ABSTRACT
Nephrogenic diabetes insipidus (NDI) is characterized by the inability to concentrate urine that results in polyuria and polydipsia, despite having normal or elevated plasma concentrations of arginine vasopressin (AVP). In this study, we review the clinical aspects and diagnosis of NDI, the various etiologies, current treatment options and potential future developments. NDI has different clinical manifestations and approaches according to the etiology. Hereditary forms of NDI are mainly caused by mutations in the genes that encode key proteins in the AVP signaling pathway, while acquired causes are normally associated with specific drug exposure, especially lithium, and hydroelectrolytic disorders. Clinical manifestations of the disease vary according to the degree of dehydration and hyperosmolality, being worse when renal water losses cannot be properly compensated by fluid intake. Regarding the diagnosis of NDI, it is important to consider the symptoms of the patient and the diagnostic tests, including the water deprivation test and the baseline plasma copeptin measurement, a stable surrogate biomarker of AVP release. Without proper treatment, patients may developcomplications leading to high morbidity and mortality, such as severe dehydration and hypernatremia. In that sense, the treatment of NDI consists in decreasing the urine output, while allowing appropriate fluid balance, normonatremia, and ensuring an acceptable quality of life. Therefore, therapeutic options include nonpharmacological interventions, including sufficient water intake and a low-sodium diet, and pharmacological treatment. The main medications used for NDI are thiazide diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), and amiloride, used isolated or in combination.
Subject(s)
Diabetes Insipidus, Nephrogenic , Diabetes Insipidus , Diabetes Mellitus , Arginine Vasopressin/genetics , Diabetes Insipidus, Nephrogenic/diagnosis , Diabetes Insipidus, Nephrogenic/etiology , Diabetes Insipidus, Nephrogenic/therapy , Humans , Mutation , Polyuria/diagnosis , Quality of LifeABSTRACT
La diabetes insípida (DI) es un síndrome caracterizado por poliuria y polidipsia asociado a la producción crónica de grandes volúmenes de orina diluida, secundario a una disminución de la secreción o acción de la hormona antidiurética (ADH) [1]. El litio es el principal fármaco implicado en la inducción de esta patología cuando se presenta de forma secundaria. [2]. Se presentan 2 reportes de casos de niños de 10 y 12 años con uso de litio por diagnóstico de trastorno del ánimo. Palabras Clave: Diabetes Melitus, trastornos del ánimo, nefrogénica, litio, hormona antidiurética
Diabetes insipidus (DI) is a syndrome characterized by polyuria and polydipsia associated with the production of large volumes of diluted urine, secondary to a decrease in the secretion or action of antidiuretic hormone (ADH) [1]. Lithium is the main drug involved in the induction of this pathology when it appears with a preventable cause [2]. Two case reports of children 10 and 12 years old with mood disorder and lithium use are presented with the intention of being alert to clinical manifestations and observation by caregivers.Key words: Diabetes insipidus, mood disorders, nephogenic, lithium, antidiuretic hormone.
Subject(s)
Humans , Male , Child , Bipolar Disorder/drug therapy , Lithium Compounds/therapeutic use , Diabetes Insipidus, Nephrogenic/etiology , Antidepressive Agents/therapeutic use , Lithium Compounds/adverse effectsABSTRACT
Introducción. Es característico del síndrome nefrótico (SN) la presencia de recaídas, aún en niños que inicialmente respondieron satisfactoriamente con prednisona y que presentaron remisión completa. Muchos de estos pacientes viven en condiciones que retardan el inicio del tratamiento o provocan la aparición de complicaciones: peritonitis, sepsis, celulitis, neumonía o trombosis venosas. Estas últimas generalmente localizada en la vena renal, pero puede presentarse en cuanquier sitio anatómico. Caso clínico. Se presenta el caso de un niño de años de edad, que durante una recaída de SN desarrolló una trombosis cerebral en el seno venoso longitudinal superior, además de diabetes insípida de origen central, así como intoxicación por fenotiazinas, que inicialmente fue causada de varias manifestaciones extrapiramidales. Se analiza la evolución de la trombosis y de la diabetes insípida, señalando la resolución favorable que se obtuvo con su manejo conservador. Conclusión. Se destaca la importancia de efectuar un estudio de tomografía axial computada de cráneo en los niños que durante una recaída de SN presentan deshidratación con cefalea o crisis convulsivas