ABSTRACT
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
Diabetes insipidus (DI) is characterized by excessive urination and thirst. This disease results from inadequate output of antidiuretic hormone (ADH) from the pituitary gland or the absence of the normal response to ADH in the kidney. We present a case of transient central DI in a patient who underwent a cardiopulmonary bypass (CPB) for coronary artery bypass grafting (CABG). A 44-yr-old male underwent a CABG operation. An hour after the operation, the patient developed polyuria and was diagnosed with central DI. The patient responded to desmopressin and completely recovered five days after surgery. It is probable that transient cerebral ischemia resulted in the dysfunction of osmotic receptors in the hypothalamus or hypothalamus-pituitary axis during CPB. It is also possible that cardiac standstill altered the left atrial non-osmotic receptor function and suppressed ADH release. Therefore, we suggest that central DI is a possible cause of polyuria after CPB.
Subject(s)
Adult , Humans , Male , Antidiuretic Agents/therapeutic use , Coronary Artery Bypass/adverse effects , Coronary Vessels , Deamino Arginine Vasopressin/therapeutic use , Diabetes Insipidus, Neurogenic/diagnosis , Hypothalamus/diagnostic imaging , Magnetic Resonance Imaging , Pituitary Gland/diagnostic imaging , Polyuria/diagnosis , Postoperative Complications/diagnosisABSTRACT
Classic Bartter syndrome, depending on the severity, presents during childhood or adolescence as failure to thrive and may be incorrectly labelled as protein–energy malnutrition, particularly in children from a low socioeconomic stratum. We encountered a 5-year-old boy who was asymptomatic till the age of 3 years. Despite adequate dietary intake, he was admitted and managed in various hospitals as a case of protein–energy malnutrition. On evaluation, he had unusual features in the form of persistent hypokalaemia and polyuria leading us to suspect a renal tubular disorder. Treatment of the condition resulted in good weight gain and normalization of serum electrolytes.
Subject(s)
Bartter Syndrome/complications , Bartter Syndrome/diagnosis , Child, Preschool , Diagnosis, Differential , Failure to Thrive/diagnosis , Failure to Thrive/etiology , Humans , Hypokalemia/diagnosis , Hypokalemia/etiology , Male , Polyuria/diagnosis , Polyuria/etiology , Protein-Energy Malnutrition/diagnosisABSTRACT
A case series of four children, of different age groups, having complaints of polyuria and failure to thrive. These cases include two infants, a toddler and a child and investigations revealed that they had hyponatremia, hypokalemia, hyperchloremia and metabolic alkalosis, leading to a diagnosis of Bartters syndrome. Two of the patients also had hypomagnesemia. All the children were put on treatment for Bartter's Syndrome, and they responded well but unfortunately one of them was lost to follow-up
Subject(s)
Humans , Male , Female , Infant , Failure to Thrive/etiology , /diagnosis , Alkalosis/diagnosis , Polyuria/diagnosis , Bartter Syndrome/blood , Bartter Syndrome/classificationABSTRACT
Sinus histiocytosis with massive lymphadenopathy [SHML], Rosai-Dorfman Disease, is a rare histiocytic syndrome first described by Rosai and Dorfman, seen predominantly in childhood and early adulthood. Even though it is considered a benign disease, fatalities may occur due to cellular infiltrates of SHML. We report a 16-year-old boy with signs of polydypsia, polyuria, weight loss and generalized lymphadenopathy. He had been receiving corticosteroid following the diagnosis of histiocytosis X. Due to hyperglycemia, the patient was admitted with the primary diagnosis of diabetic ketoacidosis and medications were initiated. All paraclinical and immunologic examinations were negative. Axillary lymph node biopsy revealed the diagnosis of Rosai-Dorfman disease
Subject(s)
Humans , Male , Adolescent , Hyperglycemia/diagnosis , Diabetic Ketoacidosis/diagnosis , Polyuria/diagnosisABSTRACT
The renal tubule plays an important role in fluid and electrolyte homeostasis. Renal tubular disorders may affect multiple ( e.g., Fanconi syndrome) or specific (e.g., nephrogenic diabetes insipidus, renal glucosuria) tubular functions. Most conditions are primary and monogenic but occasionally are secondary to other disorders (focal segmental glomerulosclerosis, cystinosis, Lowe syndrome). Tubular dysfunction should be considered in all children with failure to thrive, polyuria, refractory rickets, hypokalemia and metabolic acidosis. Careful clinical and laboratory evaluation is essential for appropriate diagnosis and specific management of these conditions.
