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  • Review Article
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Genetic screening in arterial hypertension

Nature Reviews Endocrinology volume 13, pages 289–298 (2017)Cite this article

Subjects

Key Points

  • Arterial hypertension is genetically complex, which explains why the identification of the underlying genes has not been as successful for hypertension as for other diseases

  • Genetic investigation of well-defined endocrine forms of hypertension, in which stratification of patients into homogeneous cohorts is feasible, has provided substantial accomplishments in the field

  • The prediction of adverse drug reactions and of blood pressure response to antihypertensive drugs through the identification of genetic markers is a highly promising field for personalized medicine

  • Genetic testing will also enable the design of randomized controlled trials in smaller series of patients than currently necessary, with a concomitant decrease of costs and times from drug design to clinical use

  • Genetic testing is already an option for different applications in the field of hypertension, for example in phaeochromocytomas and paragangliomas, familial hyperaldosteronism type 1 and other forms of endocrine hypertension

  • Currently, the genes and types of mutation to be searched for should be decided at referral centres, in which experience with evaluation of secondary forms of hypertension and genetic testing are both available

Abstract

Studies involving adoptive families and twins have demonstrated the genetic basis of hypertension and shown that genetic factors account for about 40% of the variance in blood pressure among individuals. Arterial hypertension is genetically complex: multiple genes influence the blood pressure phenotype through allelic effects from single genes and gene–gene interactions. Moreover, environmental factors also modify the blood pressure phenotype. This complexity explains why the identification of the underlying genes has not been as successful in hypertension as in other diseases (such as type 1 and type 2 diabetes mellitus). The identification of the genetic determinants of hypertension has been most successful in endocrine forms of hypertension, which have well-defined phenotypes that permit a precise patient stratification into homogeneous cohorts. A promising area for the application of genetic testing to personalized medicine is the prediction of responses and adverse reactions to antihypertensive drugs. The identification of genetic markers of drug response will enable the design of randomized controlled trials in much smaller series of patients than is currently possible, decreasing the costs and times from drug design to clinical use and ultimately providing patients and doctors with a larger number of tools to combat hypertension, the most important risk factor for cardiovascular disease. This Review focuses on the rapidly developing field of genetic testing in patients with arterial hypertension.

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Figure 1: The genetic complexity of hypertension.
Figure 2: Influence of a pharmacogenetically driven strategy in drug development.

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References

  1. Kearney, P. M. et al. Global burden of hypertension: analysis of worldwide data. Lancet 365, 217–223 (2005).

    Article  PubMed  Google Scholar 

  2. Perkovic, V., Huxley, R., Wu, Y., Prabhakaran, D. & MacMahon, S. The burden of blood pressure-related disease: a neglected priority for global health. Hypertension 50, 991–997 (2007).

    Article  CAS  PubMed  Google Scholar 

  3. Corvol, P., Jeunemaitre, X., Charru, A. & Soubrier, F. Can the genetic factors influence the treatment of systemic hypertension? The case of the renin-angiotensin-aldosterone system. Am. J. Cardiol. 70, 14D–20D (1992).

    Article  CAS  PubMed  Google Scholar 

  4. Lawes, C. M., Vander Hoorn, S. & Rodgers, A. Global burden of blood-pressure-related disease, 2001. Lancet 371, 1513–1518 (2008).

    Article  PubMed  Google Scholar 

  5. Padmanabhan, S., Newton-Cheh, C. & Dominiczak, A. F. Genetic basis of blood pressure and hypertension. Trends Genet. 28, 397–408 (2012).

    Article  CAS  PubMed  Google Scholar 

  6. Havlik, R. J. et al. Blood pressure aggregation in families. Am. J. Epidemiol. 110, 304–312 (1979).

    Article  CAS  PubMed  Google Scholar 

  7. Stocks, P. A. A biometric investigation of twins and their brothers and sisters. Ann. Eugen. 4, 49 (1930).

    Article  Google Scholar 

  8. Feinleib, M. et al. The NHLBI twin study of cardiovascular disease risk factors: methodology and summary of results. Am. J. Epidemiol. 106, 284–285 (1977).

