Nephrology

Question 1

What is the definition and epidemiology of AKI?

Answer 1

AKI is characterised in an abrupt fall in GFR (Glomerular Filtration Rate), clinically manifested as an abrupt and sustained rise in serum urea and creatinine. AKI is twice as common as the number of haemodialysis patients. Up to 18% of hospital patients have AKI.

Question 2

What is the aetiology of AKI?

Answer 2

Can be split into pre-renal, intrinsic and post-renal cases. Most cases tend to be pre-renal and obstructive (post-renal).

Pre-Renal:
This is due to decreased renal perfusion, secondary to:
• Hypovolaemia (haemorrhage, GI losses, urinary losses, cutaneous losses and fluid redistribution)
• Hypotension (cardiogenic shock, distributive shock e.g. sepsis or anaphylaxis)
• Renal hypoperfusion (Reduced renal perfusion plus impaired autoregulation through RAAS drug inhibition, Abdominal aortic aneurysm, Renal artery stenosis/occlusion, Hepatorenal syndrome).
• Oedema states (Cardiac failure, Hepatic cirrhosis, Nephrotic syndrome) mean that fluid moves from plasma to intracellular compartment.

Intrinsic:
Can be further split into:
• Glomerular disease - Glomerulonephritis (inflammation) or thrombosis
• Tubular injury - Acute tubular necrosis
○ Ischaemic ATN is associated with sepsis, hypotension and haemorrhage.
○ Nephrotoxic ATN is associated with drugs, radiological contrast agents, uric acid crystals, haemoglobinuria and myeloma.
• Interstitial nephritis (usually caused by drugs such as analgesics or methicillin)
• Vascular disease - vasculitis, occlusion (embolic or thrombotic), HUS (Haemolytic Uraemic Syndrome) and TTP (Thrombotic Thrombocytopaenic Purpura)

Post-Renal:
Obstructive nephropathy presents as AKI relatively infrequently. Secondary to:
• Kidney stones
• Tumour (prostate, or BPH, pelvic, bladder)
• Blood clots
• Retroperitoneal fibrosis

Question 3

What are the clinical features of uraemia?

Answer 3

Patients can present with malaise, anorexia, nausea, vomiting, pruritus, drowsiness, convulsions, and coma (caused by uraemia).

Question 4

What are the complications of AKI?

Answer 4

• Hyperphosphataemia
• Uraemia
• Pulmonary oedema
• Hyperkalaemia
• Metabolic acidosis
Later, CKD

Question 5

How can AKI be investigated?

Answer 5

Bloods:
• U&Es - acutely ↑ serum creatinine, ↑serum K+ and metabolic acidosis. ↓ Ca2+ and ↓phosphates.
• FBC - anaemia is a sign of chronic kidney disease. Eosinophilia may be present in acute intestinal nephritis.
• Coagulation studies - DIC associated with sepsis.

Urinalysis (dipstick and MC&S) to test for infection. Urinary casts point towards glomerulonephritis. Also eosinophils may be present in acute intestinal nephritis.

Immunology:
• ANA (Anti-Nuclear Antibodies) are positive in SLE and other autoimmune disorders.
• Anti-dsDNA also positive in SLE (more specific).
• ANCA - Associated with systemic vasculitis and Wegner’s granulomatosis.
• Antiglomerular basement membrane antibodies.

Renal ultrasound may show obstruction (dilated renal caylices), and other changes associated with chronic kidney disease.

Question 6

How is AKI managed?

Answer 6

Restore volume status - aiming for euvolaemia with fluids and maybe vasopressors. Careful monitoring in ITU.

Treat the cause if possible.

Treat hyperkalaemia (see Potassium Imbalance) and pulmonary oedema (see Pulmonary Oedema).