ECE2021 Eposter Presentations Adrenal and Cardiovascular Endocrinology (21 abstracts)
Acquired hypoaldosteronism as classified by circulating aldosterone levels: characteristics
Jorge Gabriel Ruiz Sánchez 1 , 2 , 3 , Mario Pazos 1 , Xavier Pérez Candel 1 , Martín Cuesta Hernández 1 , Emilia Gomez Hoyos 4 , Maria Paz De Miguel Novoa 1 , Victoria Saez de Parayuelo 1 , Alfonso Calle 1 & Isabel Runkle 1
1Hospital Clinico Universitario San Carlos, Endocrinología y Nutrición, Madrid, Spain; 2Instituto de Investigación Sanitaria San Carlos (IdISSC), Madrid, Spain; 3Hospital Universitario Fundación Jiménez Díaz, Endocrinología, Madrid, Spain; 4Hospital Clínico Valladolid, Endocrinología y Nutrición, Valladolid, Spain
Acquired Hypoaldosteronism may be caused by low circulating aldosterone levels (AD), resistance to mineralocorticoid action (MR), or a combination of both (CB). We describe the clinical/biochemical characteristics of these three types of hypoaldosteronism.
Methods
Retrospective review of a series of 177 patients with acquired hypoaldosteronism assessed by the Endocrinology Department of a tertiary teaching hospital from 2012 to 2019. We analyzed serum and urine markers of cases in which serum aldosterone (PAC) and direct renin concentration (PRC) levels were available coinciding with hyperkalemia: serum Potassium (SK) ≥5 mmol/l. Cases were classified as follows: AD: PAC <90, MR: PAC >200, or CB: PAC 90–200. PAC, PRC by Radioimmunoassay, in pg/ml. Serum/urine electrolytes in mmol/l. Mean ± s.d.
Results
| AD (n=28)(54.9%) | MR (n=9)(17.6%) | CB (n=14)(27.5%) | P | |
| Hypovolemia | 14 (50) | 8 (88.9) | 8 (57.1) | 0.087 |
| Hyponatremia | 14 (50) | 8 (88.9) | 8 (57.1) | 0.087 |
| Hypovolemic hyponatremia | 10 (35.7) | 7 (77.8) | 8 (57.1) | 0.07 |
| HMA | 8/17 (47.1) | 4/7 (57.1) | 5/8 (62.5) | 0.747 |
| SK | 5.4 ± 0.5 | 5.4 ± 0.3 | 5.3 ± 0.3 | 0.580 |
| SNa | 134 ± 7 | 130 ± 5 | 135 ± 4 | 0.155 |
| Serum Creatinine, mg/dl | 1.2 ± 0.6 | 1.3 ± 0.4 | 1.1 ± 0.5 | 0.544 |
| HCO3, mmol/l | 23.1 ± 3.8 | 23.3 ± 3.3 | 22.3 ± 3.6 | 0.828 |
| UNa | 87 ± 3 | 38 ± 15 | 68 ± 30 | 0.003 |
| UK | 30 ± 13 | 28 ± 15 | 33 ± 14 | 0.615 |
| UNa/UK ratio | 3.24 ± 1.62 | 1.5 ± 0.62 | 2.27 ± 1.17 | 0.009 |
| SK/SU ratio | 0.21 ± 0.08 | 0.22 ± 0.09 | 0.19 ± 0.08 | 0.594 |
| TTKG | 3.6 ± 1.3 | 4.8 ± 1.5 | 4.5 ± 1.2 | 0.099 |
| PAC | 43 [IQR:32–67] | 317 [IQR:256–610] | 128 [IQR:97–155] | <0.001 |
| PRC | 2.7 [IQR:1.2–10.4] | 14.4 [IQR:1.3–26.9] | 5.3 [IQR:2.8–12] | 0.279 |
51 cases analyzed, 27 (52.9%) male, age 73 ± 12 years. 30/51 were hypovolemic, 25 of whom (83.3%) presented hyponatremia. 30/51 were hyponatremic, 25/30 presenting hypovolemia. Hypovolemia was associated to hyponatremia (P<0.001). 17/32 in whom acid-base status was evaluated presented hyperchloremic metabolic acidosis (HMA). Results by group given in Table 1. No correlations were found between PAC and SK or trans-tubular-potassium gradient (TTKG) in any group, nor when all patients were grouped together (ALL). In ALL, there was a negative correlation between TTKG and urine sodium (UNa) (r= -0.333, P=0.041), TTKG and UNa/urine potassium (UK) ratio (r= -0.725, P<0.001), PAC and UNa (r= -386, P=0.007), PAC and Serum sodium (SNa) (r= -346, P=0.013), and PAC and UNa/UK ratio (r= -0.355, P=0.014).
Conclusions
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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