ABSTRACT
Los niños con lesiones selares y/o supraselares pueden presentar diabetes insípida central con posterior secreción inadecuada de hormona antidiurética. Nosotros observamos, en algunos casos, aumento de la incidencia de poliuria, natriuresis e hiponatremia, tríada diagnóstica del síndrome cerebral perdedor de sal. Aquí comunicamos la evolución de 7 pacientes con antecedentes de daño agudo del sistema nervioso central y diabetes insípida central seguida por síndrome cerebral perdedor de sal. Como tratamiento aportamos secuencialmente fluidos salinos parenterales, cloruro de sodio oral, desmopresina, mineralocorticoides e incluso tiazidas. Ante la persistencia de poliuria con hiponatremia, agregamos ibuprofeno. Como resultado de este esquema terapéutico secuencial, este grupo redujo significativamente los valores de diuresis diaria de 10 ml/kg/h a 2 ml/kg/h en un tiempo promedio de 5 días, normalizando también las natremias (de 161 mEq/L a 143 mEq/L) en un tiempo promedio de 9 días. En ningún caso observamos efectos adversos asociados al tratamiento.
Children with sellar and/or suprasellar lesions may develop central diabetes insipidus with subsequent inappropriate antidiuretic hormone secretion. An increased incidence of polyuria, natriuresis, and hyponatremia has been reported in some cases, which make up the diagnostic triad of cerebral salt wasting syndrome. Here we report the clinical course of 7 patients with a history of acute central nervous system injury and central diabetes insipidus followed by cerebral salt wasting syndrome. Treatment included the sequential use of parenteral saline solution, oral sodium chloride, desmopressin, mineralocorticoids, and even thiazides. Due to persistent polyuria and hyponatremia, ibuprofen was added. As a result of this sequential therapeutic regimen, daily urine output reduced significantly from 10 mL/ kg/h to 2 mL/kg/h over an average period of 5 days, together with a normalization of natremia (from 161 mEq/L to 143 mEq/L) over an average period of 9 days. No treatment-related adverse effects were observed in any case.
Subject(s)
Humans , Child, Preschool , Child , Adolescent , Diabetes Insipidus, Neurogenic , Hyponatremia/etiology , Hyponatremia/drug therapy , Polyuria/complications , Polyuria/etiology , Research , Ibuprofen/therapeutic useABSTRACT
In patients with acute cerebral injury, polyuric states can potentially trigger, maintain and aggravate the primary neurological damage, due to hypovolemia, arterial hypotension and alterations of osmolarity. The true incidence of the condition in this population is unknown. A widely validated definition of polyuric state is lacking and its etiology is multifactorial. There are two principal classes of polyuria: a) aqueous polyuria with diabetes insipidus as the main cause; and b) osmotic polyuria in which sodium, glucose or ureaplay the main role. Polyuric states are in close association with disorders of water and sodium metabolism and with alterations in acid-base balance. A detailed analysis of the history, clinical picture and simple laboratory determinations in blood and urine, are required for an adequate assessment of these polyuric states. The problem must be faced with pathophysiological reasoning and a systematic and sequential approach, because each disorder needs a specific therapy.
Subject(s)
Humans , Brain Injuries/complications , Polyuria/diagnosis , Polyuria/therapy , Brain Injuries/physiopathology , Polyuria/complications , Polyuria/physiopathologyABSTRACT
To investigate the efficacy and safety of desmopressin in patients with mixed nocturia, Patients aged > or =18 yr with mixed nocturia (> or =2 voids/night and a nocturnal polyuria index [NPi] >33% and a nocturnal bladder capacity index [NBCi] >1) were recruited. The optimum dose of oral desmopressin was determined during a 3-week dose-titration period and the determined dose was maintained for 4 weeks. The efficacy was assessed by the frequency-volume charts and the sleep questionnaire. The primary endpoint was the proportion of patients with a 50% or greater reduction in the number of nocturnal voids (NV) compared with baseline. Among 103 patients enrolled, 94 (79 men and 15 women) were included in the analysis. The proportion of patients with a 50% or greater reduction in NV was 68 (72%). The mean number of NV decreased significantly (3.20 to 1.34) and the mean nocturnal urine volume, nocturia index, NPi, and NBCi decreased significantly. The mean duration of sleep until the first NV was prolonged from 118.4+/-44.1 to 220.3+/-90.7 min (P<0.001). The overall impression of patients about their quality of sleep improved. Adverse events occurred in 6 patients, including one asymptomatic hyponatremia. Desmopressin is an effective and well-tolerated treatment for mixed nocturia.
Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Administration, Oral , Antidiuretic Agents/administration & dosage , Deamino Arginine Vasopressin/administration & dosage , Drug Administration Schedule , Nocturia/complications , Polyuria/complications , Prospective Studies , Surveys and Questionnaires , Sleep/drug effects , Urinary Bladder/physiopathology , Urodynamics/physiologyABSTRACT
Most cases of hydronephrosis are caused by urinary tract obstruction. However, excessive polyuric syndrome rarely gives rise to non-obstructive hydronephrosis, megaureter, and a distended bladder. The authors report here on two cases of congenital nephrogenic diabetes insipidus (NDI) with severe bilateral hydronephrosis and megaureter. It is Interesting that the patients were symptomless except for their polyuria, and they both presented with bilateral hydronephrosis. Fluid deprivation testing revealed the presence of AVP resistant NDI. Gene analysis for these patients showed the AVP receptor 2 (V2R) missense mutations (Q225X and S126F), which have previously been reported on in other studies. We made the diagnosis of NDI by using a physiologic test, and we confirmed it by mutation analysis of the V2R gene.
Subject(s)
Male , Humans , Adult , Receptors, Vasopressin/genetics , Polyuria/complications , Mutation, Missense , Hydronephrosis/complications , Diabetes Insipidus, Nephrogenic/complications , DNA Mutational AnalysisABSTRACT
La Diabetes Insípida es un síndrome caracterizado por la presencia de poliuria, polidipsia, hiperosmolidad sérica e hipostenuria en ausencia de insuficiencia renal. Se estudiaron 6 pacientes controlados por el Servicio de Nefrología del Hospital "J.M de los Rios", durante el período 1974-1989. 7 pacientes corresponden a diabetes Insípida central, y 9 pacientes de Diabetes Insípida nefrogénica. Concluimos que el mejor diagnóstico diferencial se verifica por la prueba de privación híbrica sensibilizada con vasopresina. Encontramos hallazgos de Acidosis Tubular distal e hipercalciuria concominantes. La Diabetes Insípida en una entidad que requiere minucioso estudio, con tratamiento individualizado según el tipo, y por cada paciente, y cuyo pronóstico está regido por la patología de base, y por el cumplimiento terapéutico
Subject(s)
Humans , Male , Female , Diabetes Insipidus/diagnosis , Diabetes Insipidus/therapy , Polyuria/complicationsABSTRACT
We present two patients with tumoral lesions of the hypothalamic area, which developed hypernatremia, polyuria and polydipsia due to hypodipsia and ADH deficiency related to the simultaneous compromising of the thirst regulating center and of ADH production.