Endocrine Abstracts

Pre-eclampsia is a life-threatening disease occurring in 4.6% of pregnancies characterised by multi-organ dysfunction. Placental dysfunction is implicated with release of factors causing systemic inflammation and endothelial dysfunction. Mild hyponatraemia (130–135 mmol/l) is regarded as physiological in normal pregnancy. Severe hyponatraemia (<125 mmol/l) is a rare life-threatening complication of pre-eclampsia. Severe hyponatraemia and hyperkalaemia has been reported on one occasion; we report a second case with endocrine data.

Case history: A 27 year old 34-weeks pre-eclamptic twin-pregnancy patient was referred to endocrinology with severe hyponatraemia, hyperkalaemia and metabolic acidosis: sodium 120 mmol/l, potassium 6.2 mmol/l, bicarbonate 16 mmol/l, creatinine 93 mmol/l, eGFR 63 ml/min. Five days earlier: sodium 131 mmol/L, potassium 4.5 mmol/l, creatinine 77 mmol/l, eGFR 78 ml/min. Two weeks earlier: sodium 135 mmol/l, potassium 5.1 mmol/l, creatinine 66 mmol/l, eGFR >90 ml/min. Insulin/dextrose was ineffective causing hypoglycaemia with little effect on potassium. Coincidental with deterioration in sodium and potassium levels a rise in creatinine, CRP and liver enzymes and decrease in eGFR, pH and albumin had occurred. Examination: ill, oedematous, blood pressure 140/90 mmHg on treatment with labetalol 200mg BD. Investigations at 0730 h: cortisol 483 nmol/l, ACTH 118 ng/l, PRA 1.7 nmol/l per hour, (aldosterone 2010 pmol/l, aldosterone/renin ratio 1182, results not immediately available). The abnormal electrolytes, pH and inappropriately normal cortisol level given clinical status, third trimester and elevated ACTH suggested hypoadrenalism. Hydrocortisone 100 mg IV followed by 200 mg/24 h continuous infusion did not prevent further biochemical deterioration: sodium 120 mmol/l, potassium 6.2–8.7 mmol/l, pH 7.23, creatinine 109 mmol/l and eGFR 52 ml/min. Urgent delivery was advised with a 2 healthy males outcome but a post-operative haemorrhage resulted in a hysterectomy. All laboratory data normalised post-delivery.

Conclusion: 1) This case confirms severe hyponatraemia (+/− hyperkalaemia) as a risk factor in pre-eclampsia. Existing guidelines do not address this issue. 2) There is evidence of impaired cortisol synthesis/secretion with low cortisol and high ACTH level. The adrenal ACTH receptor is a 7-membrane-spanning G protein-coupled receptor which could be affected by endothelial dysfunction. 3) Angiotensin II is also a transmembrane G protein-coupled receptor which could also be affected by endothelial dysfunction. Hyperkalaemia is a highly potent aldosterone secretagogue acting by depolarisation of the cells of the zona glomerulosa. 4) Aldosterone upregulates and enhances gene transcription of the transmembrane sodium/potassium ATPase pump which again could be affected by endothelial dysfunction explaining the lack of aldosterone effect on sodium and potassium levels.