Acute Kidney Injury Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mr Nguyen is a 69-year-old Vietnamese-Australian man with type 2 diabetes for 20 years, hypertension, ischaemic heart disease (NSTEMI 2021, DES to RCA), and stage 3a CKD (baseline creatinine 145, eGFR 42) who presents with a 5-day history of productive cough, fever, and progressive confusion. His family reports he has been taking increased doses of over-the-counter ibuprofen for pleuritic chest pain. [1]

His medications on admission are: metformin 1g BD, empagliflozin 10mg, perindopril 8mg, frusemide 40mg, atorvastatin 80mg, clopidogrel 75mg, aspirin 100mg, and ibuprofen 400mg TDS. [1]

On examination he is febrile (38.9), tachycardic (110), hypotensive (92/58), tachypnoeic (28) with right basal crackles and increased work of breathing. He is oliguric. [1]

His bloods show creatinine 345 (2.4 times baseline), K+ 6.4, pH 7.22, bicarbonate 13, lactate 3.8, CRP 210, WCC 18.4. Chest X-ray shows right lower lobe consolidation. Urine is positive for leucocytes and nitrites. [1]

His main problems are:

1. Sepsis — community-acquired pneumonia complicated by septic shock (qSOFA 3)
2. Acute kidney injury, KDIGO stage 2, multifactorial — sepsis, volume depletion, nephrotoxicity from NSAIDs and ACE inhibitor, on background diabetic CKD
3. Hyperkalaemia K+ 6.4 — requiring emergency management
4. Metabolic acidosis with raised lactate — from septic shock
5. Polypharmacy with multiple nephrotoxins" [1]

Examiner probing questions and model answers

Q1: "What is your immediate management priority?" [1]

"My first priority is the ABCDE approach. He has evidence of septic shock with hypoperfusion (hypotension, raised lactate, oliguria). I would immediately obtain IV access, take cultures (blood, urine, sputum), and administer antibiotics within one hour per Surviving Sepsis guidelines — I would use ceftriaxone plus azithromycin for community-acquired pneumonia with septic shock. I would give a 30 mL/kg balanced crystalloid fluid bolus over the first 3 hours, then reassess volume status and responsiveness. Simultaneously, I would treat his hyperkalaemia with calcium gluconate and insulin-dextrose, given K+ is 6.4. I would stop all nephrotoxic medications: ibuprofen, perindopril, metformin, and empagliflozin." [1]

Q2: "Why did you stop empagliflozin? Is it nephrotoxic?" [1]

"Empagliflozin is not directly nephrotoxic — in fact SGLT2 inhibitors are renoprotective long-term. However, during acute illness with volume depletion and AKI, SGLT2 inhibitors can worsen volume depletion through their osmotic diuretic effect and have been associated with euglycaemic ketoacidosis in the setting of acute illness. NICE and KDIGO recommend withholding SGLT2 inhibitors during acute illness as part of sick day rules. It should be reinstated after recovery given its proven cardiovascular and renal benefit in diabetic CKD." [1]

Q3: "His potassium is 6.4 with peaked T waves on ECG. Walk me through your hyperkalaemia protocol." [1]

"First, I give calcium gluconate 10 mL of 10% IV over 2 to 5 minutes to stabilise the myocardial membrane — this does not lower potassium but protects against ventricular arrhythmias, with onset in seconds. Second, I give insulin 10 units with 25 grams of IV dextrose over 15 minutes to shift potassium intracellularly, with onset in 15 minutes and duration 4 to 6 hours. I would add nebulised salbutamol 20 mg as adjunctive therapy. I would recheck potassium at 1 hour. If it is refractory or recurrent, I would prepare for renal replacement therapy. I would not rely on potassium binders such as patiromer or sodium zirconium cyclosilicate for emergency management — they are too slow." [1]

Q4: "He is volume-depleted from sepsis but also has heart failure. How do you decide how much fluid to give?" [1]

"This is the critical tension in this patient. I would assess his volume status at the bedside and use dynamic assessment. His JVP is flat, his mucous membranes are dry, and he has a postural component to his hypotension — all suggesting intravascular volume depletion. His heart failure history raises the risk of fluid overload, but the immediate threat is hypoperfusion from septic shock. I would give balanced crystalloid in 250 to 500 mL aliquots, reassessing JVP, blood pressure, oxygen saturation, and lung bases between each bolus. If I have access to point-of-care ultrasound, I would assess the IVC for collapsibility and look for B-lines as early pulmonary oedema. If he is in the ICU, I would use a passive leg raise test with cardiac output monitoring to assess fluid responsiveness. I would stop boluses when he is no longer fluid-responsive or shows signs of overload. If he develops pulmonary oedema with ongoing need for fluid, he may need early vasopressor support (noradrenaline) and, if oliguria persists, RRT for fluid management." [1]

Q5: "He does not improve after 48 hours of resuscitation. Creatinine is now 480, still oliguric, and he has developed pulmonary oedema. Do you start dialysis?" [1]

"Yes, this meets an absolute indication for RRT — the O in AEIOU: refractory volume overload with pulmonary oedema unresponsive to diuretics. I would not delay further. Given he may be haemodynamically unstable from ongoing sepsis, I would prefer continuous renal replacement therapy (CRRT, CVVHDF) for gentle fluid removal. If he is haemodynamically stable enough, sustained low-efficiency dialysis (SLED) is an alternative. I would insert a large-bore dialysis catheter in the right internal jugular or femoral vein. This is a standard — not early — initiation; the AEIOU criteria represent absolute indications that mandate RRT regardless of the timing debate from AKIKI and STARRT-AKI." [1]

