Impact of Parathormone (PTH) Levels on the Presence of Cardiovascular Disease in Patients with Primary Aldosteronism and Essential Hypertension
by
, ,
Álvaro Fernández-Sánchez
1,*, 
Diego Meneses
1,
Emma Raquel Alegre Bellasai
2,
Jersy Cárdenas-Salas
1,
Amalia Paniagua
1,
Clotilde Vázquez
1 and
Jorge Gabriel Ruiz-Sánchez
1 1
Endocrinology and Nutrition Service, Hospital Universitario Fundación Jiménez Díaz, 28040 Madrid, Spain
2
Nephrology Service, Hospital Universitario Fundación Jiménez Díaz, 28040 Madrid, Spain
*
Author to whom correspondence should be addressed.
Endocrines 2025, 6(1), 8; https://doi.org/10.3390/endocrines6010008
Submission received: 28 December 2024
/
Revised: 3 February 2025
/
Accepted: 7 February 2025
/
Published: 13 February 2025
(This article belongs to the Section Adrenal Disorders and Electrolyte Balance)
Abstract
:Background/Objectives: Primary aldosteronism (PA) is associated with a higher cardiovascular disease (CVD) risk than essential hypertension (EH) and is mainly driven by the excess of aldosterone production. Studies suggest a relationship between aldosterone and parathormone (PTH) homeostasis. Excessive PTH levels seem to also be associated with CVD. The impact of PTH levels on CVD in PA patients has not been totally elucidated. We evaluated the associations of PTH levels and hyperparathyroidism with CVD in patients with PA and EH. Methods: A cross-sectional study of a group of 67 patients was carried out, with 35 patients with PA and a control group of 32 patients with EH. We looked at the presence of CVD and data on the factors associated with its presence were collected and analyzed. A binary logistic regression was performed to assess multivariate relationships. Results: PA patients had higher PTH levels compared to the EH group (64 ± 42 vs. 39 ± 13 pg/mL, p = 0.004). Significative differences in PTH levels were observed according to the grade of hypertension in PA patients. Both hyperparathyroidism and CVD were found at higher rates in patients with PA. Patients with CVD exhibited significantly higher PAC values than patients without it (41.4 ± 18 vs. 21.4 ± 12 ng/dL, p < 0.001). Patients with hyperparathyroidism had higher rates of CVD than patients without it (58 vs. 24%, p = 0.018). Patients with PA and hyperparathyroidism manifested a higher rate of CVD than patients without this combination. A logistic regression showed an independent association of PAC and hyperparathyroidism with the presence of CVD in the total cohort. Conclusions: Hyperparathyroidism is associated with a higher probability of CVD both in PA and EH. The presence of hyperparathyroidism in PA seems to exacerbate the risk of CVD, with higher PTH levels associated with higher grades of hypertension in this cohort.
1. Introduction
Primary aldosteronism (PA) is a leading cause of secondary hypertension, representing approximately 10% of all cases of arterial hypertension [1], with values close to 40% in specialized units when Endocrine Society guideline (ESG-2016) recommendations are fulfilled [2,3].Cumulative evidence indicates that PA is related to a more severe target organ damage (TOD) and cardiovascular disease (CVD) compared to essential hypertension (EH) [4]. Thus, PA is associated with more elevated cardiovascular risk and mortality than EH, even when blood pressure (BP) is similarly controlled [5].
Several studies have shown a complex interplay between the renin–angiotensin–aldosterone (RAAS) system and parathormone (PTH) homeostasis [6]. PTH-type 1 receptors have been identified in adrenal tissue [7], and in vitro studies have demonstrated a secretagogue effect of PTH on the adrenal gland, promoting cell proliferation and aldosterone secretion [8]. Similarly, mineralocorticoid receptors have been detected in parathyroid tissue, with the activation of these receptors stimulating PTH production [7,9]. Notably, adenomatous parathyroid tissue exhibits mineralocorticoid receptor concentrations two- to four-fold higher than those of normal parathyroid glands. Since both excessive aldosterone and PTH levels can induce TOD and CVD [10], these relationships become clinically relevant beyond their pathophysiological basis.
