Acute kidney injury in pregnancy — structured SAQ (15 marks)

(a) KDIGO definition applied to pregnancy, and this patient's stage (3 marks)

Definition (1 mark), staging reasoning (1 mark), the pregnant baseline (1 mark). ^[1][5]

• KDIGO definition of AKI: rise in serum creatinine by 26.5 micromol/L (0.3 mg/dL) within 48 hours, or a rise to 1.5 times or more of baseline, or a urine output under 0.5 mL/kg/h for 6–12 hours.^[1]
• Stages: stage 1 = 1.5–1.9 times baseline or more than 26.5 micromol/L in 48 hours; stage 2 = 2.0–2.9 times; stage 3 = 3.0 times baseline, or rise to 354 micromol/L or more, or initiation of RRT.^[1]
• This patient: her baseline was 58 micromol/L; her current is 132 micromol/L — a rise of 74 micromol/L in 24 hours, more than 2.28 times baseline. She is AKI stage 2, bordering on stage 3. The pregnant baseline is critical: 58 micromol/L is normal pregnant-range (44–62 micromol/L), and 132 micromol/L is well above the pregnant abnormal threshold of 75 micromol/L (0.85 mg/dL).^[1][5]
• The urine output criterion is also met: 15 mL/h in a 70 kg woman is 0.21 mL/kg/h — under 0.5 for more than 6 hours is stage 2-3.^[1]

(b) Focused investigations and interpretation (3 marks)

One mark per group, with the pregnant interpretation. Source: ADQI 32 (Lumlertgul 2026), Jim 2017. ^[2][4]

• Cause-hunt bloods: FBC (platelets 88 — HELLP pattern; smear for schistocytes to exclude thrombotic microangiopathy), LFTs (ALT 142 — HELLP/AFLP differential), coagulation, glucose, lactate, urate, CRP. Send ADAMTS13 if TTP is on the differential, and a complement panel if aHUS is on the differential.^[2]
• Renal-interpretation bloods: creatinine trend (rising — AKI), potassium 5.9 (significant hyperkalaemia — treat per protocol), bicarbonate (likely low — metabolic acidosis), magnesium 2.4 (upper end of therapeutic; her AKI will accumulate magnesium further).^[4]
• Imaging: bedside renal ultrasound to exclude obstruction (the physiological hydronephrosis of pregnancy must not be over-called) and to assess renal size and cortical thickness; bedside echocardiography or IVC ultrasound for fluid status. Consider renal biopsy only if the diagnosis will change management (rapidly progressive glomerulonephritis, suspected lupus nephritis) — not here, where the cause is clear.^[2][4]

(c) Immediate management with magnesium dose adjustment (5 marks)

One mark per domain, with the magnesium specifics. ^[2][4]

• Treat the cause: this is severe preeclampsia with HELLP and AKI — the definitive treatment is delivery at this gestation (33 weeks). Plan delivery in consultation with neonatology; corticosteroids for fetal lung maturity already given if available. Antihypertensives to target: labetalol, nifedipine, intravenous hydralazine for acute severe hypertension.^[2]
• Magnesium sulphate for seizure prophylaxis — but dose-adjusted for the AKI. Magnesium is renally cleared and accumulates in AKI; toxicity presents as loss of deep tendon reflexes, respiratory depression and cardiac arrest. Reduce or omit the maintenance infusion, continue monitoring, check magnesium levels every 6–12 hours, monitor reflexes and respiratory rate hourly. A typical dose-adjustment: give the loading dose, then withhold or halve the maintenance infusion until the magnesium level and urine output are confirmed.^[2]
• Antidote: keep calcium gluconate 1 g IV (10 mL of 10% solution) drawn up at the bedside as the antidote for magnesium toxicity. Administer slow IV push over 10 minutes if toxicity is suspected (loss of reflexes, respiratory depression, cardiac arrhythmia).^[2]
• Fluid management: cautious — this woman has preeclampsia and is at high risk of pulmonary oedema. Small (250 mL) boluses of balanced crystalloid, frequent reassessment of fluid status (JVP, lung bases, oxygen saturation, IVC ultrasound), aim for euvolaemia. Avoid NSAIDs entirely — they block prostaglandin-mediated afferent arteriolar vasodilation and worsen the AKI.^[2][4]
• Hyperkalaemia management: potassium 5.9 mmol/L is significant; treat per protocol — calcium gluconate for cardiac membrane stabilisation if ECG changes, insulin-dextrose to shift potassium intracellularly, salbutamol, and consider bicarbonate if acidotic. Avoid NSAIDs and ACE inhibitors. If refractory or rising, escalate to RRT (see part d).^[4]

(d) RRT indications in pregnancy and the delivery decision (4 marks)

One mark per indication, one for the modality, one for the delivery decision. ^[1][3]

• AEIOU absolute indications for RRT: Acidosis refractory to medical therapy (pH under 7.1 with AKI); Electrolyte disturbance refractory to medical therapy (refractory hyperkalaemia above 6.5 mmol/L, or rising); Ingestion of a dialysable toxin; Overload of fluid refractory to diuretics (with pulmonary oedema); Uraemic complications (pericarditis, encephalopathy).^[1][4]
• Pregnancy-specific considerations: more frequent sessions, tighter fluid and urea control (high urea crosses the placenta), bicarbonate target normal for pregnancy, foetal monitoring during sessions above 23 weeks.^[3]
• Modality: continuous RRT (CRRT) preferred in the haemodynamically unstable woman; intermittent haemodialysis acceptable in the stable patient. Vascular access: internal jugular preferred; anticoagulation with heparin (or regional citrate in CRRT with careful calcium monitoring).^[3][4]
• Delivery decision: multidisciplinary — obstetrics, nephrology, anaesthetics, neonatology. In this case, the working diagnosis is severe preeclampsia with HELLP and AKI; delivery is both the definitive treatment for the preeclampsia and a key step in the renal recovery pathway. At 33 weeks, the fetus benefits from corticosteroids if not already given; the maternal condition drives the timing. RRT may need to continue after delivery as the kidney recovers.^[2][3]