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Acute Kidney Injury (AKI)

Background Knowledge ๐Ÿง 


  • A sudden decrease in kidney function, resulting in the inability to maintain fluid, electrolyte, and acid-base balance.
  • Defined by a rapid rise in serum creatinine and/or a decrease in urine output.
  • Can range from mild dysfunction to severe kidney failure requiring dialysis.


  • AKI affects approximately 13-18% of all hospitalized patients.
  • Higher incidence in elderly patients and those with pre-existing chronic kidney disease.
  • Increased risk in patients with sepsis, cardiac surgery, and those receiving nephrotoxic medications.
  • Associated with significant morbidity and mortality, particularly in critically ill patients.


Classified into prerenal, intrinsic (renal), and postrenal causes.

  • Prerenal: Decreased renal perfusion due to hypovolaemia, heart failure, or sepsis.
  • Intrinsic: Damage to kidney tissue due to acute tubular necrosis, glomerulonephritis, or interstitial nephritis.
  • Postrenal: Obstruction of urinary outflow due to stones, tumours, or strictures.


  • Involves reduced glomerular filtration rate, tubular injury, and inflammatory responses.
  • Leads to accumulation of waste products, electrolyte imbalances, and fluid overload.


  • Prerenal AKI: Due to reduced blood flow to the kidneys.
  • Intrinsic AKI: Due to direct damage to the kidney tissues.
  • Postrenal AKI: Due to obstruction of the urinary tract.
  • Acute tubular necrosis: Most common cause of intrinsic AKI.
  • Acute interstitial nephritis: Often drug-induced, causing inflammation of the kidney interstitium.
  • Acute glomerulonephritis: Involves inflammation of the glomeruli.

Clinical Features ๐ŸŒก๏ธ


  • Oliguria or anuria (reduced or no urine output).
  • Fatigue and malaise.
  • Nausea and vomiting.
  • Shortness of breath due to fluid overload.
  • Confusion or altered mental status.
  • Oedema, especially in legs and ankles.
  • Chest pain or pressure.


  • Hypertension.
  • Tachycardia in cases of sepsis or hypovolemia.
  • Decreased skin turgor and dry mucous membranes in dehydration.
  • Lung crackles or rales indicating fluid overload.
  • Jugular venous distention.
  • Pericardial friction rub in severe uraemia.
  • Elevated jugular venous pressure.

Investigations ๐Ÿงช


  • Serum creatinine: increased levels indicate impaired kidney function.
  • Blood urea nitrogen (BUN): elevated in AKI.
  • Electrolytes: monitor for hyperkalemia, hyponatremia, and metabolic acidosis.
  • Urinalysis: assess for proteinuria, hematuria, and casts.
  • Renal ultrasound: evaluate for obstruction or hydronephrosis.
  • Fractional excretion of sodium (FENa): differentiate between prerenal and intrinsic AKI.
  • ECG: check for arrhythmias due to electrolyte imbalances.
  • Blood cultures if sepsis is suspected.
  • Kidney biopsy: in certain cases to determine the underlying cause.
  • CT scan or MRI if renal ultrasound is inconclusive.

Management ๐Ÿฅผ


  • Identify and treat the underlying cause (e.g., stop nephrotoxic drugs, treat infection).
  • Fluid management: balance between resuscitation and avoiding fluid overload.
  • Electrolyte management: treat hyperkalaemia, hyponatraemia, and acidosis.
  • Renal replacement therapy (dialysis) if indicated (e.g., severe hyperkalaemia, acidosis, fluid overload).
  • Avoid nephrotoxic medications and adjust doses of renally excreted drugs.
  • Nutritional support to prevent catabolism.
  • Monitor urine output and renal function regularly.
  • Follow UK guidelines for AKI management (e.g., NICE guidelines).


  • Chronic kidney disease (CKD).
  • End-stage renal disease (ESRD).
  • Electrolyte imbalances (e.g., hyperkalemia, hyponatremia).
  • Metabolic acidosis.
  • Fluid overload and pulmonary edema.
  • Cardiovascular complications (e.g., hypertension, heart failure).
  • Increased risk of infections.
  • Anemia due to decreased erythropoietin production.
  • Uremic complications (e.g., encephalopathy, pericarditis).


  • Prognosis varies depending on the cause and severity of AKI.
  • Early diagnosis and treatment improve outcomes.
  • High mortality in critically ill patients.
  • Some patients may recover completely, while others may develop CKD or ESRD.
  • Regular follow-up required to monitor renal function and manage complications.
  • Preventive measures (e.g., avoiding nephrotoxins, managing comorbidities) are essential to reduce the risk of recurrence.
  • Public health interventions crucial for control and prevention.

Key Points

  • AKI is a common and serious condition that requires prompt diagnosis and management.
  • Understanding the underlying cause is crucial for effective treatment.
  • Fluid and electrolyte management are key components of care.
  • Renal replacement therapy may be necessary in severe cases.
  • Follow UK guidelines for the latest management protocols.
  • Regular monitoring and follow-up are essential to prevent and manage complications.
  • Patient education on risk factors and preventive measures is important.
  • Early intervention improves outcomes and reduces mortality.

For more detailed guidelines, refer to the latest UK guidelines such as those from NICE:

NICE Guidelines on Acute Kidney Injury

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