Different roles of the RAAS affect bone metabolism in patients with primary aldosteronism, Gitelman syndrome and Bartter syndrome

Tang, Wangna; Chai, Yimin; Jia, Hongwei; Wang, Baoping; Liu, Tong; Wang, Hao; Dai, Chenlin

doi:10.1186/s12902-022-00955-2

Cited by 2 publications

(2 citation statements)

References 20 publications

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“…However, Petramala et al (26) and Salcuni et al (28) found that the osteopenia and OP rates in PA patients were significantly higher than in EH patients, healthy subjects, and those with adrenal nonfunctioning tumors (NFAs). This was confirmed by another study comparing patients with PA and secondary aldosteronism (9).…”

Section: Risk Of Op In Pa Patientssupporting

confidence: 57%

Bone and mineral metabolism in patients with primary aldosteronism: A systematic review and meta-analysis

Wang

Liu³

et al. 2022

Front. Endocrinol.

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PurposePatients with primary aldosteronism (PA) tend to exhibit a high prevalence of osteoporosis (OP) that may vary by whether PA is unilateral or bilateral, and responsive to PA treatment. To explore relationships between bone metabolism, PA subtypes, and treatment outcomes, we performed a systematic review and meta-analysis.MethodsThe PubMed, Embase, and Cochrane databases were searched for clinical studies related to PA and bone metabolism markers. Articles that met the criteria were screened and included in the systematic review; the data were extracted after evaluating their quality. R software (ver. 2022-02-16, Intel Mac OS X 11.6.4) was used for the meta-analysis.ResultsA total of 28 articles were subjected to systematic review, of which 18 were included in the meta-analysis. We found that PA patients evidenced a lower serum calcium level (mean difference [MD] = –0.06 mmol/L, 95% confidence interval [CI]: −0.10 ~ −0.01), a higher urine calcium level (MD = 1.29 mmol/24 h, 95% CI: 0.81 ~ 1.78), and a higher serum parathyroid hormone (PTH) level (MD = 2.16 pmol/L, 95% CI: 1.57 ~ 2.75) than did essential hypertension (EH) subjects. After medical treatment or adrenal surgery, PA patients exhibited a markedly increased serum calcium level (MD = –0.08 mmol/L, 95% CI: –0.11 ~ –0.05), a decreased urine calcium level (MD = 1.72 mmol/24 h, 95% CI: 1.00 ~ 2.44), a decreased serum PTH level (MD = 2.67 pmol/L, 95% CI: 1.73 ~ 3.62), and an increased serum 25-hydroxyvitamin D (25-OHD) level (MD = –6.32 nmol/L, 95% CI: –11.94 ~ –0.70). The meta-analysis showed that the ser um PTH level of unilateral PA patients was significantly higher than that of bilateral PA patients (MD = 0.93 pmol/L, 95% CI: 0.36 ~ 1.49) and the serum 25-OHD lower than that of bilateral PA patients (MD = –4.68 nmol/L, 95% CI: –7.58 ~ 1.77). There were, however, no significant differences between PA and EH patients of 25-OHD, or BMD of femoral neck and lumbar spine. BMDs of the femoral neck or lumbar spine did not change significantly after treatment. The meta-analytical results were confirmed via sensitivity and subgroup analyses.ConclusionExcess aldosterone was associated with decreased serum calcium, elevated urinary calcium, and elevated PTH levels; these effects may be enhanced by low serum 25-OHD levels. The risks of OP and fracture might be elevated in PA patients, especially unilateral PA patients, but could be reduced after medical treatment or adrenal surgery. In view, however, of the lack of BMD changes, such hypothesis needs to be tested in further studies.

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Section: Risk Of Op In Pa Patientssupporting

confidence: 57%

Bone and mineral metabolism in patients with primary aldosteronism: A systematic review and meta-analysis

Wang

Liu³

et al. 2022

Front. Endocrinol.

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“…Hyperreninemic hyperaldosteronism occurring in BS patients can also play a role, as both angiotensin II and aldosterone increase PTH secretion [ 20 ]. Along with chronic high PTH, excess aldosterone, as seen in primary hyperaldosteronism, can also have direct and detrimental effects in bone of BS patients, as osteoclasts, osteoblasts, and osteocytes express mineralocorticoid receptors [ 21 – 23 ]. Indeed, low bone mineral density has been described in patients with BS types 1 and 2, and life-long bone mineral density monitoring is being recommended [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Bartter Syndrome Presenting as Arginine-Vasopressin Resistance: A Report of 2 Cases

Sousa,

Medeiros,

Rodrigues

et al. 2024

Am J Case Rep

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Case series Patients: Male, 9-month-old • Male, 6-year-old Final Diagnosis: Bartter syndrome types 1 and 2 Symptoms: Enuresis • polydipsia • polyuria • salt-craving • vomits Clinical Procedure: Short desmopressin test • ultrasonography Specialty: Nephrology Objective: Congenital defects/diseases Background: Bartter syndrome is a rare, inherited salt-wasting tubulopathy caused by mutations in 1 of 6 genes that express ion transport channels in the thick ascending limb of nephrons. Excessive prostaglandin E2 and associated hyperreninemic hyperaldosteronism occurs, causing polyhydramnios, polyuria, prematurity, failure to thrive, and characteristic physical features. Hypokalemia, hypochloremic metabolic alkalosis, and, depending on the affected gene, hypercalciuria and nephrocalcinosis are hallmarks of Bartter syndrome. Case Reports: A 9-month-old male infant, born prematurely due to polyhydramnios, presented in the Emergency Department with dehydration due to incoercible vomiting and significant polyuria. A 6-year-old male infant with a previous history of prematurity due to polyhydramnios was referred to the Pediatric Endocrinology Department due to short stature and notable polydipsia and polyuria. Considering these marked symptoms, both cases triggered suspicion and started workup for arginine-vasopressin insufficiency/resistance. However, during the investigations, a broader clinical revision revealed that both had dysmorphic physical features (triangularly shaped face, prominent forehead, protruding ears, drooping mouth), poor growth, impaired weight gain, and typical biochemical findings (hypokalemic metabolic alkalosis, hypercalciuria, secondary hyperaldosteronism) of Bartter syndrome. Genetic testing confirmed the diagnosis of Bartter syndrome types 1 and type 2, respectively, and this diagnosis allowed proper treatment and significant clinical improvements, personalized follow-up, and genetic counseling for parents desiring further healthy pregnancies. Conclusions: Here, we present clinical and follow-up findings of 2 patients with Bartter syndrome types 1 and 2 discovered upon a broader clinical revision of suspected arginine-vasopressin insufficiency/resistance. We also review pertinent data on diagnosis and management of this challenging syndrome.

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Different roles of the RAAS affect bone metabolism in patients with primary aldosteronism, Gitelman syndrome and Bartter syndrome

Cited by 2 publications

References 20 publications

Bone and mineral metabolism in patients with primary aldosteronism: A systematic review and meta-analysis

Bone and mineral metabolism in patients with primary aldosteronism: A systematic review and meta-analysis

Bartter Syndrome Presenting as Arginine-Vasopressin Resistance: A Report of 2 Cases

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