative in this setting. [15] Intrinsic AKI
A falsely low FENa may be seen in some patients with intrinsic AKI, e.g., due to glomerulonephritis, acute interstitial nephritis, rhabdomyolysis, or contrast-induced nephropathy. [15] Postrenal AKI
Imaging [17]Imaging of the kidneys and urinary tract is not necessary to establish a diagnosis of AKI but may be needed to determine the etiology. Obtain an urgent ultrasound to rule out hydronephrosis in patients with risk factors for urinary tract obstruction. While ultrasound is the initial test of choice to assess for urinary tract obstruction, CT has greater sensitivity for detecting obstructions and stones. [19] Renal biopsy [8][20]Additional specific testingUsually reserved for cases in which intrinsic AKI is initially suspected or interventions aimed at reversing presumed prerenal AKI or postrenal AKI fail to improve renal function. Studies should be guided by clinical suspicion. ManagementSupportive care and follow-upThe goal of supportive care is to avoid further renal insult and potentially aggravating factors, support adequate kidney perfusion, and ensure early identification and treatment of complications. Medications and nephrotoxic substances [9]
Calculating eGFR using conventional equations does not accurately predict the true GFR in patients with AKI. Reestimate GFR daily based on the patient's urine output and the trajectory of serum creatinine. Noncontrast imaging studies are preferred if possible. When the use of iodinated contrast is required for a critical diagnostic study or procedure (e.g., for the treatment of STEMI), the lowest clinical diagnostic dose should be used. Volume status and blood pressure [8][9]
Patients with AKI are at high risk of developing fluid overload, which can compromise renal function and may increase mortality. Avoid aggressive fluid resuscitation in patients who are not volume responsive. Consider loop diuretics ONLY in patients with signs of fluid overload. Diuretics should not be used routinely to improve urine output in patients with AKI because of their lack of benefit and potential for harm. [7] Choice of parenteral fluid [8][9][30]
The use of balanced IV fluid solutions has been associated with lower mortality and better renal outcomes compared with the use of normal saline in patients with AKI. Electrolyte and acid-base disorders
Obtain frequent (at least daily) laboratory studies to monitor for the presence of metabolic complications and response to treatment (e.g., improvement in creatinine levels). Consider urgent renal replacement therapy for patients with refractory electrolyte or acid-base disturbances. Additional considerations
The risk of GI bleeding may be increased in AKI due to uremic platelet dysfunction. [37] Consider a nutrition consult for all patients with AKI. [35] Follow-up care [38][39]
Patients who recover from AKI are at high risk of readmission, mortality, cardiovascular events, progressive renal function deterioration, and developing de novo CKD. [38][39] Adequate discharge planning and follow-up may help improve patient outcomes. [38][39] Acute management checklist
Special patient groupsPreventionIdentify patients who are at risk of AKI and implement appropriate preventive strategies. [1][7][22]
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Which pathology may result in AKI from prerenal etiology?A few of the causes of prerenal AKI include but are not limited to; intravascular volume depletion, hypotension, sepsis, shock, over diuresis, heart failure, cirrhosis, bilateral renal artery stenosis/solitary functioning kidney which is worsened by angiotensin-converting enzyme (ACE) inhibitors, and also by other ...
Which disorder is a Prerenal cause of acute kidney injury?Prerenal causes of AKI include sepsis, dehydration, excessive blood loss, cardiogenic shock, heart failure, cirrhosis, and certain medications like ACE inhibitors or NSAIDs.
What is the most common cause of Prerenal failure?Intravascular volume depletion is the most common cause of pre-renal failure. Intravascular volume depletion can be the result of poor oral intake or excessive fluid loss.
What are the 3 causes of AKI?What causes acute kidney injury? There are three major reasons why your kidneys might be injured: lack of blood flow to the kidneys, blockage in urine flow that causes infections, or direct kidney damage by infections, medications, toxins, or autoimmune conditions.
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