    Article  CAS  PubMed  Google Scholar 

  9. Annest, J. L., Sing, C. F., Biron, P. & Mongeau, J. G. Familial aggregation of blood pressure and weight in adoptive families. II. Estimation of the relative contributions of genetic and common environmental factors to blood pressure correlations between family members. Am. J. Epidemiol. 110, 492–503 (1979).

    Article  CAS  PubMed  Google Scholar 

  10. Biron, P. Normal blood pressure in offspring of persons with essential hypertension. Can. Med. Assoc. J. 119, 694–696 (1978).

    PubMed  PubMed Central  CAS  Google Scholar 

  11. Williams, C. J., Christian, J. C. & Norton, J. A. Jr. TWINAN90: a FORTRAN program for conducting ANOVA-based and likelihood-based analyses of twin data. Comput. Methods Programs Biomed. 38, 167–176 (1992).

    Article  CAS  PubMed  Google Scholar 

  12. Rossi, G. P. et al. Genetic determinants of plasma ACE and renin activity in young normotensive twins. J. Hypertens. 17, 647–655 (1999).

    Article  CAS  PubMed  Google Scholar 

  13. Snieder, H., Harshfield, G. A. & Treiber, F. A. Heritability of blood pressure and hemodynamics in African- and European-American youth. Hypertension 41, 1196–1201 (2003).

    Article  CAS  PubMed  Google Scholar 

  14. Vinck, W. J., Fagard, R. H., Loos, R. & Vlietinck, R. The impact of genetic and environmental influences on blood pressure variance across age-groups. J. Hypertens. 19, 1007–1013 (2001).

    Article  CAS  PubMed  Google Scholar 

  15. de Faire, U., Iselius, L. & Lundman, T. Biological and cultural determinants of blood pressure. Hypertension 4, 725–728 (1982).

    Article  CAS  PubMed  Google Scholar 

  16. Munroe, P. B., Barnes, M. R. & Caulfield, M. J. Advances in blood pressure genomics. Circ. Res. 112, 1365–1379 (2013).

    Article  CAS  PubMed  Google Scholar 

  17. Wellcome Trust Case Control Consortium. Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls. Nature 447, 661–678 (2007).

  18. Org, E. et al. Genome-wide scan identifies CDH13 as a novel susceptibility locus contributing to blood pressure determination in two European populations. Hum. Mol. Genet. 18, 2288–2296 (2009).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  19. Paz, M. A. et al. Treatment efficacy of anti-hypertensive drugs in monotherapy or combination: ATOM systematic review and meta-analysis of randomized clinical trials according to PRISMA statement. Medicine (Baltimore) 95, e4071 (2016).

    Article  CAS  Google Scholar 

  20. Laragh, J. H. Renin system analysis defines the special value of combination antihypertensive therapy using an antirenin agent (CEI) with a long-acting calcium channel blocker (CCB). Am. J. Hypertens. 11, 170S–174S (1998).

    Article  CAS  PubMed  Google Scholar 

  21. Cusi, D. et al. Polymorphisms of α-adducin and salt sensitivity in patients with essential hypertension. Lancet 349, 1353–1357 (1997).

    Article  CAS  PubMed  Google Scholar 

  22. Packer, M. et al. Comparison of omapatrilat and enalapril in patients with chronic heart failure: the Omapatrilat Versus Enalapril Randomized Trial of Utility in Reducing Events (OVERTURE). Circulation 106, 920–926 (2002).

    Article  CAS  PubMed  Google Scholar 

  23. Coats, A. J. Omapatrilat- the story of Overture and Octave. Int. J. Cardiol. 86, 1–4 (2002).

    Article  PubMed  Google Scholar 

  24. Mukae, S. et al. Bradykinin B2 receptor gene polymorphism is associated with angiotensin-converting enzyme inhibitor-related cough. Hypertension 36, 127–131 (2000).