PA is associated with high circulating PTH levels [11,12,13]. However, it remains unclear whether the interrelated mechanisms between PTH and the RAAS similarly influence TOD or CVD in patients with PA and EH. This study aimed to assess the impact of PTH levels on the presence of TOD and CVD in patients with PA and EH.
2. Materials and Methods
This is a cross-sectional study of hypertensive adult patients with and without PA referred to the Nephrology Department and the Endocrine Hypertension Unit of the Fundación Jiménez Díaz University Hospital over a two-year period (January 2020 to October 2022).The study was conducted according to the accepted standards of good clinical practice of the Declaration of Helsinki and approved by the Ethics Committee of the hospital.
Diagnosis of PA was based on our previously published protocol [2].Briefly, all patients with a positive screening for PA were evaluated with a Captopril-25 mg challenge test and/or oral salt loading test, according to ESG-2016. PA was diagnosed when at least one of the criteria from any of these tests was positive. In the groups of patients without PA, only those with EH were selected. EH was determined after an exhaustive evaluation was performed in all patients, excluding catecholaminergic and mineralocorticoid excess (PA or other), as well as alterations in renal Doppler and echocardiogram imaging. The inclusion criterion for the study was a baseline measurement of PTH and albumin-corrected calcium. Exclusion criteria for the study were a prior diagnosis of primary hyperparathyroidism, secondary hyperparathyroidism due to moderate/severe vitamin D deficiency (<20ng/mL), chronic kidney disease (CKD) stage G3-A or higher, the prior use of supplements affecting phospho-calcium metabolism (including calcimimetics and vitamin D compounds), and pregnancy (Figure 1).
2.1. Data Collection
The following variables were collected from clinical records: age, sex, weight, BP, duration of hypertension, grade of hypertension, number and types of current antihypertensive medications, the presence of obesity, dysglycosis (either prediabetes or type 2 diabetes), CKD (if estimated glomerular filtration rate [eGFR] < 60 mL/min/1.73 m2, as estimated by the CKD-EPI equation), obstructive sleep apnea (OSA), the presence of TOD, and a previous history of CVD (ischemic cardiopathy [acute or chronic], ictus, atrial fibrillation, heart failure, or vascular arteriopathy if documented). TOD was defined as a composite variable encompassing any of the following: a history of left ventricular hypertrophy, CVD, urine albumin-to-creatinine ratio (UACR) > 30 mg/g, or CKD. Biochemical data on the screening day were registered, which included levels of plasma aldosterone concentration (PAC), plasma renin activity (PRA, measured in ng/mL/h), the aldosterone-to-renin ratio (ARR), serum sodium, potassium, glucose, creatinine, eGFR, albumin-corrected calcium, phosphate, vitamin D (25-OH vitamin D), PTH, and UACR.
Hyperparathyroidism was defined as PTH above 65 pg/mL, and it was hypercalcemic if albumin-corrected calcium was ≥10.5 mg/dL.
2.2. Statistical Analysis
Categorical variables were represented as frequencies and percentages; meanwhile, quantitative variables were summarized using means and standard deviations (SDs). Comparative tests were ruled out. For categorical data, chi-square tests were used. For quantitative data, the Mann–Whitney U test, Kruskal–Wallis test, Student’s t-test, or ANOVA were applied, depending on the context. Post hoc multiple comparisons were made with the Bonferroni test.
An analysis with a binary logistic regression was performed to assess relationships between variables with a previous association in univariate analysis. Correlation analyses were performed with Spearman’s or Pearson’s method according to distribution.
Statistical significance was set at a p-value less than 0.05 in a two-tailed analysis. SPSS version 25 (IBM Corp., New York, NY, USA) was used for statistical analyses.
3. Results
A total of 35 patients with PA and 32 patients with EH (control group) were finally included in the study. The mean age was 56 ±13 years and 65% were female. A total of 19% of cases had hyperparathyroidism in the entire cohort, with one case being a patient diagnosed with hypercalcemic hyperparathyroidism. The remaining cases were normocalcemic hyperparathyroidism. Table 1 shows the comparative characteristics between PA and EH patients.
