Acute Kidney Injury (AKI)

• 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.

• 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.

• Serum creatinine: Increased levels indicate impaired kidney function.
• Blood urea nitrogen (BUN): Elevated in AKI.
• Electrolytes: Monitor for hyperkalaemia, hyponatremia, and metabolic acidosis.
• Urinalysis: Assess for proteinuria, haematuria, 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.

• 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., hyperkalaemia, hyponatremia).
• Metabolic acidosis.
• Fluid overload and pulmonary oedema.
• Cardiovascular complications (e.g., hypertension, heart failure).
• Increased risk of infections.
• Anaemia 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.

• 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.