Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Klotho gene displays an extremely shortened life span with loss of function missense mutations leading to premature multiple organ failure, thus resembling human premature aging syndromes. The transmembrane form of Klotho protein functions as an obligatory co-receptor for FGF23. Klotho and FGF23 are crucial components for the regulation of vitamin D metabolism and subsequently blood phosphate levels. The secreted Klotho protein has multiple regulatory functions, including effects on electrolyte homeostasis, on growth factor pathways as well as on oxidative stress, which are currently the object of extensive research. Klotho protein deficiency is observed in many experimental and clinical disease models. Genetic polymorphisms such as the G-395A polymorphism in the promoter region of the Klotho gene have been associated with the development of essential hypertension. The kidneys are the primary site of Klotho production, and renal Klotho is decreased in CKD, followed by a reduction in plasma Klotho. Klotho deficiency has been both associated with progression of CKD as well as with its cardinal systemic manifestations, including cardiovascular disease. Thus, Klotho has been suggested both as a risk biomarker for early detection of CKD and additionally as a potential therapeutic tool in the future.
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PMID:Klotho, the Holy Grail of the kidney: from salt sensitivity to chronic kidney disease. 2721 57

Fibroblast growth factor 23 (FGF 23), an endocrine hormone regulating the homeostasis of phosphate and vitamin D, has been shown to play a role in cardiovascular disease. Increased blood FGF 23 is found to be associated with elevated blood pressure in adults. However, measurement of FGF 23 in hypertensive children has not been documented. In this study, a total of 98 children with primary hypertension and 37 controls were recruited, and blood FGF 23 was comparatively investigated. Additionally, FGF 23 levels were compared between the subgroups of patients after hypertensive children were sub-grouped according to their cardiac geometry, hypertension stages, insulin levels, and weight. The case group had a FGF 23 level of 48.99 (16.42), expressed as the median (the interquartile range), significantly higher than the 41.72 (7.05) from the control group (p = 0.0002). While no remarkable differences were observed in FGF 23 levels between non-obese and obese hypertensive children, between patients with stage 1 and stage 2 hypertension, or between patients with normal and high insulin levels; hypertensive children with abnormal cardiac geometry had significantly higher levels of FGF 23 than patients with normal cardiac geometry (p = 0.0085). Our data revealed for the first time that hypertensive children have higher levels of FGF 23. Further studies are needed to examine if lowering FGF 23 improves the cardiac geometry in hypertensive children with higher FGF 23.
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PMID:Plasma Fibroblast Growth Factor 23 Is Elevated in Pediatric Primary Hypertension. 3105 17