3.1. Interplays Between PA and PTH Levels
In the PA group, 28% of patients had vitamin D levels > 30 ng/mL, and 72% had levels between 20 and 30 ng/mL, while in the EH group, 25% of patients had levels > 30 ng/mL, and the remaining patients had levels between 20 and 30 ng/mL, with no statistical differences in the rates between groups. Despite comparable levels of vitamin D between PA and EH, the former had significantly higher PTH values and lower corrected calcium levels (Table 1). Furthermore, PA patients had a higher rate of hyperparathyroidism than EH (29% vs. 9.4%, p = 0.047).
In the group of patients with PA, but not in those with EH, a significant correlation was found between the values of PTH and PRA (r2 = 0.6, p = 0.001). However, no correlations were found between PAC with PTH and calcium (Figure 2).
PTH levels were directly associated with the grade of hypertension in patients with PA, but not in those with EH. Thus, a statistically significant difference in PTH levels was observed according to the grade of hypertension in the former group (p = 0.014) which remained when grade III hypertension was individually compared with the other hypertension grades (Figure 3). Nevertheless, there were no statistically significant differences in PTH levels among patients taking more than three antihypertensive medications at screening, neither in the entire cohort nor in the PA group or the EH group.
The analysis of PTH levels performed in each hypertension grade group in PA showed no significant differences based on the type of antihypertensive medication used, including an individual analysis for thiazide diuretics (ANOVA analysis p = 0.33).
3.2. Impact of PA and Hyperparathyroidism on Prevalence of TOD and CVD
At screening, TOD and CVD were found in 42% and 31% of the entire cohort, respectively. Both patients with TOD and CVD exhibited significantly higher PAC values than patients without them (TOD: 33.1 ± 13 vs. 23.7 ± 18 ng/dL, p = 0.05; CVD: 41.4 ± 18 vs. 21.4 ± 12 ng/dL, p < 0.001). Likewise, a significantly higher prevalence of TOD was observed in PA as compared to EH. However, no significant differences were found in CVD rates (Table 1).
In the entire cohort, patients with TOD and CVD did not show significant differences in PTH levels compared to patients without them (TOD: 52 ± 32 vs. 50 ± 33 pg/mL, p = 0.851; CVD: 64 ± 41 vs. 46 ± 27 pg/mL, p = 0.108). The differences in PTH levels according to the presence of TOD and CVD, grouped by PA and EH, are described in Table 2. Univariate regression analysis showed no association of PTH levels with CVD in the entire cohort nor when grouped by PA and EH. Patients with hyperparathyroidism had no significant differences in rates of TOD as compared to patients without it (33 vs. 41%, p = 0.749), but they had a higher percentage of CVD than patients without hyperparathyroidism (58 vs. 24%, p = 0.018).
In patients with PA, the presence of hyperparathyroidism was not associated with different percentages of TOD (44 vs. 55%, p = 704), but it was associated with higher rates of CVD (68 vs. 27%, p = 0.056), as compared to its absence. Similarly, when the nine patients presenting both PA and hyperparathyroidism were compared to all patients of the entire cohort without this combination, the rates of TOD were 44 vs. 39%, p = 0.99, and those of CVD were 68 vs. 24%, p = 0.017.
In the entire cohort, a multivariate logistic regression analysis, including sex, age, grade of hypertension, PAC, serum sodium, potassium, corrected calcium, and the presence of hyperparathyroidism, showed an independent association of PAC levels (OR: 1.11, 95%CI: 1.03 to 1.2, p = 0.01) with TOD. In a similar model, excluding the grade of hypertension, both hyperparathyroidism (OR: 12.9, 95%CI: 1.6 to 106.9, p = 0.017) and PAC levels (OR: 1.1, 95%CI: 1.02 to 1.19, p = 0.011) were independently associated with CVD. In patients with PA, in a model adjusted by sex, age, hyperparathyroidism, and PAC levels, only PAC was found to be associated with CVD (OR: 1.11, 95%CI: 1.014 to 1.23, p = 0.025). The same model did not reveal the significance of any variable for TOD.
