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Renal & Urinary System

Acute Kidney Injury (AKI)

Acute impairment of renal function, previously known as Acute Renal Failure. Can result from reduced kidney perfusion, direct kidney damage, or urinary tract obstruction.

Also known as: Acute Renal Failure, ARF, AKI

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Referral and warning signs

When to refer

Refer ALL suspected AKI cases to hospital (HC4/H/RR) for diagnosis, management, and monitoring. Urgent referral needed for: Anuria, Severe hyperkalaemia, Severe acidosis, Pulmonary oedema, Uraemic complications (encephalopathy, pericarditis), Need for dialysis.

Red flags

  • Anuria or severe oliguria (<100ml/24h)
  • Signs of severe fluid overload (pulmonary oedema, severe peripheral oedema)
  • Signs of hyperkalaemia (ECG changes - peaked T waves, wide QRS)
  • Signs of uraemia (confusion, drowsiness, pericardial rub, asterixis)
  • Rapidly rising creatinine/urea

Signs and symptoms

  • Oliguria (urine output <1 ml/kg/hour or <400-500ml/day in adults)
  • Anuria (urine output <100 ml/24 hours) - suggests obstruction or severe injury
  • Generalised oedema
  • Hypertension
  • Signs of heart failure / fluid overload (dyspnoea)
  • Nausea, vomiting, anorexia
  • Lethargy, confusion, drowsiness
  • Convulsions (due to uraemia or electrolyte imbalance)

Risk factors

  • Pre-renal causes (compromised perfusion): Dehydration, Haemorrhage, Shock, Heart failure, Sepsis.
  • Renal (intrinsic) causes (damage to kidney tissue): Glomerulonephritis, Acute tubular necrosis (ATN) due to ischemia or toxins (nephrotoxic drugs like aminoglycosides, NSAIDs; contrast dye; poisons/herbs), Interstitial nephritis (drug reaction, infection).
  • Post-renal causes (obstructed urinary flow): Kidney stones, Benign Prostatic Hyperplasia (BPH), Tumours (prostate, bladder, cervical), Urethral strictures, Bilateral ureteric obstruction.

Diagnosis

Clinical assessment

Suspected based on rapid decline in urine output (oliguria/anuria) and/or rise in serum creatinine/urea. Assess fluid status (dehydration vs overload), blood pressure, identify potential cause (sepsis, drugs, obstruction). Differentiate from chronic kidney disease (history, kidney size on ultrasound).

Investigations

  • Urinalysis: Assess for blood (haematuria), protein (proteinuria), white blood cells (pyuria), casts (e.g., granular/muddy brown casts in ATN; red cell casts in glomerulonephritis).
  • Serum Urea, Creatinine, Electrolytes: Assess severity of renal impairment, check for hyperkalaemia, acidosis.
  • Kidney Ultrasound: Assess kidney size (usually normal/large in AKI, small in CKD), rule out hydronephrosis (obstruction), assess parenchyma.
  • Complete Blood Count (CBC): Assess for anaemia, infection.
  • Further tests based on suspected cause: Blood cultures (sepsis), ECG (hyperkalaemia, heart failure), specific tests for glomerulonephritis (ASOT, autoimmune screen - specialist).

Diagnostic criteria

Rapid increase in serum creatinine, and/or decrease in urine output, meeting standard AKI criteria (e.g., KDIGO criteria).

Management

Non-pharmacological management

  • Identify and Treat Underlying Cause: Crucial (e.g., fluids for dehydration, antibiotics for sepsis, relieve obstruction).
  • Fluid Management: Careful monitoring of fluid input and output. Replace losses appropriately (Daily requirement ~10ml/kg + measured losses). Avoid fluid overload; fluid restriction may be needed if oliguric/anuric and overloaded.
  • Monitoring: Monitor BP (treat hypertension), daily weight, urine output.
  • Dietary Management: Restrict salt (<2g/day), restrict potassium (avoid high-K+ foods like bananas, oranges). Moderate protein intake. Ensure adequate caloric intake.
  • Renal Replacement Therapy (Dialysis): Indicated for severe AKI with refractory fluid overload, hyperkalaemia, acidosis, uraemic complications (encephalopathy, pericarditis). Requires referral.

Pharmacological treatment

  • Treat Underlying Cause (e.g., antibiotics for infection).
  • Manage Fluid Overload: Diuretics (e.g., IV Furosemide). High doses may be needed in AKI. Response may be poor if severe injury/anuria.
  • Manage Hyperkalaemia (Emergency - See electrolyte imbalance section).
  • Manage Metabolic Acidosis (Sodium bicarbonate - specialist guidance).
  • Manage Hypertension (See CV006, adjust doses for renal impairment).
  • Adjust dosages of renally excreted drugs.
  • Avoid Nephrotoxic Drugs: NSAIDs, aminoglycosides (use with caution if essential), contrast dye.

Monitoring

Monitor fluid balance (I/O chart, daily weight), vital signs (BP, HR), urine output frequently. Monitor serum urea, creatinine, electrolytes (esp. potassium) daily or as needed. Monitor acid-base status (if severe). Monitor for uraemic complications.

Complications

  • Fluid overload, pulmonary oedema, heart failure
  • Hyperkalaemia (life-threatening arrhythmia risk)
  • Metabolic acidosis
  • Uraemia (encephalopathy, pericarditis, bleeding)
  • Infections
  • Progression to Chronic Kidney Disease (CKD)
  • Death

Prevention

  • Maintain adequate hydration, especially in sick patients.
  • Avoid/monitor nephrotoxic drugs carefully.
  • Prompt treatment of shock, sepsis, heart failure.
  • Manage conditions predisposing to AKI (diabetes, hypertension).

Patient education

  • Explanation of AKI and potential causes.
  • Importance of fluid/dietary restrictions.
  • Need for close monitoring.
  • Avoidance of nephrotoxic drugs/herbs.
  • Follow-up plan after recovery to assess for CKD.

Uganda-specific notes

Common causes include dehydration (diarrhoea, vomiting), sepsis (malaria, bacterial), nephrotoxic traditional remedies, and obstetric complications. Access to dialysis is extremely limited. Focus on prevention, early recognition, fluid management, treating underlying cause, and cautious drug use.

References

  • Uganda Clinical Guidelines (UCG) 2023

    Chapter 7, Section 7.1.1

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