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]

SAQ 2 — Investigation Interpretation and RRT Decision (15 marks, 20 minutes)

Prompt: A 62-year-old man in the ICU with perforated diverticulitis and septic shock develops AKI. Day 3 of admission: creatinine 410 (baseline 90), K+ 6.8 mmol/L, pH 7.12 (bicarbonate 10), he is intubated and on noradrenaline 0.3 mcg/kg/min. Urine output 50 mL over 12 hours. Despite calcium gluconate and insulin-dextrose, his potassium is 6.5 on recheck at 1 hour. Interpret his clinical status and outline your RRT decision. [1]

Model Answer

Clinical status (4 marks): [1]

This patient has KDIGO stage 3 AKI (creatinine 4.6 times baseline, anuric) in the setting of septic shock. He now meets two absolute indications for RRT: [1]

1. Refractory hyperkalaemia — K+ 6.8 initially, persisting at 6.5 despite calcium and insulin-dextrose (E for Electrolytes in AEIOU)
2. Severe metabolic acidosis — pH 7.12, refractory to medical therapy (A for Acidosis in AEIOU) [1]

He also has oliguria/anuria with likely progressive volume overload risk (O for Overload). [1]

RRT decision (5 marks): [1]

This patient must receive RRT now. These are absolute (not relative) indications — the question of timing strategy (AKIKI, STARRT-AKI) applies only to patients WITHOUT absolute indications. When AEIOU criteria are met, RRT is mandatory regardless of trial evidence about timing. [1]

Modality choice: Given he is haemodynamically unstable (intubated, on noradrenaline 0.3 mcg/kg/min), the preferred modality is continuous renal replacement therapy (CRRT) — typically CVVHDF (continuous veno-venous haemodiafiltration). CRRT provides gentle, continuous fluid and solute removal that does not cause the haemodynamic swings of intermittent haemodialysis. It allows precise fluid balance management in a patient needing ongoing vasopressor and fluid management. [1]

Preparation (3 marks):

• Urgent vascular access: large-bore dual-lumen haemodialysis catheter (right internal jugular or femoral vein)
• Discuss with ICU, nephrology, and ICU nursing team
• Anticoagulation: regional citrate anticoagulation preferred (if no hepatic dysfunction); alternatively heparin or no anticoagulation if bleeding risk
• Confirm electrolyte panel, coagulation, platelet count before circuit setup
• Continue all standard sepsis management (antibiotics, source control for perforated diverticulitis) [1]

Prognosis discussion (3 marks): [1]

ICU patients with septic AKI requiring CRRT have approximately 50 to 60% in-hospital mortality — driven by the underlying sepsis and multi-organ failure. Of survivors, approximately 60 to 70% recover renal function, 15 to 20% have partial recovery (new or worsened CKD), and 5 to 10% remain dialysis-dependent at discharge. He should have renal function monitored closely during and after CRRT to determine if and when it can be discontinued. Transition to intermittent haemodialysis may occur once he is haemodynamically stable, with monitoring for ongoing need. [1]