4. Discussion
The present study identified PAC levels and hyperparathyroidism as independent factors associated with the presence of CVD both in patients with PA and EH. Furthermore, the combination of hyperparathyroidism and PA was associated with a higher rate of CVD than that observed in patients without this combination. Thus, this highlights the impact of hyperparathyroidism on the presence of CVD, even in populations with elevated cardiovascular risk, such as patients with PA.
We observed that patients with PA had higher PTH levels than patients with EH, confirming what has been reported for over three decades. Furthermore, it was observed to coincide with lower and similar levels of albumin-corrected calcium and vitamin D, respectively, similar to those reported in a recent meta-analysis by Wang et al. [14]. One could think that these data are in accordance with the bidirectional relationship between RAAS and PTH: aldosterone can directly induce PTH production, and vice versa. However, we did not find correlations between PTH and PAC. Thus, other mechanisms could be involved in these findings. The fact that calcium levels were lower despite similar circulating vitamin D suggests that PA could induce a reduction inblood calcium, which in turn triggers a compensatory increase in PTH secretion [15]. In fact, aldosterone increases renal calcium excretion and suppresses intestinal calcium absorption. The resulting decrease in calcium levels would stimulate PTH secretion and may contribute to PA-induced secondary hyperparathyroidism [15,16].
While increased PAC levels are a well-documented contributor to CVD [17], the role of high PTH levels is not yet fully understood. The known effect of high PTH levels on CVD in the general population comes from cases of primary (hypercalcemic) hyperparathyroidism. In these cases, after surgical treatment, a reduction in CVD comorbidities has been observed [18]. Nevertheless, the impact of normocalcemic hyperparathyroidism, especially in patients with PA, is not totally elucidated, although it has been suggested that it could be similar to that of hypercalcemic hyperparathyroidism [19]. Physiologically, PTH induces vasodilation. However, high PTH values have been associated with increased blood pressure. The mechanisms behind this paradoxical action are unclear, being attributed to hypercalcemia and/or RAAS effects [16]. In any case, it is evident that the high prevalence of CVD is not limited to hypercalcemic hyperparathyroidism but is also observed in normocalcemic hyperparathyroidism, as demonstrated in our study, revealing other potential mechanisms beyond hypercalcemia. In this regard, the continuous increase in PTH levels, in the absence of hypercalcemia, across the grades of hypertension observed in cases with PA of our cohort might reflect the interplay of PTH influencing vascular tone and remodeling, potentially exacerbating hypertension already caused by PA [20], which could also explain the association of hyperparathyroidism with CVD. Thus, it looks like the presence of hyperparathyroidism would be associated with a more severe phenotype of PA, as suggested by Asbach et al. [18]. Nevertheless, given the absence of differences in PTH levels between patients with and without CVD, as well as those receiving fewer or more than three antihypertensive drugs, it appears that the overall state of hyperparathyroidism, rather than an elevation of PTH levels beyond a specific threshold, is what may be associated with a higher cardiovascular risk. In fact, our multivariate analysis suggests a synergistic risk profile for CVD in patients with high PAC values and hyperparathyroidism, but not with PTH levels. Further investigations are needed to fully elucidate the mechanisms of these combined factors and the role of hyperparathyroidism on PA as a potential therapeutic target.
Limitations of the Study
Our results should be interpreted based on some limitations. First, PTH and PAC levels were registered from the screening, where some RAAS-interfering drugs could be used, which could alter the values of variables. Second, we were unable to establish differences in PTH levels after treatment compared to initial levels. Third, no data regarding creatinine-adjusted or filtered calciuria were registered. On the other hand, a significant strength of the study is the exhaustive evaluation conducted to exclude potential secondary causes of both hyperparathyroidism and hypertension, thereby minimizing selection bias.
