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El riñón tiene un papel importante en la síntesis, metabolismo y eliminación de gran cantidad de hormonas. Así, la enfermedad renal crónica (ERC) cursa de forma natural con diversas alteraciones hormonales. Esta revisión aborda la posible conexión entre alteraciones en el eje hipotalámico-pituitario-gonadal y factores de riesgo cardiovascular en el paciente con ERC. Las anomalías hormonales analizadas son la retención de prolactina, deficiencia de testosterona y síndrome de T3 baja, todas ellas entendidas tradicionalmente como testigos inocentes de uremia y que han recibido una atención relativamente escasa por la comunidad nefróloga. En este revisamos interesantes vinculos entre estas alteraciones hormonales y complicaciones como la inflamación sistemica, la disfunción endotelial, la rigidez arterial, el desgaste proteico-energético y otras alteraciones cardiometabólicas inherentes a la excesiva mortalidad observada en la ERC. Proponemos que estas disfunciones hormonales pueden ser nuevos o previamene no apreciados factores de riesgo en el paciente urémico, existiendo la posibilidad de que puedan servir como objetivos terapéuticos.
Palabras clave:
Prolactina
Palabras clave:
Hormonas tiroideas
Palabras clave:
Testosterona
The kidney plays an important role in synthesis, metabolism and elimination of a plethora of hormones. Thus, chronic kidney disease (CKD) naturally progresses with hormonal disorders. This review will focus in emerging evidence regarding the association between CKD-associated disturbances in the hypothalamic-pituitary-gonadal axis and cardiovascular risk factors. Hormonal derangements discussed are prolactin retention, testosterone deficiency and the low trioodothyronine syndrome, all of which have traditionally been interpreted as innocent bystanders of uremia and received relatively scarce attention by the Nephrology community. We here show that these disorders share intriguing links with inflammation, endothelial dysfunction, arterial stiffness, protein-energy wasting and other cardiometabolic alterations inherent to CKD-related excess mortality. We argue that these disorders may be novel uremic risk factors with possibility to serve as therapeutic targets.
Keywords:
Prolactin
Keywords:
Thyroid hormones
Keywords:
Testosterone
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