Q6: "Tell me about the AKIKI and STARRT-AKI trials and how they changed your practice." [1]

"AKIKI, published in NEJM in 2016, randomised 620 critically ill patients with KDIGO stage 3 AKI to early versus delayed RRT. There was no difference in 60-day mortality — 48.5% early versus 49.7% delayed. Critically, 49% of the delayed group never needed RRT at all, meaning early initiation exposed half the patients to an unnecessary procedure and its complications. [1]

STARRT-AKI, published in NEJM in 2020, was much larger — over 3000 patients in 168 hospitals across 15 countries. It compared an accelerated strategy (RRT within 12 hours of meeting criteria) with a standard strategy (RRT only for absolute indications or persistent AKI at 72 hours). Again, no mortality difference — 43.9% versus 43.7%. But the accelerated group had worse outcomes: higher RRT dependence at 90 days (10.4% versus 6.0%) and more adverse events. [1]

The ELAIN trial, a single-centre German study, showed a mortality benefit for very early initiation at KDIGO stage 2, but this has not been replicated in larger multicentre trials, and the population was predominantly surgical. [1]

These trials changed my practice to favour a standard or delayed strategy — I initiate RRT for absolute indications (AEIOU) or for progressive AKI that is not recovering despite treating the cause. I do not initiate early based on stage alone. This approach avoids exposing patients to unnecessary RRT while not compromising outcomes." [1]

Q7: "What is his long-term prognosis if he survives?" [1]

"Even if his creatinine returns to near baseline, he is at significant long-term risk. Every AKI episode approximately doubles the risk of progression to CKD stage 4 or 5 over the subsequent 3 to 5 years, and this risk is amplified by his baseline diabetic CKD. He has a 20 to 30% risk of recurrent AKI within 1 year. I would arrange close follow-up: creatinine at discharge, 1 month, and 3 months. If his eGFR remains below baseline at 3 months, I would refer to nephrology. I would reinstate his ACE inhibitor and SGLT2 inhibitor after recovery given their proven renoprotective and cardioprotective benefits. I would provide thorough sick day rules education: during any future acute illness with reduced intake, he should hold his ACE inhibitor, SGLT2i, diuretics, metformin, and all NSAIDs, and resume when recovered. I would emphasise avoiding all over-the-counter NSAIDs permanently given his diabetic CKD and this AKI episode." [1]

Short Case Discussion

Scenario: "Assess this patient's volume status"

Candidate presentation (model): [1]

"I assessed this patient's volume status. The hands are cool peripherally with capillary refill of 4 seconds, suggesting poor peripheral perfusion. The pulse is regular at 104 beats per minute, of reduced volume. Blood pressure is 96/62 lying and 84/55 standing — a significant postural drop of 12 mmHg systolic. The JVP is not visible above the sternal angle at 45 degrees, consistent with low right atrial pressure. The mucous membranes are dry and the tongue is furrowed. Skin turgor over the clavicle is reduced with persistent tenting. The lungs are clear with no crackles. Heart sounds are dual with no gallop. There is no peripheral or sacral oedema. The abdomen is soft with no ascites. [1]

In summary, these findings are consistent with significant intravascular volume depletion. I would manage this patient with intravenous balanced crystalloid resuscitation, giving 500 mL boluses with reassessment of volume status, blood pressure, and oxygen saturation between each." [1]

Examiner: "What is the significance of the postural drop?" [1]

"A postural systolic blood pressure drop of more than 20 mmHg or a diastolic drop of more than 10 mmHg on standing indicates significant volume depletion — typically at least 10 to 15% reduction in circulating volume. It is a more sensitive marker of hypovolaemia than supine hypotension, which is a late sign. In this patient, the combination of postural drop, flat JVP, delayed capillary refill, and dry mucous membranes gives me high confidence that he is volume-depleted and requires fluid resuscitation rather than diuretics or fluid restriction." [1]

Examiner: "If you could only use one sign to assess volume status, what would it be and why?" [1]

"The JVP. It is the only bedside sign that directly reflects right atrial pressure and therefore intravascular volume. A flat JVP at 45 degrees indicates low right atrial pressure and volume depletion; a JVP elevated more than 3 cm above the sternal angle indicates elevated right atrial pressure and volume overload. Its limitations are that it can be difficult to see in obese patients, in patients with high ventilator pressures, and in atrial fibrillation where the waveform is irregular. In those situations, point-of-care ultrasound of the IVC is a useful adjunct — a small, collapsible IVC suggests low volume, while a dilated, non-collapsible IVC suggests volume overload. However, the JVP remains the single most useful bedside sign when it can be assessed." [1]

Examiner: "What fluid would you give and why?" [1]

"I would use a balanced crystalloid such as Plasma-Lyte or Hartmann's solution, not 0.9% saline. The SMART trial, published in 2019, showed that in critically ill adults, balanced crystalloids reduced the composite outcome of major adverse kidney events at 30 days compared with saline. The mechanism is that large-volume saline causes hyperchloraemic metabolic acidosis, which causes renal vasoconstriction of the afferent arteriole and reduces renal blood flow. Balanced crystalloids avoid this by maintaining a more physiological strong ion difference. The one situation where I would preferentially use saline is if the patient has significant hyponatraemia, hypochloraemia, or specific saline-responsive conditions." [1]