5. Conclusions
The results indicate that both the excess of PAC and the presence of hyperparathyroidism are associated with the risk of CVD, both in patients with PA and EH. The presence of hyperparathyroidism in PA seems to exacerbate the risk of CVD, with higher PTH levels associated with higher grades of hypertension in this cohort. The precise role of PTH hypersecretion in contributing to cardiovascular risk, especially when not associated with hypercalcemia, remains unclear and warrants further investigation. Addressing both aldosterone and PTH elevations could offer novel therapeutic chances for patients with PA and other conditions associated with hyperparathyroidism and RAAS activation.
Author Contributions
Conceptualization: J.G.R.-S. and Á.F.-S.; methodology: Á.F.-S. and J.G.R.-S.; validation: J.G.R.-S., D.M., E.R.A.B., J.C.-S., A.P. and C.V.; formal analysis: J.G.R.-S. and Á.F.-S.; investigation: J.G.R.-S., D.M. and J.C.-S.; writing—original draft preparation: Á.F.-S. and J.G.R.-S.; writing—review and editing: J.G.R.-S., Á.F.-S. and E.R.A.B.; supervision and reviewing: J.G.R.-S. All authors have read and agreed to the published version of the manuscript.
Funding
This research received no external funding.
Institutional Review Board Statement
Not applicable.
Informed Consent Statement
Patient consent was waived due to the retrospective nature of the study.
Data Availability Statement
Data are contained within the article.
Conflicts of Interest
The authors declare no conflicts of interest.
Abbreviations
The following abbreviations are used in this manuscript:
| ARR | aldosterone-to-renin ratio |
| BP | blood pressure |
| CKD | chronic kidney disease |
| CVD | cardiovascular disease |
| EH | essential hypertension |
| PA | primary aldosteronism |
| PAC | plasma aldosteroneconcentration |
| PRA | plasma reninactivity |
| PTH | parathormone |
| RAAS | renin–angiotensin–aldosterone |
| TOD | target organ damage |
| UACR | albumin-to-creatinine ratio |
References
- Dogra, P.; Bancos, I.; Young, W.F. Primary Aldosteronism: A Pragmatic Approach to Diagnosis and Management. Mayo Clin. Proc. 2023, 98, 1207–1215. [Google Scholar] [CrossRef]
- Ruiz-Sanchez, J.G.; Sanchez, Á.F.; Cardenas-Salas, J.; Fernandez-Cagigao, Y.; Bellassai, E.R.A.; Rossello, M.G.; Fernandez-Fernandez, B.; Moreno, B.J.; Paniagua, A.; Vazquez, C.; et al. Primary aldosteronism prevalence enhanced by strict adherence to 2016 Endocrine Society guidelines: Insights from an endocrine hypertension unit. J. Hypertens. 2024, 42, 1813–1822. [Google Scholar] [CrossRef]
- Funder, J.W.; Carey, R.M.; Mantero, F.; Murad, M.H.; Reincke, M.; Shibata, H.; Stowasser, M.; Young, W.F. The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline. J. Clin. Endocrinol. Metab. 2016, 101, 1889–1916. [Google Scholar] [CrossRef]
- Rossi, G.P.; Seccia, T.M.; Maiolino, G.; Cesari, M. The cardiovascular consequences of hyperaldosteronism. Ann. Endocrinol. 2021, 82, 174–178. [Google Scholar] [CrossRef]
