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Carbamazepine and oxcarbazepine are antiepileptic drugs which can induce hyponatremia, being this disorder more frequent with the latter.In this report we present a clinical case regarding an oxcarbazepine induced hyponatremia, and we hypothesized that oxcarbazepine could induce hyponatremia as a consequence of its influence on distal nephron where it could promote free water retention, urinary sodium loss, or both of them.Besides, we proposed that a greater tubular sesitivity to oxcarbazepine than to carbamazepine could explain the different hyponatremia inducing capability between these two drugs

La carbamazepina y la oxcarbazepina son drogas antiepilépticas potencialmente inductoras de hiponatremia, siendo este disturbio más frecuente con ésta última.En este reporte presentamos un caso de hiponatremia inducida por oxcarbazepina, y proponemos una potencial explicación fisiopatológica para esta entidad, a la cual se la considera consecuencia de un aumento a nivel de los túmulos colectores de la reabsorción de agua libre, de la pérdida urinaria de sodio, o de ambos fenómenos combinados.Además, postulamos que la mayor propensión a la aparición de hiponatremia con el uso de oxcarbazepina respecto del empleo de carbamazepina podría ser consecuencia de una mayor sensibilidad de los túmulos colectores a la primera de las drogas mencionadas.

Gaucher´s disease consists of a genetic autosomic recesive alteration that leads to a reduction in the acid glucosil-ceramide beta-glucosidase enzyme. This enzyme brakes the glucosilceramide, a substance from which many esphingo and glucolipids are synthesized. Even though the renal compromise is not frequent in Gaucher disease, proteinuria (in nephrotic range or not) and glomerulonephritis have been described in this illness.Fanconi syndrome is charaterized by a dysfunction in the proximal tubular reabsorption. Among the etiologies of Fanconi syndrome there are many metabolic diseases, but no association has been described yet in the literature between Fanconi syndrome and Gaucher disease. We present the following case report where this association was observed.

La enfermedad de Gaucher es un trastorno genético autosómico recesivo generador de un déficit de la enzima lisosomal glucosilceramida-beta-glucosidasa ácida. Dicha enzima degrada la glucosilceramida, sustancia a partir de la cual se sintetizan muchos esfingo y glucolípidos. La falta de su degradación conduce a su almacenamiento en los macrófagos tisulares con las consiguientes complicaciones mecánicas y funcionales. El compromiso renal es infrecuente en esta enfermedad, pero cuando se presenta lo hace bajo la forma de proteinuria aislada o glomerulonefritis.El sindrome de Fanconi consiste en la disfunción parcial o total de los túbulos proximales renales. Existen diversas entidades que pueden inducir este síndrome, pero no hay hasta ahora informes en la literatura que lo vinculen con la enfermedad de Gaucher.Presentamos un caso clínico en el cual se logró documentar dicha asociación.

El síndrome de secreción inadecuada de hormona antidiurética (SIADH) es una condición que puede asociarse a diversas neumopatías.En el presente reporte clínico se presenta un caso de SIHAD asociado a un tromboembolismo pulmonar. Hasta donde sabemos, la asociación entre TEP y SIHAD no había sido reportada aun en la literatura, y presentamos como hipótesis etiológica la liberación de citoquinas inductoras de la secreción de vasopresina, secundaria al daño parenquimatoso pulmonar del TEP.Conclusion: El tromboembolismo de pulmón podría ser incorporado a las causas pulmonares de SIADH.

Syndrome of inadequate secretion of antidiuretic hormone (SIADH) is a condition that can be associated to various sort of lung diseases.In this report we present a clinical case where a SIADH associated to pulmonary thromboembolism was documented. As long as we know, this association has not been described yet in the literature, and we hypothesized that lung cytokines released due to pulmonary necrosis could be the main stimulus to vasopressin secretion in this entity.Conclusion: Pulmonary thromboembolism should be incorporated in the list of lung causes of SIADH.

