Hypoaldosteronism laboratory findings

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Akshun Kalia M.B.B.S.[2]

Overview

Laboratory findings consistent with the diagnosis of hypoaldosteronism include hyperkalemia and mild non-anion gap metabolic acidosis. Other lab findings include hyponatremia, decreased aldosterone level, and variable amounts of plasma renin activity (depends upon the underlying condition).

Laboratory Findings

Laboratory findings consistent with the diagnosis of hypoaldosteronism include:^[1]^[2]
- Hyperkalemia
- Mild non-anion gap metabolic acidosis

Laboratory investigations to be performed in hypoaldosteronism includes:^[3]
- Serum potassium: Hypoaldosteronism patients have hyperkalemia and should be categorised into mild hyperkalemia (5.5–6.5 mmol/l), moderate hyperkalemia (6.5–7.5 mmol/l) and severe hyperkalemia (>7.5 mmol/l).
- Serum sodium: In general, hyponatremia is unusual in hypoaldosteronism but if the cause of hypoaldosteronism is adrenal insufficiency, hyponatremia may be present. Hyponatremia must be categorized into mild hyponatremia (130-134 mmol/L), moderate hyponatremia (125-129 mmol/L) and severe hyponatremia(<125 mmol/L).
- Patients suspects of hypoaldosteronism should be checked for plasma renin activity (PRA), serum aldosterone, and serum cortisol.
- The following table distinguishes among various subtypes of hypoaldosteronism:^[4]^[5]^[6]^[7]

Disorder	Plasma Renin Activity	Plasma Aldosterone	Plasma Cortisol
Hyporeninemic hypoaldosteronism	Low	Low	Normal
Hypereninemic hypoaldosteronism	Increased	Low	Normal/↓
Primary adrenal insufficiency	High	Low	Low
Pseudohypoaldosteronism type I	High	High	Normal
Pseudohypoaldosteronism type II	Normal/↓	Normal/↓	Normal

References

↑ Shiah CJ, Wu KD, Tsai DM, Liao ST, Siauw CP, Lee LS (1995). “Diagnostic value of plasma aldosterone/potassium ratio in hypoaldosteronism”. J. Formos. Med. Assoc. 94 (5): 248–54. PMID 7613258.
↑ Lehnhardt, Anja; Kemper, Markus J. (2010). “Pathogenesis, diagnosis and management of hyperkalemia”. Pediatric Nephrology. 26 (3): 377–384. doi:10.1007/s00467-010-1699-3. ISSN 0931-041X.
↑ Palmer BF (2010). “A physiologic-based approach to the evaluation of a patient with hyperkalemia”. Am. J. Kidney Dis. 56 (2): 387–93. doi:10.1053/j.ajkd.2010.01.020. PMID 20493606.
↑ Oster JR, Singer I, Fishman LM (1995). “Heparin-induced aldosterone suppression and hyperkalemia”. Am. J. Med. 98 (6): 575–86. PMID 7778574.
↑ Mayes D, Furuyama S, Kem DC, Nugent CA (1970). “A radioimmunoassay for plasma aldosterone”. J. Clin. Endocrinol. Metab. 30 (5): 682–5. doi:10.1210/jcem-30-5-682. PMID 5444558.
↑ Choi MJ, Ziyadeh FN (2008). “The utility of the transtubular potassium gradient in the evaluation of hyperkalemia”. J. Am. Soc. Nephrol. 19 (3): 424–6. doi:10.1681/ASN.2007091017. PMID 18216310.
↑ Ruecker B, Lang-Muritano M, Spanaus K, Welzel M, l’Allemand D, Phan-Hug F, Katschnig C, Konrad D, Holterhus PM, Schoenle EJ (2015). “The Aldosterone/Renin Ratio as a Diagnostic Tool for the Diagnosis of Primary Hypoaldosteronism in Newborns and Infants”. Horm Res Paediatr. 84 (1): 43–8. doi:10.1159/000381852. PMID 25968592.

Overview