Acute Kidney Injury — Viva

Q1: Define AKI and reproduce the KDIGO criteria. Classify AKI by cause and state the relative frequencies. (3 min)

Definition (KDIGO 2012):^[1] AKI is a rapid decline in kidney function — any one of: (a) creatinine rise of 0.3 mg/dL (26.5 micromol/L) or more within 48 hours; (b) creatinine 1.5 times baseline or more within 7 days; (c) urine output under 0.5 mL/kg/h for 6 hours or more.

Classification by cause:^[1] pre-renal (hypoperfusion, about 60 per cent — hypovolaemia, heart failure, sepsis, NSAIDs, ACE inhibitors); intrinsic (about 35 per cent — ATN is commonest, then glomerular, interstitial, vascular); post-renal (obstruction, about 5 per cent — BPH, stones, tumour, retroperitoneal fibrosis).

KDIGO staging:^[1] Stage 1 — Cr 1.5 to 1.9 times baseline or up by 0.3 mg/dL, UO under 0.5 mL/kg/h for 6 to 12 h; Stage 2 — Cr 2.0 to 2.9 times, UO under 0.5 for 12 h or more; Stage 3 — Cr 3 times baseline, or over 4.0 mg/dL, or RRT; UO under 0.3 for 24 h or more or anuria for 12 h or more.

Q2: A 68-year-old man on ramipril and ibuprofen is admitted with diarrhoea and vomiting, creatinine 320 (baseline 90). How will you investigate and distinguish pre-renal from ATN? (3 min)

Investigations:^[1] U&E trend, FBC, CRP, lactate, CK, venous gas, urinalysis and microscopy, urine sodium and creatinine (FENa), renal ultrasound and bladder scan, ECG (hyperkalaemia).

Pre-renal vs ATN:^[1] FENa under 1 per cent, urine Na under 20, urine osmolality over 500, BUN/Cr over 20:1, bland sediment, and rapid recovery with fluids = pre-renal. FENa over 2 per cent, urine Na over 40, osmolality under 350, BUN/Cr 10 to 20:1, muddy brown granular casts, no recovery with fluids = ATN. Caution: FENa is misleading after diuretics — use FEurea, where under 35 per cent supports pre-renal.

This patient has the triple whammy (NSAID + ACE inhibitor + diuretic on volume depletion) — initially pre-renal, may progress to ischaemic ATN if untreated.^[1]

Q3: What is the management of AKI? Reproduce the indications for dialysis and the hyperkalaemia treatment ladder with doses. (3 min)

Four-step ladder:^[1] (1) treat the cause (fluids, antibiotics, relieve obstruction, stop nephrotoxins, immunosuppression); (2) optimise haemodynamics (MAP over 65 mmHg); (3) manage complications (K+, acidosis, fluid, nutrition); (4) renal replacement therapy.

AEIOU:^[1] Acidosis (refractory, pH under 7.1 to 7.15), Electrolytes (refractory hyperkalaemia), Ingestion (lithium, salicylate, methanol, ethylene glycol, metformin), Overload (refractory pulmonary oedema), Uraemia (pericarditis, encephalopathy).

Hyperkalaemia ladder: calcium gluconate 10 per cent 10 mL IV; insulin 10 units + 50 per cent dextrose 50 mL IV; salbutamol 10 to 20 mg nebulised; potassium binders; dialysis.^[2]

Q4: Discuss the evidence on the timing of dialysis and the long-term consequences of AKI. (2 min)

Timing (AKIKI 2016, STARRT-AKI 2020):^[3] neither trial showed a mortality benefit of early over delayed initiation of RRT in critically-ill Stage 3 AKI — a delayed strategy meant 49 per cent of that group never received renal replacement therapy. Start for AEIOU, persistent AKI, or worsening course; early prophylactic RRT is not recommended.

Long-term: AKI is a risk factor for incident and progressive CKD, end-stage kidney disease, cardiovascular events and long-term mortality (James et al, Nature Reviews Nephrology, 2020); risk is proportional to severity and recurrence.^[1] — establish AKI and CKD as a continuum, and follow up survivors.

Q5: Briefly, what are the pitfalls in AKI management? (1 min)

Missing obstruction (always ultrasound); failing to stop nephrotoxins including over-the-counter NSAIDs;^[1] over-resuscitation causing pulmonary oedema; using FENa after diuretics; attributing CKD to AKI; missing rapidly progressive glomerulonephritis; missing rhabdomyolysis (dipstick blood, no red cells); treating the number rather than the patient with furosemide.

References3ShowHide

1. [1]Kellum JA, Lameire N Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care, 2013.PMID 23394211
2. [2]Long B, Warix JR, Koyfman A. Controversies in Management of Hyperkalemia. J Emerg Med, 2018.PMID 29731287
3. [3]Gaudry S, Hajage D, Schortgen F, et al. Initiation Strategies for Renal-Replacement Therapy in the Intensive Care Unit. N Engl J Med, 2016.PMID 27181456