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Isolated Hypoaldosteronism: an Overlooked Cause of Hyponatraemia ⁎ I

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Isolated Hypoaldosteronism: an Overlooked Cause of Hyponatraemia ⁎ I European Journal of Internal Medicine 18 (2007) 246–248 www.elsevier.com/locate/ejim Brief report Isolated hypoaldosteronism: An overlooked cause of hyponatraemia ⁎ I. Talapatra , S. Kalavalapalli, D.J. Tymms Royal Albert Edward Infirmary, Wigan Lane, Wigan, WN1 2NN United Kingdom Received 14 April 2006; received in revised form 20 August 2006; accepted 19 September 2006 Abstract We report three patients with hyponatraemia due to isolated hypoaldosteronism. Addison's disease was ruled out in each of these patients by a normal short synacthen test. Two patients had severe hyponatraemia and fluid restriction helped improve the sodium level only marginally. One was treated with demeclocycline, which did not prove to be effective. Subsequently, all three patients were found to have aldosterone deficiency and treatment with fludrocortisone caused their sodium levels to return to normal. © 2007 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. Keywords: Hyponatraemia; Hypoaldosteronism; Renin; Fludrocortisone 1. Introduction plasma sodium had ranged from 124 to 130 mmol/l (normal 135–145 mmol/l) for the past 2 years. The patient had Isolated hypoaldosteronism is often overlooked as a cause postural hypotension causing his dizziness. Investigations of hyponatraemia. A patient with hyponatraemia is assessed undertaken showed the following results: plasma osmolality for plasma volume depletion or overloading, Addison's 280 mosmol/kg H2O (normal 280–298 mosmol/kg H2O), disease, SIADH (syndrome of inappropriate ADH secretion) urine osmolality 370 mosmol/kg H2O, urine sodium and urinary or gastric loss of sodium and is then treated 30 mmol/l, random cortisol 546 nmol/l, plasma sodium accordingly. There have not been many case reports of 128 mmol/l, potassium 5.2 mmol/l (normal 3.5–5.3 mmol/l), isolated hypoaldosteronism as a cause of hyponatraemia urea 7 mmol/l (normal 2.5–7 mmol/l) and creatinine with a normal potassium level. Treatment with fludrocorti- 100 μmol/l (normal 95–140 μmol/l). Chest X-ray was sone was found to be highly effective in all of our patients, unremarkable. with restoration of plasma sodium level to normal. Hence, An aldosterone short synacthen test was performed that estimation of plasma aldosterone constitutes an important showed normal results for baseline cortisol (416 nmol/l) and investigation for hyponatraemia. its response (761 nmol/l) to ACTH injection. However, the aldosterone (80 pmol/l) and renin levels (b0.2) were low, 2. Case reports suggesting an isolated form of secondary hypoaldosteronism (hyporeninaemic hypoaldosteronism), which was treated Our first patient was an 82-year-old gentleman referred with fludrocortisone 50 μg daily. Plasma sodium improved for persistent hyponatraemia and dizziness. The patient's to 138 mmol/l with potassium of 3.8 mmol/l with correction of postural hypotension. Our second patient was a 64-year-old lady, a known hypertensive and type 2 diabetic, who presented with col- ⁎ Corresponding author. Diabetes centre, Royal Albert Edward Infirmary, Wigan Lane, Wigan WN1 2NN United Kingdom. Tel.: +44 1942264713; lapse with a capillary blood glucose of 3 mmol/l and se- fax: +44 1942822191. vere hyponatraemia. Investigations undertaken showed the E-mail address: [email protected] (I. Talapatra). following results: plasma sodium 116 mmol/l, potassium 0953-6205/$ - see front matter © 2007 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.ejim.2006.09.026 I. Talapatra et al. / European Journal of Internal Medicine 18 (2007) 246–248 247 Table 1 Various findings in the three patients with hyponatraemia Patient 1 Patient 2 Patient 2 Patient 3 (test repeated) Cortisol: baseline 416 nmol/l (normal: 220–720); Cortisol: baseline 635 nmol/l and Cortisol: baseline 385 nmol/l and 761 nmol 30 min after ACTH(synacthen) 981 nmol/l after synacthen injection 780 nmol/l after synacthen injection injection (normal: N580 nmol/l) Aldosterone: baseline: 80 pmol/l and 190 pmol/l Aldosterone: baseline: 100 pmol/l and Aldosterone: Aldosterone: baseline: 60 pmol/l after synacthen injection (normal: 250 pmol/l after synacthen injection baseline: 85 pmol/l baseline 110–450 pmol/l and a rise of N150 pmol/l after synacthen injection) Renin: baselineb0.2 pmol/ml/h (normal: 1.1–2.7) Renin: baseline 2.9 pmol/ml/h (raised) Urea: 7 mmol/l on presentation Urea: 4 mmol/l on presentation Urea: 3.8 mmol/l on presentation and and 6.5 nmol/l after correction and 5.1 nmol/l after correction 4.2 mmol/l after correction of of hyponatraemia of hyponatraemia hyponatraemia Creatinine: 100 μmol/l on presentation and Creatinine: 95 μmol on presentation Creatinine: 89 μmol/l on presentation 103 μmol/l after correction and 102 μmol/l after correction and 80 μmol/l after correction of of hyponatraemia (normal values) of hyponatraemia (normal values) hyponatraemia.