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Pediatric endocrine hypertension

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      Abstract

      Endocrine causes of hypertension are rare in children and screening for endocrine hypertension in children should be carried out only after ruling out renal and renovascular causes. Excess levels and/or action of mineralocorticoids associated with low renin levels lead to childhood hypertension and this can be caused by various conditions which are discussed in detail in the article. Childhood pheochromocytomas are being increasingly diagnosed because of the improved application of genetic testing for familial syndromes associated with pheochromocytomas. Adolescents with polycystic ovarian syndrome (PCOS) can also have hypertension associated with their obese phenotype.

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      Most cited references 29

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      The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents.

        (2004)
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        Human hypertension caused by mutations in WNK kinases.

         Z Farfel,  B Dussol,  D. Simon (2001)
        Hypertension is a major public health problem of largely unknown cause. Here, we identify two genes causing pseudohypoaldosteronism type II, a Mendelian trait featuring hypertension, increased renal salt reabsorption, and impaired K+ and H+ excretion. Both genes encode members of the WNK family of serine-threonine kinases. Disease-causing mutations in WNK1 are large intronic deletions that increase WNK1 expression. The mutations in WNK4 are missense, which cluster in a short, highly conserved segment of the encoded protein. Both proteins localize to the distal nephron, a kidney segment involved in salt, K+, and pH homeostasis. WNK1 is cytoplasmic, whereas WNK4 localizes to tight junctions. The WNK kinases and their associated signaling pathway(s) may offer new targets for the development of antihypertensive drugs.
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          Hypertension caused by a truncated epithelial sodium channel gamma subunit: genetic heterogeneity of Liddle syndrome.

          Sensitivity of blood pressure to dietary salt is a common feature in subjects with hypertension. These features are exemplified by the mendelian disorder, Liddle's syndrome, previously shown to arise from constitutive activation of the renal epithelial sodium channel due to mutation in the beta subunit of this channel. We now demonstrate that this disease can also result from a mutation truncating the carboxy terminus of the gamma subunit of this channel; this truncated subunit also activates channel activity. These findings demonstrate genetic heterogeneity of Liddle's syndrome, indicate independent roles of beta and gamma subunits in the negative regulation of channel activity, and identify a new gene in which mutation causes a salt-sensitive form of human hypertension.
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            Author and article information

            Affiliations
            Department of Endocrinology and Diabetes, Amrita Institute of Medical Sciences, Cochin, Kerala, India
            Author notes
            Corresponding Author: Dr. Nisha Bhavani, Department of Endocrinology and Diabetes, Amrita Institute of Medical Sciences, Cochin – 682 041, Kerala, India. E-mail: nishab@ 123456aims.amrita.edu
            Journal
            Indian J Endocrinol Metab
            IJEM
            Indian Journal of Endocrinology and Metabolism
            Medknow Publications & Media Pvt Ltd (India )
            2230-8210
            2230-9500
            October 2011
            : 15
            : Suppl4
            : S361-S366
            3230094
            22145140
            IJEM-15-361
            10.4103/2230-8210.86980
            Copyright: © Indian Journal of Endocrinology and Metabolism

            This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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