    Article  CAS  PubMed  Google Scholar 

  25. Weinshilboum, R. Inheritance and drug response. N. Engl. J. Med. 348, 529–537 (2003).

    Article  PubMed  Google Scholar 

  26. Rossi, G. P., Seccia, T. M. & Pessina, A. C. Clinical use of laboratory tests for the identification of secondary forms of arterial hypertension. Crit. Rev. Clin. Lab. Sci. 44, 1–85 (2007).

    Article  CAS  PubMed  Google Scholar 

  27. Neumann, H. P. et al. New genetic causes of pheochromocytoma: current concepts and the clinical relevance. Keio J. Med. 54, 15–21 (2005).

    Article  CAS  PubMed  Google Scholar 

  28. Lenders, J. W. et al. Pheochromocytoma and paraganglioma: an endocrine society clinical practice guideline. J. Clin. Endocrinol. Metab. 99, 1915–1942 (2014).

    Article  CAS  PubMed  Google Scholar 

  29. Fliedner, S. M., Lehnert, H. & Pacak, K. Metastatic paraganglioma. Semin. Oncol. 37, 627–637 (2010).

    Article  PubMed  PubMed Central  Google Scholar 

  30. van der Mey, A. G., Maaswinkel-Mooy, P. D., Cornelisse, C. J., Schmidt, P. H. & van de Kamp, J. J. Genomic imprinting in hereditary glomus tumours: evidence for new genetic theory. Lancet 2, 1291–1294 (1989).

    Article  CAS  PubMed  Google Scholar 

  31. O'Toole, S. M., Denes, J., Robledo, M., Stratakis, C. A. & Korbonits, M. The association of pituitary adenomas and phaeochromocytomas or paragangliomas. Endocr. Relat. Cancer 22, T105–T122 (2015).

    Article  CAS  PubMed  Google Scholar 

  32. Hansson, J. H. et al. A de novo missense mutation of the β subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activity. Proc. Natl Acad. Sci. USA 92, 11495–11499 (1995).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  33. Lifton, R. P. Molecular genetics of human blood pressure variation. Science 272, 676–680 (1996).

    Article  CAS  PubMed  Google Scholar 

  34. Schumacher, F. R. et al. Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia. EMBO Mol. Med. 7, 1285–1306 (2015).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  35. O'Shaughnessy, K. M. Gordon syndrome: a continuing story. Pediatr. Nephrol. 30, 1903–1908 (2015).

    Article  PubMed  Google Scholar 

  36. Wilson, R. C. et al. A genetic defect resulting in mild low-renin hypertension. Proc. Natl Acad. Sci. USA 95, 10200–10205 (1998).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Dave-Sharma, S. et al. Examination of genotype and phenotype relationships in 14 patients with apparent mineralocorticoid excess. J. Clin. Endocrinol. Metab. 83, 2244–2254 (1998).

    CAS  PubMed  Google Scholar 

  38. Geller, D. S. et al. A novel form of human mendelian hypertension featuring nonglucocorticoid-remediable aldosteronism. J. Clin. Endocrinol. Metab. 93, 3117–3123 (2008).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  39. Pacak, K., Koch, C. A. & Eisenhofer, G. Current approaches and new advances in endocrine hypertension. Trends Endocrinol. Metab. 13, 96–97 (2002).

    Article  CAS  PubMed  Google Scholar 

  40. Teo, A. E. et al. Pregnancy, primary aldosteronism, and adrenal CTNNB1 mutations. N. Engl. J. Med. 373, 1429–1436 (2015).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  41. Murtha, T. D., Carling, T. & Scholl, U. I. Pregnancy, primary aldosteronism, and somatic CTNNB1 mutations. N. Engl. J. Med. 374, 1492–1493 (2016).