- Hundemer, G.L.; Curhan, G.C.; Yozamp, N.; Wang, M.; Vaidya, A. Cardiometabolic outcomes and mortality in medically treated primary aldosteronism: A retrospective cohort study. Lancet Diabetes Endocrinol. 2018, 6, 51–59. [Google Scholar] [CrossRef] [PubMed]
- Zheng, M.-H.; Li, F.-X.; Xu, F.; Lin, X.; Wang, Y.; Xu, Q.-S.; Guo, B.; Yuan, L.-Q. The Interplay Between the Renin-Angiotensin-Aldosterone System and Parathyroid Hormone. Front. Endocrinol. 2020, 11, 539. [Google Scholar] [CrossRef]
- Maniero, C.; Fassina, A.; Guzzardo, V.; Lenzini, L.; Amadori, G.; Pelizzo, M.R.; Gomez-Sanchez, C.; Rossi, G.P. Primary hyperparathyroidism with concurrent primary aldosteronism. Hypertension 2011, 197958, 341–346. [Google Scholar] [CrossRef]
- Mazzocchi, G.; Aragona, F.; Malendowicz, L.K.; Nussdorfer, G.G. PTH and PTH-related peptide enhance steroid secretion from human adrenocortical cells. Am. J. Physiol. Endocrinol. Metab. 2001, 280, E209–E213. [Google Scholar] [CrossRef]
- Lenzini, L.; Prisco, S.; Vanderriele, P.E.; Lerco, S.; Torresan, F.; Maiolino, G.; Seccia, T.M.; Iacobone, M.; Rossi, G.P. PTH Modulation by Aldosterone and Angiotensin II is Blunted in Hyperaldosteronism and Rescued by Adrenalectomy. J. Clin. Endocrinol. Metab. 2019, 104, 3726–3734. [Google Scholar] [CrossRef] [PubMed]
- Gruson, D. PTH and cardiovascular risk. Ann. Endocrinol. 2021, 82, 149–150. [Google Scholar] [CrossRef]
- Kometani, M.; Yoneda, T.; Aono, D.; Gondoh-Noda, Y.; Matsuoka, T.; Higashitani, T.; Yoshikura, S.; Sawada, K.; Takeda, Y.; Fujimoto, A.; et al. Primary Aldosteronism with Parathyroid Hormone Elevation: A Single-center Retrospective Study. Intern. Med. 2021, 60, 993–998. [Google Scholar] [CrossRef]
- Pilz, S.; Kienreich, K.; Drechsler, C.; Ritz, E.; Fahrleitner-Pammer, A.; Gaksch, M.; Meinitzer, A.; März, W.; Pieber, T.R.; Tomaschitz, A. Hyperparathyroidism in patients with primary aldosteronism: Cross-sectional and interventional data from the GECOH study. J. Clin. Endocrinol. Metab. 2012, 97, E75–E79. [Google Scholar] [CrossRef] [PubMed]
- Ruiz-Sánchez, J.G.; Guerra, M.P.; Meneses, D.; Runkle, I. Primary Hyperaldosteronism: When to Suspect It and How to Confirm Its Diagnosis. Endocrines 2022, 3, 29–42. [Google Scholar] [CrossRef]
- Wang, A.; Wang, Y.; Liu, H.; Hu, X.; Li, J.; Xu, H.; Nie, Z.; Zhang, L.; Lyu, Z. Bone and mineral metabolism in patients with primary aldosteronism: A systematic review and meta-analysis. Front. Endocrinol. 2022, 13, 1027841. [Google Scholar] [CrossRef] [PubMed]
- Gao, X.; Yamazaki, Y.; Tezuka, Y.; Onodera, Y.; Ogata, H.; Omata, K.; Morimoto, R.; Nakamura, Y.; Satoh, F.; Sasano, H. The crosstalk between aldosterone and calcium metabolism in primary aldosteronism: A possible calcium metabolism-associated aberrant ‘neoplastic’ steroidogenesis in adrenals. J. Steroid Biochem. Mol. Biol. 2019, 193, 105434. [Google Scholar] [CrossRef] [PubMed]
