M12AKI, electrolytes and kidney support

Clinical overview

Pregnancy lowers serum creatinine through increased glomerular filtration. A value that appears “normal” on a nonpregnant laboratory report can therefore represent important kidney injury, especially when rising from baseline. Acute kidney injury (AKI) in obstetrics commonly follows haemorrhage, sepsis, severe pre-eclampsia/HELLP, acute fatty liver, thrombotic microangiopathy, nephrotoxic exposure or obstruction. Early management is cause-directed: restore perfusion without causing congestion, stop nephrotoxins, control infection/bleeding/hypertension and detect obstruction.

Electrolyte emergencies are managed according to maternal danger. Pregnancy does not alter the need to stabilise a hyperkalaemic myocardium, treat symptomatic hyponatraemia or correct magnesium toxicity. It does create characteristic contexts: oxytocin-associated water intoxication, hyperemesis, DKA, magnesium sulphate treatment, massive transfusion and postpartum fluid shifts.

Core knowledge

Recognising AKI

The operative published KDIGO definition (2012) includes any of:

• serum creatinine rise of at least 26.5 µmol/L within 48 hours;
• rise to at least 1.5 times baseline within seven days; or
• urine output below 0.5 mL/kg/hour for six hours.

These thresholds were not designed specifically for pregnancy and can be late against a low gestational baseline. Use trend and clinical context. The KDIGO 2026 AKI/AKD guideline available in August 2026 is a public-review draft, not final normative guidance and should not be cited as operative.

Classify causes:

• Reduced perfusion: haemorrhage, sepsis, dehydration, cardiac failure or excessive diuresis.
• Intrinsic kidney injury: acute tubular injury, pre-eclampsia/HELLP, glomerular disease, interstitial nephritis, TTP/aHUS, acute fatty liver-related multi-organ failure, pigment or drug injury.
• Obstruction: stones, infected collecting-system obstruction, pelvic mass/surgical injury or catheter blockage.

Oliguria does not prove reduced preload. Congestion and raised venous pressure can reduce kidney filtration despite total-body fluid excess.

Investigation

Review baseline creatinine, pregnancy/postpartum timing, blood loss, infection, hypertension, urine/protein, medicines and contrast. Examine perfusion and congestion. Check urinalysis/microscopy, protein quantification where appropriate, FBC/platelets, haemolysis markers, electrolytes, bicarbonate/gas, liver/coagulation and kidney ultrasound when obstruction is possible.

A rapidly falling platelet count with haemolysis and neurological/renal injury requires urgent distinction among HELLP, TTP and aHUS. Coagulation tests and pregnancy timing help but overlap is substantial; haematology/nephrology input and disease-specific therapy cannot wait for prolonged diagnostic certainty.

AKI prevention and treatment

Treat cause and physiology. Stop nonessential nephrotoxins and adjust renally cleared drugs. Use balanced crystalloid in measured doses when perfusion is volume responsive; use blood for haemorrhage and vasoactive support for vasoplegia. Avoid both under-resuscitation and fluid overload. Do not use diuretics to “treat the creatinine”; use them to manage congestion when a response is expected.

Contrast studies are not withheld when they answer a life-threatening question. Optimise haemodynamics, avoid duplicate exposure and use appropriate dose/technique. A needed CTPA, coronary study or CT for source control often carries less risk than delayed diagnosis.

Kidney replacement therapy

Dialysis is initiated for clinical indications rather than a creatinine number: refractory hyperkalaemia, severe acid–base disturbance, pulmonary oedema/fluid overload causing organ compromise, uraemic complications, selected toxins or inability to manage solute/fluid needs. Modality depends on haemodynamic stability, urgency, cerebral status, resources and local expertise.