Subject(s)
Acid-Base Equilibrium , Acidosis, Renal Tubular , Calcium/urine , Child , Humans , Hypokalemia/diagnosis , Kidney Diseases/diagnosis , Kidney Tubules/physiopathology , Polyuria/diagnosis , Urine/chemistryABSTRACT
Se sospecha Síndrome Poliúrico (SP) cuando el volumen urinario excede en 2 a 3 veces lo esperado para la edad o cuando a raíz de una deshidratación o restricción hídrica no se produce concentración urinaria adecuada. El volumen y la osmolaridad de los líquidos orgánicos se regulan con gran precisión gracias a la actividad de la hormona antidiurética (HAD), producida en el eje hipotálamo hipofisiario, que maneja la permeabilidad del agua de los túbulos distales y colectores renales. El SP se clasifica en dos grandes grupos: 1) con niveles plasmáticos bajos de HAD (diabetes insípida central DIC o neurogénica y polidipsia primaria) y 2) con niveles plasmáticos normales de HAD (diuresis osmótica y diabetes insípida nefrogénica DIN). El diagnóstico diferencial se hace con la prueba de deprivación acuosa y el tratamiento consiste en reemplazo hormonal con HAD en DIC y en la DIN reducción del aporte calórico proteico con la ingesta libre de agua, más diuréticos tiazídicos y antiinflamatorios. En el presente artículo se hace una revisión actualizada del SP.
Subject(s)
Humans , Renal Agents/therapeutic use , Polyuria/diagnosis , Polyuria/etiology , Polyuria/drug therapy , Hormone Replacement Therapy , Vasopressins/biosynthesis , Vasopressins/therapeutic use , Diagnosis, Differential , Diabetes Insipidus, Nephrogenic/therapy , Polyuria/classification , SyndromeSubject(s)
Humans , Female , Child, Preschool , Polyuria/diagnosis , Nutrition Disorders/diagnosis , ArgentinaSubject(s)
Adult , Humans , Diabetes Insipidus/diagnosis , Polyuria/diagnosis , Diagnosis, DifferentialABSTRACT
Se entiende por poliuria, la presencia de una diuresis mayor de 80 ml/hr/m* de superficie corporal; habitualmente se trata de una diuresis de 2 a 10 litros por día, la orina presenta, en la mayoría de los casos, una densidad urinaria inferior a 1.005 con osmolaridad de 40 a 200 mOsm/l. Para entender la fisiopatogenia de este signo renal se tienen que conocer los mecanismos normales que intervienen en la concentración de la orina, entendiendo la relación existente entre excreción renal de solutos, concentración urinaria y volumen de orina. El ser humano no puede excretar solutos sin agua, por lo que tiene una pérdida obligatoria de agua a nivel renal, la cual es de aproximadamente 55 ml de agua por cada 100 calorías. En el adulto normal se excretan 600 mOsm por día, en un volumen aproximadamente 2.000 ml, lo que da una osmolaridad urinaria de 300 mOsm/litro. Si un adulto sano se encuentra en el desierto, requiere evitar pérdidas de agua, para lo cual sus riñones concentrarán la orina al máximo, al hacer esto la concentración urinaria aumenta 4 veces de 300 a 1.200 mOsm/l y su volumen urinario disminuye 4 veces de 2.000 a 500 ml, con lo que su organismo se ahorra la pérdida de 1.500 ml. Ahora bien, bajo otra situación, si la ingesta de líquidos ha sido cuantiosa, para evitar una intoxicación acuosa, sus riñones diluyen la orina a su máxima capacidad, con lo cual la osmolaridad urinaria disminuye 5 veces de 300 a 60 mOsm/l y el volumen urinario aumenta 5 veces de 2.000 ml a 10.000 ml