    Article  PubMed  Google Scholar 

  42. Beuschlein, F. et al. Constitutive activation of PKA catalytic subunit in adrenal Cushing's syndrome. N. Engl. J. Med. 370, 1019–1028 (2014).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  43. Goh, G. et al. Recurrent activating mutation in PRKACA in cortisol-producing adrenal tumors. Nat. Genet. 46, 613–617 (2014).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  44. Sato, Y. et al. Recurrent somatic mutations underlie corticotropin-independent Cushing's syndrome. Science 344, 917–920 (2014).

    Article  CAS  PubMed  Google Scholar 

  45. Cao, Y. et al. Activating hotspot L205R mutation in PRKACA and adrenal Cushing's syndrome. Science 344, 913–917 (2014).

    Article  CAS  PubMed  Google Scholar 

  46. Assie, G. et al. ARMC5 mutations in macronodular adrenal hyperplasia with Cushing's syndrome. N. Engl. J. Med. 369, 2105–2114 (2013).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  47. Espiard, S. et al. ARMC5 mutations in a large cohort of primary macronodular adrenal hyperplasia: clinical and functional consequences. J. Clin. Endocrinol. Metab. 100, E926–E935 (2015).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  48. Gagliardi, L. et al. ARMC5 mutations are common in familial bilateral macronodular adrenal hyperplasia. J. Clin. Endocrinol. Metab. 99, E1784–E1792 (2014).

    Article  CAS  PubMed  Google Scholar 

  49. Alencar, G. A. et al. ARMC5 mutations are a frequent cause of primary macronodular adrenal hyperplasia. J. Clin. Endocrinol. Metab. 99, E1501–E1509 (2014).

    Article  CAS  PubMed  Google Scholar 

  50. Lodish, M. & Stratakis, C. A. A genetic and molecular update on adrenocortical causes of Cushing syndrome. Nat. Rev. Endocrinol. 12, 255–262 (2016).

    Article  CAS  PubMed  Google Scholar 

  51. Carney, J. A., Lyssikatos, C., Lodish, M. B. & Stratakis, C. A. Germline PRKACA amplification leads to Cushing syndrome caused by 3 adrenocortical pathologic phenotypes. Hum. Pathol. 46, 40–49 (2015).

    Article  CAS  PubMed  Google Scholar 

  52. Faillot, S. & Assie, G. The genomics of adrenocortical tumors. Eur. J. Endocrinol. 174, R249–R265 (2016).

    Article  CAS  PubMed  Google Scholar 

  53. Rossi, G. P. A comprehensive review of the clinical aspects of primary aldosteronism. Nat. Rev. Endocrinol. 7, 485–495 (2011).

    Article  PubMed  Google Scholar 

  54. Sutherland, D. J., Ruse, J. L. & Laidlaw, J. C. Hypertension, increased aldosterone secretion and low plasma renin activity relieved by dexamethasone. Can. Med. Assoc. J. 95, 1109–1119 (1966).

    PubMed  PubMed Central  CAS  Google Scholar 

  55. Salti, I. S., Stiefel, M., Ruse, J. L. & Laidlaw, J. C. Non-tumorous “primary” aldosteronism. I. Type relieved by glucocorticoid (glucocorticoid-remediable aldosteronism). Can. Med. Assoc. J. 101, 1–10 (1969).

    PubMed  PubMed Central  CAS  Google Scholar 

  56. Lifton, R. P. et al. Hereditary hypertension caused by chimaeric gene duplications and ectopic expression of aldosterone synthase. Nat. Genet. 2, 66–74 (1992).

    Article  CAS  PubMed  Google Scholar 

  57. Gioco, F., Seccia, T. M., Gomez-Sanchez, E. P., Rossi, G. P. & Gomez-Sanchez, C. E. Adrenal histopathology in primary aldosteronism: is it time for a change? Hypertension 66, 724–730 (2015).

    Article  PubMed  CAS  Google Scholar 

  58. Mulatero, P. et al. Prevalence and characteristics of familial hyperaldosteronism: the PATOGEN study (Primary Aldosteronism in TOrino-GENetic forms). Hypertension 58, 797–803 (2011).