- Brown, S.J.; Ruppe, M.D.; Tabatabai, L.S. The Parathyroid Gland and Heart Disease. Methodist DeBakey Cardiovasc. J. 2017, 13, 49–54. [Google Scholar] [CrossRef] [PubMed]
- Monticone, S.; Burrello, J.; Tizzani, D.; Bertello, C.; Viola, A.; Buffolo, F.; Gabetti, L.; Mengozzi, G.; Williams, T.A.; Rabbia, F.; et al. Prevalence and Clinical Manifestations of Primary Aldosteronism Encountered in Primary Care Practice. J. Am. Coll. Cardiol. 2017, 69, 1811–1820. [Google Scholar] [CrossRef] [PubMed]
- Asbach, E.; Bekeran, M.; König, A.; Lang, K.; Hanslik, G.; Treitl, M.; Ladurner, R.; Bidlingmaier, M.; Beuschlein, F.; Quinkler, M.; et al. Primary and Secondary Hyperparathyroidism in Patients with Primary Aldosteronism—Findings From the German Conn’s Registry. Exp. Clin. Endocrinol. Diabetes 2020, 128, 246–254. [Google Scholar] [CrossRef] [PubMed]
- Pepe, J.; Cipriani, C.; Sonato, C.; Raimo, O.; Biamonte, F.; Minisola, S. Cardiovascular manifestations of primary hyperparathyroidism: A narrative review. Eur. J. Endocrinol. 2017, 177, R297–R308. [Google Scholar] [CrossRef]
- Pilz, S.; Tomaschitz, A.; Drechsler, C.; Ritz, E.; Boehm, B.O.; Grammer, T.B.; März, W. Parathyroid hormone level is associated with mortality and cardiovascular events in patients undergoing coronary angiography. Eur. Heart J. 2010, 31, 1591–1598. [Google Scholar] [CrossRef] [PubMed]
Figure 1.
Exclusion criteria used in our study.
Figure 2.
Correlations between the values of PTH and PRA (A),PTH and PAC (B), and PTH and corrected calcium (C) in the PA group.
Figure 2.
Correlations between the values of PTH and PRA (A),PTH and PAC (B), and PTH and corrected calcium (C) in the PA group.
Figure 3.
PTH levels grouped by grades of hypertension in patients with primary aldosteronism.
Table 1.
Comparative characteristics between patients with PA and EH.
| Total (n = 67) | PA (n = 35) | EH (n = 32) | p-Value | |
|---|---|---|---|---|
| Age, years | 56 ± 13 | 57 ± 10 | 53 ± 15 | 0.239 |
| Female, n (%) | 44 (65) | 25 (71) | 19 (59) | 0.299 |
| Morbidity data | ||||
| Cardiovascular disease, n (%) | 21 (31) | 14 (40) | 7 (21) | 0.110 |
| Target organ damage, n (%) Left ventricular hypertrophy, n (%) Atrial fibrillation, n (%) Heart failure, n (%) Ictus, n (%) Ischemic cardiopathy, n (%) Albuminuria > 30 mg/g, n (%) | 28 (42) 28 (42) 5 (7) 3 (5) 5 (7) 5 (7) 16 (24) | 19 (54) 23 (67) 3 (9) 1 (3) 2 (6) 4 (11) 11 (32) | 9 (28) 5 (15) 2 (6) 2 (6) 3 (9) 1 (3) 5 (15) | 0.03 * <0.001 * 0.718 0.603 0.680 0.358 0.150 |
| Hypertension grade, n (%) Grade I, n (%) Grade II, n (%) Grade III, n (%) | 13 (40) 33 (49) 21 (31) | 0 15 (42) 20 (36) | 13 (40) 18 (56) 1 (3.1) | 0.001 * |
| Evolution of hypertension, years | 9 ± 8 | 11 ± 9 | 7 ± 6 | 0.061 |
| Number of antihypertensive medications Need 3 or more drugs, n (%) | 2.9 ± 1.2 32/54 (59.3) | 3 ± 1.4 14 (61) | 2.8 ± 1.1 18 (58) | 0.639 0.836 |
| Chronic kidney disease, n (%) | 6 (9) | 5 (15) | 1 (3.1) | 0.100 |
| Obstructive sleep apnea, n (%) | 31 (46) | 11 (32) | 20 (59) | 0.420 |
