Acute kidney injury overview

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Acute Kidney Injury from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT scan

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Interventions

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

Definition

Over 30 different definitions of AKI have been used in the literature since it was first described, which prompted the need for a uniform definition. In 2002, The Acute Dialysis Quality Initiative (ADQI) proposed the first consensus definition known as the RIFLE criteria. The acronym combines a classification of 3 levels of renal dysfunction (Risk, Injury, Failure) with 2 clinical outcomes (Loss, ESRD). This unified classification was proposed to enable a viable comparison in trials of prevention and therapy and to observe clinical outcomes of the defined stages of AKI.[1]

RIFLE criteria for the definition of acute kidney injury (AKI)
Classification GFR criteria Urine output criteria
Risk 1.5x increase in SCr or GFR decrease >25% <0.5 mL/kg/h for 6 hours
Injury 2x increase in SCr or GFR decrease >50% <0.5 mL/kg/h for 12 hours
Failure 3x increase in SCr or GFR decrease >75% <0.3 mL/kg/h for 24 hours or anuria for 12 hours
Loss Complete loss of renal function >4 weeks
End-stage Renal Disease Complete loss of renal function >3 months

In 2007, the Acute Kidney Injury Network (AKIN) proposed a modified diagnostic criteria based on the RIFLE criteria. The initiative separated the definition and staging into 2 separate entities previously combined in the RIFLE criteria. This made the definition more clinically applicable. AKI was defined as either one of the following:[2]

  • An increase in serum creatinine by 0.3 mg/dL in 48 hours
  • An increase in serum creatinine by more than 50% of baseline or 1.5 times baseline occuring in the past 7 days
  • A decrease in urine volume <0.5 mL/kg/h for 6 hours

In March 2012, the Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for Acute Kidney Injury retained the AKIN definition while implementing modifications to the staging criteria of AKI. [3]

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

Initially, the staging of AKI was a part of the proposed definition by the ADQI initiative and the RIFLE criteria. In 2007, AKIN proposed separated the 2 and created a new staging scheme modified from the RIFLE criteria. Prior to the 2012 KDIGO AKI guidelines, RIFLE and AKIN criteria were used interchangeably to stage patients with renal injury.

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 damage to renal parenchyma. 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

Oliguria is typically present in AKI. So, AKI should be differentiated from other causes of oliguria.

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

Symptoms of acute kidney injury include decreased urine output, dark colored urine, fatigue and malaise, nausea and vomiting.

Physical Examination

Patients with acute kidney injury usually appear ill. Physical examination of patients with acute kidney injury is usually remarkable for hypotension, edema of the lower extremities, maculopapular rash and rales o chest ausculatation.

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

There are no x-ray specific findings associated with AKI. However, AKI may lead to fluid overload leading to pulmonary edema.

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

99m Technetium (Tc) scan may be helpful in the diagnosis of acute kidney injury. 99m Technetium (Tc) scan may be hehpful in assessing renal blood flow and tubular function.

Other Diagnostic Studies

There are no other diagnostic studies associated with the acute kidney injury.

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.

Primary Prevention

Effective measures for the primary prevention of acute kidney injury include volume expansion and/or fluid therapy, optimization of blood pressure,tight glycemic control, avoidance of drug- and nephrotoxin-induced AKI, recheck renal function 48-72 hours following the radiological contrast media, and low doses of corticosteroids in septic shock patients.

Secondary Prevention

There are no established measures for the secondary prevention of acute kidney injury.

References

  1. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P, Acute Dialysis Quality Initiative workgroup (2004). "Acute renal failure - definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group". Crit Care. 8 (4): R204–12. doi:10.1186/cc2872. PMC 522841. PMID 15312219.
  2. Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG; et al. (2007). "Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury". Crit Care. 11 (2): R31. doi:10.1186/cc5713. PMC 2206446. PMID 17331245.
  3. Kidney Disease Improving Global Outcomes Work Group (2012). "2012 KDIGO Clinical Practice Guideline for Acute Kidney Injury". Kidey Int Supp. 2: 69–88. doi:10.1038/kisup.2011.34.

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