    Article  CAS  PubMed  Google Scholar 

  59. Torpy, D. J. et al. Familial hyperaldosteronism type II: description of a large kindred and exclusion of the aldosterone synthase (CYP11B2) gene. J. Clin. Endocrinol. Metab. 83, 3214–3218 (1998).

    CAS  PubMed  Google Scholar 

  60. Carss, K. J., Stowasser, M., Gordon, R. D. & O'Shaughnessy, K. M. Further study of chromosome 7p22 to identify the molecular basis of familial hyperaldosteronism type II. J. Hum. Hypertens. 25, 560–564 (2011).

    Article  CAS  PubMed  Google Scholar 

  61. Choi, M. et al. K+ channel mutations in adrenal aldosterone-producing adenomas and hereditary hypertension. Science 331, 768–772 (2011).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  62. Boulkroun, S. et al. Prevalence, clinical, and molecular correlates of KCNJ5 mutations in primary aldosteronism. Hypertension 59, 592–598 (2012).

    Article  CAS  PubMed  Google Scholar 

  63. Scholl, U. I. et al. Hypertension with or without adrenal hyperplasia due to different inherited mutations in the potassium channel KCNJ5. Proc. Natl Acad. Sci. USA 109, 2533–2538 (2012).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  64. Charmandari, E. et al. A novel point mutation in the KCNJ5 gene causing primary hyperaldosteronism and early-onset autosomal dominant hypertension. J. Clin. Endocrinol. Metab. 97, E1532–E1539 (2012).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  65. Monticone, S. et al. A case of severe hyperaldosteronism caused by a de novo mutation affecting a critical salt bridge Kir3.4 residue. J. Clin Endocrinol. Metab. 100, E114–E118 (2015).

    Article  CAS  PubMed  Google Scholar 

  66. Sertedaki, A. et al. Functional characterization of two novel germline mutations of the KCNJ5 gene in hypertensive patients without primary aldosteronism but with ACTH-dependent aldosterone hypersecretion. Clin. Endocrinol. 85, 845–851 (2016).

    Article  CAS  Google Scholar 

  67. Rossi, G. P., Gioco, F., Fassina, A. & Gomez-Sanchez, C. E. Normoaldosteronemic aldosterone-producing adenoma: immunochemical characterization and diagnostic implications. J. Hypertens. 33, 2546–2549 (2015).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  68. Azizan, E. A. et al. Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension. Nat. Genet. 45, 1055–1060 (2013).

    Article  CAS  PubMed  Google Scholar 

  69. Scholl, U. I. et al. Somatic and germline CACNA1D calcium channel mutations in aldosterone-producing adenomas and primary aldosteronism. Nat. Genet. 45, 1050–1054 (2013).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  70. Scholl, U. I. et al. Recurrent gain of function mutation in calcium channel CACNA1H causes early-onset hypertension with primary aldosteronism. eLife 4, e06315 (2015).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  71. Lenzini, L. & Rossi, G. P. The molecular basis of primary aldosteronism: from chimeric gene to channelopathy. Curr. Opin. Pharmacol. 21, 35–42 (2015).

    Article  CAS  PubMed  Google Scholar 

  72. Zennaro, M. C. & Jeunemaitre, X. SFE/SFHTA/AFCE consensus on primary aldosteronism, part 5: genetic diagnosis of primary aldosteronism. Ann. Endocrinol. (Paris) 77, 214–219 (2016).

    Article  Google Scholar 

  73. Maniero, C. et al. Primary hyperparathyroidism with concurrent primary aldosteronism. Hypertension 58, 341–346 (2011).

    Article  CAS  PubMed  Google Scholar 

  74. Maniero, C. et al. Mild hyperparathyroidism: a novel surgically correctable feature of primary aldosteronism. J. Hypertens. 30, 390–395 (2012).

    Article  CAS  PubMed  Google Scholar 

  75. Rossi, G. P. et al. Hyperparathyroidism can be useful in the identification of primary aldosteronism due to aldosterone-producing adenoma. Hypertension 60, 431–436 (2012).

