Acute kidney injury overview

# 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.
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:
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. 

# 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.