This report concerns a patient with cystic h'brosis, who initially presented hipokalemia, hypochloremia and metabolic alkalosis, associated with normal blood pressure. Sweat test was positive. We studied the chloride reabsortion in trie distal collector tubule, wich was normal.We analize the pathophysiology of"the metabolic alkalosis and its relationship with chloride metabolism.El diagnostico direrencial de la alcalosis metabolica hipokalemica cuando se acornpana de hiperaldosteronismo secundario y presion arterial normal suele ser un problema diagnostico. La identiticacion de la via por donde se pierde potasio, ha sido en el pasado el camino usual para llegar al diagnostico etiologico. Sin,embargo, la alcalosis "per se", ya sea metabolica o respiratoria, puede indueir perdida renal de potasio, 1 con lo cual la mera eonstatacion de kaliuresis adquiere una utilidad diagn6stica relativa.No ocurre lo mismo con el cloro, cuyo inanejo renal suele ser diterente segiin cual sea la etiologia de la alcalosis. En el Sindrorne de Bartter, que frecuentemente es considerado en el diagnostico diferencial de estos pacientes, debido a que se presenta con hipokalemia, kaliuresis, alcalosis metabolica, hiperplasia del aparato yuxtaglome- rular con hiper-reninemia, hiperaldosteronisino secundario y presion arterial nonnal, se he descrito perdida "obligatoria" de cloro por el rinon. 2En cambio, cuando la alcalosis se debe a un trastorno extra-renal el rinon puede electuar ajustes que se traducen en mayor reabsorcion de cloro con minima excrecion urinaria de este anion. Deseamos destacar la importancia de estos mecanismos a proposito del caso de un paciente con alcalosis metabolica hipokalemica en quien se pudo descartar el diagnostico de Sindrome de Bartter, a traves del estiidio de la absorcion renal de cloro, llegandose posteriormente al diagnostico de fibrosis qnistica del pancreas. CASOCLIMCO L.G.S., sexo masculino. P.N. 4.050 grs. Sin antecedentes de importancia.Su historia comienza a los 28 dias de edad, consultando pordiarrea, vomitos y tos. Al examen tisico solo se encuentran escasos estestores bronquiales, sin signos de condensacion. Es tratado solo con indicaciones dieteticas. Este episodio se repite en 4 oportunidades con las mismas carac-233

Eight children with end-stage renal failure were treated by intermittent peritoneal dialysis (IPD) from 19iS3 to 1985 in a Metropolitan hospital at Santiago, Chile. Six females and two males ranging 2 years 1 month to 12 years 10 months of age were included. The Tenckhoff catheter was used and all the patients were mantained on peritoneal dialysis every 3 days, during 24 hours, for periods of 1 to 7 months. Anthropometric, biochemical and hematological evaluations were performed twice a month. Six out of 8 patients were grafted with kidneys from live related donnors, the other two are waiting a donnor. Peritonitis was detected in a 3 patients, and catheter obstruction ocurred in other two children. It is concluded that IPD is useful in the treatment of uremic children and is valuable in end-stage renal failure waiting for transplantation. La dialisis peritoneal ha tenido una buena aceptacion entre los pediatras debido a los resultados obtenidos en comparacion con la hemodialisis 1 ' 2 . En muchos pai'ses se usa la peritoneo dialisis ambulatoria como im procedimiento que ha salvado innumerables vidas y ha permitido realizar transplantes renales en mejores condiciones. La mayor experiencia existe con el uso de la dialisis peritoneal continua ambulatoria (DPCA) y en menor escala con dialisis peritoneal intermitente (DPI), aunque esta ultima data de 1962 3 . La DPI se realiza habitualmente con sistemas automatizados, que nan permitido obtener resultados muy satisfactorios dado lo eficiente del sistema y la pocaincidencia de complicaciones 4 " 7 ,aunque con DPI manual se nan publicado experiencias similares 8 -9 . Durante los ultimos anos se han efectuado varias publicaciones acerca de la peritoneo dialisis en nifios con insuficiencia renal cronica terminal, y recientemente Fine y Gruskin resumen esta experiencia desde el punto de vista historico,

Renal scars and P blood subgroup Possible relationships between renal scars and P blood group have been 'ecently emphasized. Urinary tract infections, an important factor in the production of renal scar, are mainly caused by specific types of E. coll, which has the ability to adhere through fimbriae, to receptors of the urinary tract epithelium that are structurally related to antigens detected in people with blood group P1. We looked for Pi subgroup in 30 children with vesicourete r a5 reflux and rena! scar and 30 patients with equivalent degrees of reflux but without evidence of renal scar. Sex and age were unmatched. Thefrequency of PI blood subgroup was similar in both kinds of patients (56.7% vs. 66.7, n.s.) so we could not demonstrate that P1 subgroup can be a useful Indirect risk marker for rena' scar formation.

A seven years olf female was admitted to Luis Calvo Mackenna Children's Hospital. Her past history was remarkable in that she had had fever for the preceding months. Her physical, examination disclosed no pulses at her right brachial artery. Blood pressure in her left upper extremity was 200/150 and the erytrosedimentation rate was 124mm. in the first hour, Aortography showed contour irregularities, and the presence of stenosis and dilations subtantiated. a diagnosis of Takayasu disease. After treatment with steroids and a ntihy per tensive drugs improvement was noted. A review of the current theory of the etiology of this disease as well as the modes of treatment and follow up are included.

According to the heterogenous nature of hemolityc uremic syndrome in relation to the etiology, pathophisiology, treatmente and diagnosis, we wich to draw attention to the main characteristics about its epidemiological clinical and immunopathological aspects. The HUS's distributes through all the world, but in Argentina, North oÊ urope, South Africa and west of USA the incidence is higher than the rest of the counties. The immune-pathological studies shows thrombotic angiopatic lesion, consisting ir generalized alte'ation of the capilar and arteriolar epithelium. Decreased levels OT PGI 2 , Von Willebrand's factor and bacterial toxins are apparently involved among mechanism that are able to produce HUS. Dial'sis is one of the main helps in the treatment of HUS, and in spite of our continued advances in knowledge about this disease, still 'urther developments are needed in pathophisiology and therapeutics to enlight its intimate mechanisms.(Key words: haemolityc uremic syndrome).El sindrome hemolitico uremico (SHU) resulta de la accion de numerosos factores etiologicos y patogenicos. En la decada del 50 Gasser y col. sistematizaron la informacion existente sobre este problema y acufiaron el terrain o de SHU 1 ' 8 .La informacidn reciente ha aclarado considerablemente la naturaleza del cuadro. En la actualidad se observa aumento de su incidencia y expansion a niveles etarios de adolescentes, adultos y ancianos 9 ' 11 , por lo tanto, el pediatra, el internista y el geriatra deben familiarizarse con el SHU. Este escrito enfoca algunos aspectos etiologicos, patogenicos y terapeuticos de relevancia clinica practica del smdrome, cuyas consecuencias pueden ser devastadoras. El tema ha sido evaluado en forma exhaustiva en otras publicaciones 2 ' 6 > 12 > 17 > 57 . Caracterfsticas clinicas y epidemiologicasEl SHU puede ocurrir a cualquiera edad, es precedido generalmente por infeccion respira-