    Article  CAS  PubMed  Google Scholar 

  76. 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. 280, E209–E213 (2001).

    Article  CAS  PubMed  Google Scholar 

  77. Widimsky, J. Jr et al. Vascular disturbances in primary aldosteronism: clinical evidence. Kidney Blood Press. Res. 35, 529–533 (2012).

    Article  CAS  PubMed  Google Scholar 

  78. Mackenzie-Feder, J., Sirrs, S., Anderson, D., Sharif, J. & Khan, A. Primary hyperparathyroidism: an overview. Int. J. Endocrinol. 2011, 251410 (2011).

    Article  PubMed  PubMed Central  Google Scholar 

  79. Alevizaki, M. & Saltiki, K. Primary hyperparathyroidism in MEN2 syndromes. Recent Results Cancer Res. 204, 179–186 (2015).

    Article  PubMed  Google Scholar 

  80. Mayr, B., Schnabel, D., Dorr, H. G. & Schofl, C. Gain and loss of function mutations of the calcium-sensing receptor and associated proteins: current treatment concepts. Eur. J. Endocrinol. 174, R189–R208 (2016).

    Article  CAS  PubMed  Google Scholar 

  81. Murphy, H. et al. Neonatal severe hyperparathyroidism caused by homozygous mutation in CASR: a rare cause of life-threatening hypercalcemia. Eur. J. Med. Genet. 59, 227–231 (2016).

    Article  PubMed  Google Scholar 

  82. Pichardo-Lowden, A. R., Manni, A., Saunders, B. D. & Baker, M. J. Familial hyperparathyroidism due to a germline mutation of the CDC73 gene: implications for management and age-appropriate testing of relatives at risk. Endocr. Pract. 17, 602–609 (2011).

    Article  PubMed  Google Scholar 

  83. Costa-Guda, J. & Arnold, A. Genetic and epigenetic changes in sporadic endocrine tumors: parathyroid tumors. Mol. Cell. Endocrinol. 386, 46–54 (2014).

    Article  CAS  PubMed  Google Scholar 

  84. Koulouridis, E. & Koulouridis, I. Molecular pathophysiology of Bartter's and Gitelman's syndromes. World, J. Pediatr. 11, 113–125 (2015).

    Article  CAS  Google Scholar 

  85. Simon, D. B. et al. Bartter's syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na-K-2Cl cotransporter NKCC2. Nat. Genet. 13, 183–188 (1996).

    Article  CAS  PubMed  Google Scholar 

  86. Ji, W. et al. Rare independent mutations in renal salt handling genes contribute to blood pressure variation. Nat. Genet. 40, 592–599 (2008).

    Article  PubMed  PubMed Central  CAS  Google Scholar 

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Acknowledgements

The authors thank the Foundation for Advanced Research in Hypertension and Cardiovascular Diseases (www.forica.it) and the FP7-funded COST ADMIRE network (BM1301), and acknowledge the support of Horizon2020 Grant SEP-210176891. This work was supported by The Foundation for Advanced Research in Hypertension and Cardiovascular Diseases, the Società Italiana dell'Ipertensione Arteriosa and the University of Padua, Italy.

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  1. Department of Medicine (DIMED), Clinica dell'Ipertensione Arteriosa, University of Padua, Via Giustiniani 2, 35126, Padua, Italy

    Gian Paolo Rossi, Giulio Ceolotto, Brasilina Caroccia & Livia Lenzini

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G.P.R. was responsible for conceiving, drafting and finalizing the manuscript. L.L. contributed to drafting the manuscript. G.C. and B.C. searched the literature, revised the manuscript and contributed to preparing the draft, correcting it and preparing the references.

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Rossi, G., Ceolotto, G., Caroccia, B. et al. Genetic screening in arterial hypertension. Nat Rev Endocrinol 13, 289–298 (2017). https://doi.org/10.1038/nrendo.2016.196

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