| Type 2 diabetes, n (%) | 16 (24) | 7 (20) | 9 (28) | 0.393 |
| Biochemical data | ||||
| Serum Na+, mmol/L | 141.9 ± 2.8 | 143.2 ± 2.4 | 140 ± 2.5 | <0.001 * |
| Serum K+, mmol/L | 4.1 ± 0.5 | 3.9 ± 0.4 | 4.4 ± 0.4 | <0.001 * |
| PAC, ng/dL | 28.1 ± 16.77 | 32.0 ± 15.4 | 16.2 ± 15.7 | <0.001 |
| ARR, ng/dL/mL/h | 99 ± 89 | 129 ± 84.0 | 8.0 ± 6.1 | <0.001 |
| eGFR, mL/min/1.73 m2 | 87.2 ± 15.3 | 88.5 ± 14.5 | 86.0 ± 16.3 | 0.509 |
| UACR, mg/g | 148 ± 634 | 326 ± 55 | 55 ± 95 | 0.311 |
| PTH, pg/mL | 51.4 ± 33.1 | 64.3 ± 42.2 | 39.4 ± 13.5 | 0.004 * |
| Albumin-corrected Ca, mg/dL | 9.3 ± 0.4 | 9.12 ± 0.40 | 9.6 ± 0.38 | <0.001 * |
| 25-OH vitamin D, ng/mL | 28.9 ± 10.9 | 28.91 ± 8.9 | 28.8 ± 12.8 | 0.97 |
PAC: plasma aldosterone; ARR: aldosterone-to-renin ratio; eGFR: estimated glomerular filtration rate; UACR: urine albumin-to-creatinine ratio * p < 0.05.
Table 2.
PTH levels according to the presence of TOD and CVD, grouped by PA and EH.
| Cardiovascular Disease | |||
| Yes | No | ||
| Primary aldosteronism | 79 ± 45 | 55 ± 39 | 0.13 |
| Essential hypertension | 38 ± 15 | 40 ± 13 | 0.747 |
| Target Organ Damage | |||
| Yes | No | ||
| Primary aldosteronism | 63 ± 37 | 66 ± 48 | 0.887 |
| Essential hypertension | 33 ± 5 | 42 ± 15 | 0.023 |
TOD: target organ damage; CVD: cardiovascular disease; PA: primary aldosteronism; EH: essential hypertension.
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content. |
© 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
Share and Cite
MDPI and ACS Style
Fernández-Sánchez, Á.; Meneses, D.; Bellasai, E.R.A.; Cárdenas-Salas, J.; Paniagua, A.; Vázquez, C.; Ruiz-Sánchez, J.G. Impact of Parathormone (PTH) Levels on the Presence of Cardiovascular Disease in Patients with Primary Aldosteronism and Essential Hypertension. Endocrines 2025, 6, 8. https://doi.org/10.3390/endocrines6010008
AMA Style
Fernández-Sánchez Á, Meneses D, Bellasai ERA, Cárdenas-Salas J, Paniagua A, Vázquez C, Ruiz-Sánchez JG. Impact of Parathormone (PTH) Levels on the Presence of Cardiovascular Disease in Patients with Primary Aldosteronism and Essential Hypertension. Endocrines. 2025; 6(1):8. https://doi.org/10.3390/endocrines6010008
Chicago/Turabian StyleFernández-Sánchez, Álvaro, Diego Meneses, Emma Raquel Alegre Bellasai, Jersy Cárdenas-Salas, Amalia Paniagua, Clotilde Vázquez, and Jorge Gabriel Ruiz-Sánchez. 2025. "Impact of Parathormone (PTH) Levels on the Presence of Cardiovascular Disease in Patients with Primary Aldosteronism and Essential Hypertension" Endocrines 6, no. 1: 8. https://doi.org/10.3390/endocrines6010008
APA StyleFernández-Sánchez, Á., Meneses, D., Bellasai, E. R. A., Cárdenas-Salas, J., Paniagua, A., Vázquez, C., & Ruiz-Sánchez, J. G. (2025). Impact of Parathormone (PTH) Levels on the Presence of Cardiovascular Disease in Patients with Primary Aldosteronism and Essential Hypertension. Endocrines, 6(1), 8. https://doi.org/10.3390/endocrines6010008
