ECE2016 Eposter Presentations Adrenal cortex (to include Cushing's) (85 abstracts)
Moderate/severe Hypovolemic Hyponatremia with urinary sodium loss secondary to Hypoaldosteronism: analysis of 28 cases
Rona Penso 1 , Ana Ortola 1 , Angela Amengual 1 , Irene Crespo 1 , Teresa Ruiz-Gracia 1 , Martin Cuesta-Hernandez 2 , Emilia Gomez-Hoyos 3 , Clara Marcuello 1 , Alfonso Calle 1 & Isabelle Runkle 1
1Hospital Clinico San Carlos, Madrid, Spain; 2Beaumont Hospital, Dublin, Ireland; 3Hospital Clinico Valladolid, Valladolid, Spain.
Introduction: Hypoaldosteronism (HA), a cause of hypovolemic hyponatremia (HN) with urinary(U) sodium(Na) loss, is often underdiagnosed. We studied 28 patients with an episode of HA-induced moderate/severe hyponatremia.
Methods: Retrospective 2012–2015. In all patients, Nadir(N) serum(S) Na <130 mmol/l (corrected for total proteins and glycemia), low internal yugular venous pressure, low ocular pressure. Addison’s Disease ruled (ACTH, cortisol and/or Synacthen test). UNa>25 mmol/l, U osmolality(Osm)> Plasma(P) Osm, Transtubular Potassium Gradient (TTKG)< 5. Group I (GrI) (10/28) had risk factors for aldosterone deficit (heparin, ARBs, ACEi, aliskiren, NSAIDs, and/or tacrolimus), Group II (GrII) (2/28) risk factors for mineralocorticoid resistance (obstructive uropathy, urinary infection, renal transplant, NSAIDs, trimetroprim, and/or spironolactone), Group III (GrIII) (16/28): both. Na, Potassium (K) values in mmol/l, Osm mOsm/kg. t-test, X2, Spearman’s Rho, Kruskal-Wallis, Mann–Whitney U. Results given as Mean (S.D.) unless stated otherwise.
Results: 12/28 females, age: 71.36 (15.55). 78.6% had either chronic renal disease (12/28), diabetes (13/28) or both (3/28). NSNa: 121.82 (5.19) with SK of 5.08 (0.63). Values at diagnosis (D): SNa: 126.07 (5.62), SK: 4.93 (0.62). UNa:73.03 (38.66), TTKG:3.6(0.85), POsm:277.78 (12.47), UOsm:392.53(167.75), In mg/dl: SUrea 50.78 (25.23) SCreatinine:1.12 (0.56), uricemia:5.26 (1.45). NSNa GrI:123.9 (3.18), GrII:121.2 (2.83), 83), GrIII:120.63(6.12). Corresponding SK GrI:4.85 (0.62), GrII:4.65 (0.49). GrIII:5.27 (0.62). GrII aldosteronemia-345.5 pg/ml (20.51)- was higher than in GrI:103 (60.3) or GrIII:117.85 (88.4). Median reninemia tended to be lower in GrI: 7 pg/ml (3.5–11.5) than GrII+III: 21 (5–67), P=0.08. Patients with both high renin(>25) and low aldosterone(<100), all in GrIII, had significantly lower NSNa:113.33(4.04) than the rest:123.19(4.2), P=0.033. Heparin(11/28), trimpetroprim (8/28), or both (6/28) were precipitating factors in 46.4% patients, and associated with significantly lower DSNa:123.7 (5.82) vs128.13 (4.69) P=0.038, and lower DPOsm:271.23 (11.45) vs 283.47 (10.63), P=0.007.
Conclusion: Hypoaldosteronism can induce marked hyponatremia. Most patients had risk factors for both inhibition of aldosterone secretion and mineralocorticoid resistance. Heparin and/or trimetroprim use was associated with lower SNa and SOsm levels.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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