DIABETES INSIPIDA NEFROGENICA PDF

La diabetes inspida nefrognica consiste en un defecto en la respuesta renal a la ADH. Aunque la secrecin de ADH de la hipfisis posterior es normal, un defecto en el receptor, la protena Gs, o la adenilil ciclasa hace que las clulas principales no respondan a la ADH. En consecuencia, la ADH no consigue aumentar la permeabilidad al agua en el tbulo distal final y los tbulos colectores. Como ocurre en la diabetes inspida central, el agua no puede reabsorberse en estos segmentos y se excretan grandes volmenes de orina diluida. La osmolaridad plasmtica aumenta, lo que estimula la hipfisis posterior para segregar an ms ADH.

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Aunque se trata de una enfermedad rara, su prevalencia no se conoce con exactitud. Mucosas ligeramente secas e hipocoloreadas. Boca con saliva espesa. Fontanela anterior puntiforme. Foto No. El AMPc, a su vez activa una proteincinasa que inicia una secuencia de acontecimientos que llevan al aumento de la permeabilidad de la membrana luminar.

Pediatr Nephrol. Madrid: Ediciones Norma. En: Gordillo PG. Madrid: Elsevier Science; Inheritance of nephrogenic diabetes insipidus. Am Hum Genet. Areses R, Urbieta M A. Santos F. Linshaw MA. Congenital Nephrogenic Diabetes Insipidus. Pediatrics in review. Characterization o fan aquaporin-2 water channel gene mutation causing partial nephrogenic diabetes insipidus in a Mexican Family: evidence of increased frequency of the mutation in the town oringin.

J Am Soc Nephrol. Cell biological aspects of the vasopressin type-2 receptor and aquaporin 2 water channel in nephrogenic diabetes insipidus.

Am J Physiol Renal Physiol. Molecular biology of hereditary diabetes insipidus. Nephrogenic diabetes insipidus. Ann Internal Med. SUMMARY Tubulopaties gather an important quantity of entities having in common renal tubular dysfunction generally traduced in the reabsortion alteration of one or several elements, determinant in the clinical manifestations. Anomalies in the tubular transport could be primary or could be developed as a result of other disorders.

The primary ones have a hereditary, congenital character, explaining why the first symptoms are generally precocious and, therefore, their diagnosis is made by the pediatrician.

We describe its pathogeny, hereditary transmission way, and also the most relevant clinical aspects of this malady, having into account how infrequent it is and that its prevalence is not known exactly.

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