Acute Kidney Injury

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Introduction

Acute kidney injury (AKI):

• A sudden (within hours) decline in kidney function, which includes both injury (structural damage) and impairment (loss of function).

• Often referred to as acute renal failure (ARF), is a sudden episode of kidney damage or failure that occurs within a few hours or days and is indicated by a sharp rise in serum creatinine, a decline in urine output, or both.

• AKI is known to occur in between 10% and 15% of hospitalized patients, with more than 50% of patients need intensive care.

• AKI is distinct from chronic kidney disease, which causes the kidneys to slowly lose function over time.

Epidemiology

There are significant disparities in the incidence and etiology of AKI between developing and industrialized nations.

In developing nations' cities, the most prevalent causes of AKI are hospital acquired (renal ischaemia, sepsis, and nephrotoxic medications), but in rural regions, it is more usually a result of community acquired illness (diarrhoea, dehydration, viral diseases, animal venoms, and so on).

The incidence of AKI is rising in industrialized nations. It is believed to occur up to 15% of the time in hospital inpatients, and it is more prevalent in critically sick patients, where it is anticipated to occur up to 60% of the time.

Etiology

The causes of acute kidney injury are classified as:

• Prerenal
• Intrinsic renal
• Postrenal

Prerenal AKI occurs due to inadequate blood flow to the kidney. The main causes are:

• Extracellular fluid volume depletion (caused, for example, by insufficient fluid intake, diarrheal disease, and sepsis)
• Decompensated liver disease (cirrhosis)
• Cardiovascular illness (such as heart failure and cardiogenic shock)

Intrinsic Renal causes of AKI involve intrinsic kidney disease or damage. Blood arteries, glomeruli, tubules, and the interstitium can all be affected. The most frequent reasons include:

• Acute glomerulonephritis
• Acute tubular necrosis
• Nephrotoxins (including over-the-counter and prescription medications)

Postrenal AKI (obstructive nephropathy) is due obstruction in the voiding and collecting sections of the urinary system such as Bladder outlet blockage brought on by an enlarged prostate.

Clinical Presentation

Depending on the underlying cause, signs and symptoms of acute kidney injury may include:

• Low urine output
• Swelling in the ankles, legs, and around the eyes
• Fatigue or exhaustion
• Breathing difficulty
• Confusion
• Nausea
• Seizures, or in severe situations, coma
• Chest pressure or discomfort

AKI can occasionally go unnoticed and only be detected by a healthcare professional through additional testing.

Diagnosis

According to the KDIGO (Kidney Disease: Improving Global Outcomes), AKI can be diagnosed if any one of the following is present:

• Increase in the serum creatinine value of ≥ 0.3 mg/dL (26.52 micromol/L) in 48 hours
• Increase in serum creatinine of ≥ 1.5 times baseline within the prior 7 days
• Urine volume < 0.5 mL/kg/hour for 6 hours.

Once the diagnosis of AKI is made, further testing is often required to determine the underlying cause. Other investigations include:

• Blood tests: complete blood count (CBC), BUN, creatinine, and electrolytes (including calcium and phosphate)

• Urine tests: sodium, urea, protein, and creatinine concentration; and microscopic analysis of sediment.
• Imaging: Renal ultrasonography, noncontrast CT.

Treatment

The therapy of AKI is dependent on identifying and treating the underlying cause.  In addition to treating the underlying illness, AKI is usually managed by avoiding nephrotoxins, or chemicals that are harmful to the kidneys. These include nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen or naproxen, iodinated contrasts like those used in CT scans.

The primary goals of early management are to address life-threatening problems, ideally in a critical care unit.

• Immediate treatment of pulmonary edema and hyperkalemia

• Dialysis is used when necessary to control hyperkalemia, pulmonary edema, metabolic acidosis, and uremic symptoms
• Adjustment of drug regimen for degree of renal dysfunction
• Restriction of water, sodium, phosphate, and potassium intake, but provision of adequate protein
• Possibly intestinal potassium binders for hyperkalemia and phosphate binders for hyperphosphatemia.

Physiotherapy management

An exercise rehabilitation programme for AKI patients could ultimately improve renal recovery following AKI, reduce progression to CKD and improve long term patient outcomes. See Renal Rehabilitation.

Prevention

Acute kidney injury (AKI) can be prevented in patients with trauma, burns, or significant bleeding, as well as those having major surgery, by maintaining normal fluid balance, blood volume, and blood pressure.

Iodinated contrast agents should be avoided, especially in high-risk patients (e.g., the elderly and those with pre-existing renal insufficiency, volume depletion, diabetes, or heart failure).