DEFINITION

Acute kidney injury (AKI) is characterized by a sudden decrease in kidney

function resulting in an increase in serum creatinine concentration and the
accumulation of nitrogenous excretory products over a course of hours to
days.
 
AKI is commonly accompanied by decreased urine output, fluid retention,
metabolic acidosis, hyperkalemia, and hyperphosphatemia. 

AKI is associated with high morbidity, mortality, and health care

costs
• AKI is associated with high morbidity, mortality, and health care costs
• Patients with AKI have an increased risk for developing chronic kidney
disease (CKD) and end-stage kidney disease (ESKD).
•  patients with preexisting CKD are at an increased risk for developing
acute-on-chronic kidney failure.
• AKI care should be focused on prevention, early recognition and
diagnosis, and management of complications.
Epidemiology and Pathophysiology

• The reported incidence of AKI varies markedly depending on the

definition of AKI applied and the patient population studied
• The incidence of AKI based on the KDIGO definition is estimated to be
21% of all hospital admissions, with 11% requiring dialysis support. In
the ICU, AKI affects >50% of patients.
• Critically ill patients with AKI in the context of multiorgan failure have
been reported to have mortality rates >50%, especially when dialysis
therapy is required.
DIAGNOSTIC CRITERIA
AKIN: Acute Kidney Injury Network
• Increase in serum creatinine of ≥0.3 mg/dL or ≥50% within 48 hours
• OR
• Urine output of <0.5 mL/kg/hour for >6 hours
Kidney Disease: Improving Global Outcomes
• Increase in serum creatinine of ≥0.3 mg/dL within 48 hours or ≥50%
within 7 days
• OR
• Urine output of <0.5 mL/kg/hour for >6 hours
• AKI can be divided into prerenal, intrinsic, and postrenal 
• KDIGO covers both the AKIN and RIFLE criteria, taking into account
changes in creatinine within 48 hours or a decline in the glomerular
filtration rate (GFR) over 7 days. Moreover, patients under 18 with a
GFR <35mL/min and patients with a serum creatinine >4.0mg/dL
(absolute value) were added to AKIN stage 3. 
Clinical Manifestations

• Patients with AKI can be asymptomatic until extreme loss of kidney function
occurs, and patients with mild to moderate AKI are often diagnosed by
laboratory studies only
• Patients with AKI can also present with oliguria (urine output <500 mL/d or
<0.3 mL/kg/h) or anuria (urine output <50 mL/d).
• Severe AKI can lead to symptoms from volume overload, electrolyte
abnormalities, anemia, platelet dysfunction, and uremia. 
• Uremic symptoms include nausea, vomiting, anorexia, weight loss, fatigue,
muscle cramps, restless legs, mental status changes, pruritus, asterixis,
seizures, and pericarditis.
• Key Point
COVID-19: Issues related to acute kidney
injury
• In a meta-analysis of approximately 13,000 mostly hospitalized patients, the incidence of AKI was 17 percent
• Approximately 5 percent of patients required kidney replacement therapy (KRT)

• In two large observational studies of over 5000 patients hospitalized with COVID-19, AKI was noted among 32 to 37 percent of
patients
• Among patients with AKI, approximately one-half had mild disease (1.5- to 2-fold increase in serum creatinine), and the remaining had
moderate or severe disease (more than doubling of creatinine). AKI requiring KRT was noted in 12 to 15 percent of patients.

• One study compared the incidence of AKI among hospitalized patients with and without COVID-19 [17]. The incidence of AKI was
higher among the 2600 patients who had COVID-19 compared with over 19,500 patients who were hospitalized for other reasons (31
versus 18 percent)

•
Robbins-Juarez SY, Qian L  Issues related to acute kidney injury, glomerular disease, and hypertension’
•

Bowe B, Cai M Acute Kidney Injury in a National Cohort of Hospitalized US Veterans with COVID-19.
Prerenal

• Prerenal AKI (prerenal azotemia) is caused by underperfusion of the

kidney with a subsequent decrease in GFR, which is reversible with
appropriate therapy.
• Renal hypoperfusion can occur due to intravascular volume depletion,
decreased effective arterial circulation, renal vasoconstriction, and/or
medications.
• atients may have a history of acute hemorrhage, loss of gastrointestinal
fluids, heart failure, decompensated liver disease, sepsis, or recent
diuretic or NSAID use. Physical signs of hypovolemia include
hypotension, tachycardia, orthostasis, and decreased skin turgor. 
• In prerenal AKI, the kidney responds by reabsorbing urea, sodium, and water, often resulting
in a BUN-creatinine ratio >20:1
• Prerenal AKI due to hypovolemia can be distinguished from ATN by the renal response to a
fluid challenge. If serum creatinine recovers to baseline with fluid
• ug-induced prerenal AKI typically results from decreased blood flow to the kidney or
intraglomerular hemodynamic alterations. Diuretics can cause prerenal AKI from volume
depletion. Drugs affecting vasodilatation of the afferent arterioles or vasoconstriction of the
efferent arterioles can cause prerenal AKI, especially in the setting of volume depletion,
decreased effective arterial circulation, or CKD. NSAIDs, including cyclooxygenase-2 inhibitors,
cause AKI by diminishing the renal vasodilatory effect of prostaglandins. ACE inhibitors and
angiotensin receptor blockers (ARBs) prevent efferent vasoconstriction by inhibiting
angiotensin II. Calcineurin inhibitors such as cyclosporine and tacrolimus can cause prerenal
AKI from afferent and efferent vasoconstriction. repletion, the cause of AKI is likely to be
prerenal.
• Management of prerenal AKI includes discontinuing nephrotoxins and
increasing renal perfusion by treating the underlying cause, such as
correcting volume deficits. If prerenal AKI is not recognized and
treated in a timely fashion, prolonged renal hypoperfusion will result
in ATN and progressive intrinsic kidney failure