Acute renal failure is a frequent entity in the elderly. This is due on one hand to the structural and physiological changes of the aged kidney, and on the other hand to the exposure of this population to polypharmacy and their reduced capability to metabolize drugs. In the present report we present a case of a seventy year-old woman who developed acute renal failure secondary to severe dehydration with a clinical and laboratory pattern of intermediate syndrome: laboratory results compatible with parenchymal renal insufficiency (elevated urinary sodium, plasma urea and creatinine), but with a positive response to hydration. The main characteristics of the aged kidney that predispose to the development of an intermediate syndrome are: the vascular dysautonomy and reduced capability of sodium and water reabsorption. The intermediate syndrome is a typical pattern of pre-renal insufficiency in the elderly. RESUMEN: La insuficiencia renal aguda es frecuente en el anciano. Esto se debe por un lado a los cambios estructurales y funcionales propios del riñón senil, y por otro a la gran exposición que esta población tiene a la polifarmacia, y su reducida capacidad para metabolizar los medicamentos. En este reporte presentamos el caso de una mujer de 70 años que desarrolló una insuficiencia renal aguda secundaria a severa deshidratación, mostrando un patrón clínico y de laboratorio propio de un sindrome intermedio: laboratorios compatibles con una insuficiencia renal parenquimatosa (sodio urinario, uremia y creatininemia elevadas), pero con una respuesta favorable a la hidratación. Las principales características del riñón senil que predisponen al desarrollo del sindrome intermedio: son la disautonomía vascular y la reducida capacidad en la recuperación de sodio y agua El sindrome intermedio es un patrón típico de insuficiencia prerrenal en el anciano.

Acute renal failure is a frequent entity in the elderly. This is due on one hand to the structural and physiological changes of the aged kidney, and on the other hand to the exposure of this population to polypharmacy and their reduced capability to metabolize drugs. In the present report we present a case of a seventy year-old woman who developed acute renal failure secondary to severe dehydration with a clinical and laboratory pattern of intermediate syndrome: laboratory results compatible with parenchymal renal insufficiency (elevated urinary sodium, plasma urea and creatinine), but with a positive response to hydration. The main characteristics of the aged kidney that predispose to the development of an intermediate syndrome are: the vascular dysautonomy and reduced capability of sodium and water reabsorption. The intermediate syndrome is a typical pattern of pre-renal insufficiency in the elderly. RESUMEN: La insuficiencia renal aguda es frecuente en el anciano. Esto se debe por un lado a los cambios estructurales y funcionales propios del riñón senil, y por otro a la gran exposición que esta población tiene a la polifarmacia, y su reducida capacidad para metabolizar los medicamentos. En este reporte presentamos el caso de una mujer de 70 años que desarrolló una insuficiencia renal aguda secundaria a severa deshidratación, mostrando un patrón clínico y de laboratorio propio de un sindrome intermedio: laboratorios compatibles con una insuficiencia renal parenquimatosa (sodio urinario, uremia y creatininemia elevadas), pero con una respuesta favorable a la hidratación. Las principales características del riñón senil que predisponen al desarrollo del sindrome intermedio: son la disautonomía vascular y la reducida capacidad en la recuperación de sodio y agua El sindrome intermedio es un patrón típico de insuficiencia prerrenal en el anciano.

Chronic dialysis is a valid therapeutic option in very elderly ESRD patients, even though the decision to dialyze or not has little impact on survival. Additionally, very old patients usually do not agree with starting chronic dialysis. Even though, activated charcoal is a cheap treatment for working as adsorbent for nitrogenous products its utility is very limited. We studied the combination of a low protein diet and oral activated charcoal to reduce serum urea and crea-tinine levels in very old ESRD patients who had refused to start chronic dialysis. Nine lucid, very old > 80 years, ESRD patients who had refused to start dialysis were prescribed a treatment based on a combination of a very low protein diet and oral activated charcoal (30 gram/day). None of the patients had anuria, oliguria, edema, significant metabolic acidosis or hyperkalemia. None of them had significant gastrointestinal symptoms. After one week and ten months of charcoal use signi-ficant decrease in blood urea and creatinine levels was observed and none of them required emer-gency dialysis during this time. In conclusion, in patients more than 80 years of age low protein diet and oral activated charcoal may control the uremic symptoms effectively.

