Acute Kidney Injury — Written Clinical Reasoning

SAQ 1 — Integrated Management of Multifactorial AKI (25 marks, 30 minutes)

Prompt: Outline your immediate and integrated management plan for this patient, including emergency management, problem list, investigation interpretation, pharmacological changes, drug dosing, and follow-up planning. Justify each decision with reference to evidence and guidelines. [1]

Model Answer

Immediate emergency management — hyperkalaemia (3 marks): [1]

K+ 6.3 mmol/L is a medical emergency requiring immediate treatment. The patient has no ECG changes described but K+ is above 6.0 with metabolic acidosis — treat urgently: [1]

1. Calcium gluconate 10 mL of 10% IV over 2 to 5 minutes to stabilise the myocardium (if any ECG changes present).
2. Insulin-dextrose: 10 units Actrapid in 25 g IV dextrose over 15 minutes to shift potassium intracellularly.
3. Salbutamol 10 to 20 mg nebulised as adjunctive potassium-shifting therapy.
4. Recheck K+ within 1 to 2 hours. If refractory, prepare for RRT. [1]

Treat metabolic acidosis by addressing the cause (hypoperfusion from volume depletion). Sodium bicarbonate is not routinely indicated for lactic acidosis in AKI. If pH remains <7.1 despite resuscitation, discuss RRT. [1]

Problem list (4 marks): [1]

1. Acute kidney injury, KDIGO stage 2 (creatinine 2.3 times baseline) — multifactorial
2. Hyperkalaemia K+ 6.3 — requiring emergency management
3. Metabolic acidosis (pH 7.24, bicarbonate 14) — from AKI and hypoperfusion
4. Volume depletion — postural hypotension, flat JVP, delayed capillary refill
5. Nephrotoxicity — ibuprofen (NSAID, afferent arteriolar vasoconstriction) and perindopril (ACE inhibitor, efferent arteriolar dilation), both on a background of diabetic CKD where autoregulation is impaired
6. Possible sepsis — CRP 85, diarrhoea and vomiting (could be infective); source to identify
7. Polypharmacy — metformin (contraindicated in significant AKI due to lactic acidosis risk) [1]

Classification of AKI (3 marks): [1]

This is predominantly pre-renal AKI progressing toward ATN — the kidney is structurally intact but functionally impaired from volume depletion (gastroenteritis) compounded by nephrotoxic drugs that have removed both compensatory mechanisms:

• NSAIDs block prostaglandin-mediated afferent arteriolar vasodilation
• ACE inhibitor blocks angiotensin II-mediated efferent arteriolar vasoconstriction
• In a diabetic patient with CKD, renal autoregulation is already impaired, making the kidney exquisitely sensitive to these insults [1]

The FENa cannot be reliably interpreted because she has received frusemide. If measured, FEUN <35% would support pre-renal. The bland urinalysis (only trace blood and protein, no casts) is consistent with pre-renal rather than intrinsic glomerular disease. [1]

Fluid resuscitation (3 marks): [1]

She is clearly hypovolaemic (postural drop, flat JVP, dry mucous membranes, delayed capillary refill). Resuscitate with balanced crystalloid (Plasma-Lyte or Hartmann's) — not 0.9% saline:

• Give 500 mL boluses, reassessing volume status, JVP, blood pressure, and oxygen saturation between each bolus
• Target: restoration of intravascular volume (JVP visible, postural drop resolved, capillary refill <2 seconds, MAP >65 mmHg)
• The SMART trial supports balanced crystalloids over saline in patients at risk of AKI — saline causes hyperchloraemic metabolic acidosis which worsens renal vasoconstriction
• Stop resuscitation if she develops signs of volume overload (rising JVP, pulmonary crackles) [1]

Pharmacological changes — stop nephrotoxins (4 marks): [1]

Investigations and source identification (3 marks): [1]

• Blood cultures, stool culture (infective diarrhoea?), urine culture
• Chest X-ray — exclude pneumonia as source of sepsis
• ECG — for hyperkalaemia changes; repeat after treatment
• Repeat U&E every 6 to 12 hours initially; monitor K+ and creatinine trajectory
• Venous blood gas — monitor acid-base and lactate
• Renal ultrasound — if no improvement after volume resuscitation, to exclude occult obstruction (especially in a diabetic patient with autonomic bladder dysfunction)
• Do NOT give contrast (CT) unless absolutely essential and after resuscitation
• Consider autoimmune/infective screen if no recovery despite removing nephrotoxins and volume repletion (ANA, ANCA, anti-GBM, complements, hepatitis, HIV) [1]

Drug dosing in AKI (2 marks): [1]

If antibiotics are needed for sepsis (e.g., pyelonephritis, pneumonia):

• Use the current (worsened) eGFR for dosing, not baseline
• Piperacillin-tazobactam: reduce frequency (e.g., 4.5 g IV QID becomes TDS or BD depending on eGFR)
• Vancomycin: trough-level guided dosing, not fixed interval
• Aminoglycosides: avoid if possible in AKI; if essential, extended-interval with trough monitoring
• If hyperkalaemia persists or she develops volume overload, consider renal replacement therapy [1]

Prognosis and follow-up (3 marks): [1]

• If this is predominantly pre-renal and volume-responsive, creatinine should plateau within 24 to 48 hours of resuscitation and begin improving within 3 to 5 days. Complete recovery is expected in 60 to 70% of pre-renal AKI cases.
• She is at higher risk of incomplete recovery due to baseline CKD and diabetes. Even partial recovery may worsen her CKD trajectory.
• Creatinine should be checked at discharge, at 1 month, and at 3 months to confirm recovery or detect new CKD stage progression.
• Sick day rules education: During future acute illness with reduced oral intake, she should temporarily hold perindopril, frusemide, metformin, any SGLT2i, and all NSAIDs. Resume when recovered and eating/drinking normally. This education is critical to prevent recurrent AKI.
• Perindopril should be reinstated after recovery (eGFR returned to near baseline) because of its proven renoprotective and cardioprotective benefit in diabetes and CKD.
• Refer to nephrology if creatinine has not returned to baseline by 3 months, or if recurrent AKI. [1]