(normal values) Sodium: 128 mmol/l on presentation and Sodium: 116 mmol/l on presentation Sodium: 117 mmol/l on presentation 138 mmol/l after correction of hyponatraemia and 135 mmol/l after correction and 136 mmol/l after correction of hyponatraemia of hyponatraemia Potassium: 5.2 mmol/l Potassium: 5.0 mmol/l on presentation Potassium: 5.1 mmol/l on presentation on presentation and 3.8 mmol/l after and 4.4 mmol/l after correction and 4.2 mmol/l after correction correction of hyponatraemia of hyponatraemia of hyponatraemia Albumin: 36 mmol/l on presentation and Albumin: 35 mmol/l on presentation and Albumin: 36 mmol/l on presentation 37 mmol/l (normal) after correction of 36 mmol/l after presentation and 37 mmol/l after correction hyponatraemia of hyponatraemia of hyponatraemia Haemoglobin: 14.2 g/dl Haemoglobin: 11.7 g/dl on presentation and Haemoglobin: 10.7 g/dl on on presentation and 13.7 g/dl after 12.3 g/dl after correction of hyponatraemia presentation and 11 g/dl on correction of hyponatraemia correction of hyponatraemia BP: on presentation: 150/90 (lying) and BP: on presentation: BP 130/80 (lying) and BP: on presentation 140/70 (lying) 120/70 (standing); BP 155/90 on correction 110/70 (standing); BP 135/90 on correction and 130/70 (standing); BP 150/80 of hyponatraemia with no postural drop of hyponatraemia with no postural drop on correction of hyponatraemia with no postural drop Pulse rate: on presentation 80/min (lying) Pulse rate: 100/min on presentation Pulse rate: 96/min (lying) and and 90/min (standing); pulse 76/min (lying down) and 112/min (standing); 102/min (on standing); pulse rate on correction of hyponatraemia with not pulse rate 72/min (lying) after correction 64/min on correction of hyponatraemia much change with posture of hyponatraemia with not much change with not much change with posture with posture. Body weight: 62.6 kg initially; 64.4 kg after Body weight: 63.4 kg initially; 65 kg after Body weight 53.4 kg initially; 56 kg correction of hyponatraemia correction of hyponatraemia on recovery from hyponatraemia 5 mmol/l, urea 4 mmol/l, normal creatinine, plasma os- shadow. A short synacthen test was normal for cortisol, with the molality 249, urine osmolality 658 and urine sodium levels being 385 and 780 nmol/l, respectively, before and 128 mmol/l. Chest X-ray was unremarkable. BP was 130/ after synacthen injection. Fluid restriction and treatment 80 (on lying) and 110/70 mmHg (on standing). Fluid intake with demeclocycline caused the sodium to improve to restriction to 1 l/day caused the sodium to improve to 124 mmol/l. Early morning aldosterone was 60 pmol/l (↓) 122 mmol/l. A short synacthen test was normal for cortisol. and the patient was treated with fludrocortisone 100 μg/day Plasma cortisol levels were 635 and 981 nmol/l, respective- with an improvement of plasma sodium to 136 mmol/l. ly, before and after the synacthen injection. However, early morning plasma aldosterone was 85 pmol/l (low) and PRA 3. Discussion 2.9 pmol/ml/h (high). The patient was diagnosed with aldo- sterone deficiency and treated with fludrocortisone 100 μg/ Aldosterone causes reabsorption of sodium and chloride day. Plasma sodium improved to 135 mmol/l. and excretion of potassium and hydrogen ion in the distal The third patient, a 73-year-old lady who was on convulated tubule. In aldosterone deficiency, renal sodium loss amiodarone for hypertrophic cardiomyopathy, presented with occurs, resulting in hyponatraemia. With volume depletion, a blackout. BP was 140/70 (on lying) and 130/70 mmHg (on ADH (anti-diuretic hormone) release is expected by a reflex standing). Investigations undertaken showed: plasma sodium mechanism via the carotid sinus baroreceptors. This was 117 mmol/l, potassium 5.1 mmol/l, urea 3.8 mmol/l, plasma possibly responsible for a SIADH-like biochemical picture in osmolality 256, urine osmolality 455 and urine sodium our second and third patients. However, aldosterone deficien- 170 mmol/24 h. Chest X-ray showed an enlarged cardiac cy, as the cause for it, needed to be treated with fludrocortisone 248 I. Talapatra et al. / European Journal of Internal Medicine 18 (2007) 246–248 for the plasma sodium level to normalise. These patients did an early morning aldosterone level be measured in all not respond well to water restriction. patients with hyponatraemia. Isolated hypoaldosteronism Idiopathic SIADH with low aldosterone and postural may be present despite the patient's having a normal cortisol hypotension can occur in elderly subjects. Chronic mild level, contributing to the patient's hyponatraemia, and it may hyponatraemia can occur with idiopathic SIADH in be easily overlooked. Treatment with fludrocortisone in individuals above 80 years of age; it is usually asymptomatic small doses is very effective [6]. and does not require fludrocortisone therapy [1].
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