The handling of renal creatinine in human beings has classically been described as the result of two particular physiological processes: glomerular filtration and proximal tubular secretion. However, there are particular physiological situations in which tubular creatinine reabsorption has been documented, such as in the case of healthy newborns and premature babies. We performed a prospective study in order to evaluate if there is tubular creatinine reabsorption in healthy elderly people. We studied prospectively nine healthy volunteers, four of them young (20–33 years old) and the remaining five, old (65–73 years old). Since creatinine is secreted in the proximal tubules, and its secretion can be completely blocked by cimetidine administration, a creatinine clearance with cimetidine reliably represents the glomerular filtration rate. Therefore, if the ratio creatinine clearance (Ccr)/creatinine clearance with cimetidine (CcrWC) is higher than one, this would indicate net creatinine secretion, whereas a ratio lower than one would indicate a net renal creatinine tubular reabsorption; a ratio equal to one indicates creatinine filtration. Finally, the Ccr, CcrWC, and Ccr/CcrWC ratios were compared between the young and old group. Mann-Whitney and Wilcoxon tests were used. As expected, creatinine clearance in the elderly was significantly lower than in the young [Ccr: 74.4 ml/min (47.9–100.9) (old) vs. 153.8 ml/min (108.3–199.2) (young), p = 0.014]. Similarly, the creatinine clearance with cimetidine (CcrWC) was significantly lower in the elderly compared to the young [CcrWC: 81.8 ml/min (69.2–94.5) (old) vs. 122.5 ml/min (82.6–162.4) (young), p = 0.028]. The ratio of Ccr/CcrWC was 0.9 in the elderly vs. 1.26 in the young (p = 0.014), indicating net creatinine reabsorption in the elderly and net creatinine secretion in the young. Our findings indicate that there seems to be a net reabsorption of creatinine in the renal tubules of healthy old persons.

Furosemide test is a simple and useful test of renal physiology used to evaluate the capability of the collecting ducts to secrete potassium under the effect of serum aldosterone. Its behaviour pattern has been established in children and young adults but not described in very old healthy people, which we explored in this study.Twenty-six healthy volunteers on a standard Western diet (50 mmol of K/day) were studied: 20 of them were young (between 17 and 40 years old) and the rest were very old (between 75 and 85 years old). They suffered from no diseases and were not on any medication. Before, during the test and 180 min after a single dose of intravenous furosemide (1 mg/kg), urine and blood samples were obtained for creatinine and electrolytes levels. From these data we calculated fractional excretion (FE) of electrolytes; serum aldosterone was measured pre and post furosemide infusion. Statistical analysis was performed by applying Student's t-test.There was no significant difference regarding pre-furosemide (basal) FE of potassium between the very old and young group. Post-furosemide average FE of potassium was significantly lower in the very old group (27.4 +/- 2%) compared with the young group (35.4 +/- 9%) (P = 0.04). Even though there was no significant difference in post-furosemide peak FE of potassium value, it was reached later in the very old (120 min) compared with the young (30 min). Serum aldosterone levels were significantly higher post furosemide in both groups: 18.3 +/- 12.2 ng/dl (pre) versus 32.5 +/- 18.6 ng/dl (post) in the young (P = 0.007) and 69.8 +/- 13.7 ng/dl (pre) versus 113.3 +/- 54.8 ng/dl (post) in the very old (P = 0.04). Furthermore, all serum aldosterone values (pre and post furosemide) were significantly higher in very old people compared with young people (P0.001). Basal fractional excretion of sodium and chloride were slightly higher in the very old group compared with the young group (P = 0.05). Average post-furosemide FE of sodium and chloride were slightly and significantly lower in the very old (P = 0.05 and P = 0.03), respectively. However, there was no significant difference in peak post-furosemide FE of sodium and chloride values, which were reached later in the very old (120 min) compared with the young (30 min).Furosemide test showed a significantly lower average post-furosemide FE of potassium value, delayed post-furosemide peak FE of Na, K and Cl and a hormonal pattern of aldosterone resistance in very old people.