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Acute Kidney Injury

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function occurring within seven days. This condition is characterised by an increase in serum creatinine or a decrease in urine output, or both. AKI is primarily categorised into prerenal, intrinsic renal, and postrenal causes.

Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury.
Pathologic kidney specimen showing marked pallor of the cortex, contrasting to the darker areas of surviving medullary tissue. The patient died with acute kidney injury.

Signs and Symptoms

The symptoms of AKI are typically dominated by the underlying cause and the disturbances in kidney function. Common symptoms include fatigue, loss of appetite, headache, nausea, and vomiting, all due to the accumulation of urea and other nitrogen-containing substances in the bloodstream. High potassium levels can lead to severe and life-threatening abnormal heart rhythms. Pain in the flanks, thirst, and evidence of fluid depletion may also be observed. Physical examinations may reveal additional clues such as a rash in interstitial nephritis or a palpable bladder in obstructive nephropathy.

Causes

Prerenal

Prerenal causes of AKI are due to decreased blood flow to the kidneys, resulting in a reduced glomerular filtration rate (GFR). Common prerenal causes include dehydration, excessive blood loss, heart failure, and certain medications like NSAIDs.

Intrinsic or Intrarenal

Intrinsic AKI results from direct damage to the kidney itself and can affect the glomeruli, tubules, or interstitium. Causes include glomerulonephritis, acute tubular necrosis, and acute interstitial nephritis. Certain medications, such as calcineurin inhibitors, can also directly damage the kidney.

Postrenal

Postrenal AKI is caused by obstructions in the urinary tract downstream of the kidney. This can result from conditions such as benign prostatic hyperplasia, kidney stones, and bladder cancer.

Diagnosis

Definition and Staging

AKI can be diagnosed based on criteria established by the Kidney Disease: Improving Global Outcomes (KDIGO) in 2012, which include an increase in serum creatinine by ≥0.3 mg/dL within 48 hours, an increase in serum creatinine to ≥1.5 times baseline within the prior 7 days, or urine volume < 0.5 mL/kg/h for 6 hours. The RIFLE criteria further aid in assessing the severity of AKI, ranging from Risk to End-stage kidney disease.

Evaluation

Diagnosis often involves measuring urine output and blood tests for urea and creatinine. Further testing might include urine sediment analysis, renal ultrasound, and kidney biopsy. Imaging studies such as renal ultrasonography, CT scans, and MRI are used to examine the acute changes in the kidney and identify any structural abnormalities.

Renal ultrasonograph of acute pyelonephritis with increased cortical echogenicity and blurred delineation of the upper pole.
Renal ultrasonograph of acute pyelonephritis with increased cortical echogenicity and blurred delineation of the upper pole.
Renal ultrasonograph in renal failure after surgery with increased cortical echogenicity and kidney size. Biopsy showed acute tubular necrosis.
Renal ultrasonograph in renal failure after surgery with increased cortical echogenicity and kidney size. Biopsy showed acute tubular necrosis.
Renal ultrasonograph in renal trauma with laceration of the lower pole and subcapsular fluid collection below the kidney.
Renal ultrasonograph in renal trauma with laceration of the lower pole and subcapsular fluid collection below the kidney.

Treatment

The management of AKI involves treating the underlying cause and providing supportive care. Avoiding nephrotoxic substances is very important. Monitoring of kidney function through serial serum creatinine measurements and urine output is routinely performed.

Prerenal

In prerenal AKI without fluid overload, intravenous fluids are typically administered to improve kidney function. If low blood pressure persists, vasopressors and inotropes may be given to enhance blood flow to the kidney.

Intrinsic

Treatment of intrinsic AKI depends on the specific cause. For example, AKI due to vasculitis or glomerulonephritis may respond to steroids, cyclophosphamide, and plasma exchange. Discontinuation of nephrotoxic drugs is often required.

Postrenal

Postrenal AKI necessitates relieving the obstruction, which may involve procedures such as nephrostomy or urinary catheterisation.

Renal Replacement Therapy

In some cases, renal replacement therapy like haemodialysis is required. Both intermittent and continuous renal replacement therapies are used, depending on the patient's condition and response to treatment.

Prognosis and Epidemiology

Mortality rates for AKI are high, particularly in ICU settings, with a death rate as high as 50%. AKI can lead to chronic kidney disease and end-stage kidney disease, requiring lifelong dialysis or a kidney transplant. AKI is common among hospitalised patients, affecting 3-7% of those admitted to the hospital and 25-30% of ICU patients. The incidence of AKI has increased over the past 20 years, making it one of the most expensive conditions seen in hospitals.


Self-assessment MCQs (single best answer)

What is the primary characteristic of Acute Kidney Injury (AKI)?



Which of the following is NOT a common symptom of AKI?



What is a prerenal cause of AKI?



Which medication is known to cause direct damage to the kidney, leading to intrinsic AKI?



What does postrenal AKI result from?



According to KDIGO criteria, what urine volume is indicative of AKI?



What diagnostic tool is commonly used to examine acute changes in the kidney and identify structural abnormalities?



Which treatment is typically administered for prerenal AKI without fluid overload?



When might renal replacement therapy be required in the management of AKI?



Which of the following is a potential long-term consequence of AKI?



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