The cardiovascular markers copeptin and high-sensitive C-reactive protein decrease following specific therapy for primary aldosteronism

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Abstract

Context:

Copeptin and high-sensitive C-reactive protein (hsCRP) are biomarkers associated with increased mortality in patients with cardiovascular and cerebrovascular disease as well as in the general population. No data exist regarding these markers in patients with primary aldosteronism.

Objective:

To evaluate copeptin and hsCRP levels as cardiovascular risk markers in primary aldosteronism patients.

Methods:

A total of 113 primary aldosteronism patients (64% male) from two centers of the prospective German Conn's Registry were identified, for whom a full data set and blood samples at baseline and follow-up (14 ± 3.4 months) after initiation of specific primary aldosteronism treatment were available. These cases were matched 1 : 3 (n = 339) for sex, renal function, BMI, age and SBP with participants from the Cooperative Health Research in the Region of Augsburg F4 survey. Copeptin and hsCRP were determined by sandwich fluoroimmunoassay.

Results:

HsCRP was significantly higher in primary aldosteronism patients at baseline compared with matched controls. Following specific therapy, hsCRP and copeptin decreased significantly in primary aldosteronism patients [median (25th and 75th percentile): 1.6 (0.8, 3.4) to 1.2 (0.6, 2.1) mg/l, P < 0.001; 7.8 (4.6, 13.5) to 5.0 (3.1, 8.9) pmol/l, P < 0.001, respectively]. Men had higher hsCRP and copeptin levels at baseline and follow-up compared with women. The combination of sex, hypokalemia, lateralization index and blood pressure were the best predictors of outcome. However, copeptin and hsCRP had no predictive value despite the association of lower copeptin levels with better outcome regarding cure of primary aldosteronism.

Conclusion:

Copeptin and hsCRP levels decrease following specific primary aldosteronism therapy reflecting successful cardiovascular risk reduction. However, they are no independent predictors regarding cure of primary aldosteronism.

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