Postdiarrheal Shiga toxin-mediated hemolytic uremic syndrome similar to septic shock

The inflammatory response of host endothelial cells is included in the development of vascular damage observed in enterohemorrhagic Escherichia coli (EHEC) infection, resulting in hemolytic uremic syndrome (HUS). The response to a non-conventional treatment for a group of D+ HUS (diarrhea positive HUS) patients, with clinical hemodynamic parameters of septic shock was evaluated in this prospective study (1999-2003). Twelve children 2.8 +/- 0.6 years old, with D+ HUS produced by E. coli infection with serological evidence of Shiga toxin, presenting severe unstable hemodynamic parameters and neurological dysfunction at onset, were studied. The protocol included fresh frozen plasma infusions, methylprednisolone pulses (10mg/k/day) for three consecutive days and plasma exchange for five days, starting after admission to the intensive care unit (ICU). The twelve patients with increased pediatric risk of mortality (PRISM) score: 18 +/- 2 after admission to intensive care unit (ICU), required dialysis for 17.4 +/- 4 days, mechanical ventilator assistance for 10 +/- 1 days and early inotropic drugs support for 10.5 +/- 1 days. Neurological dysfunction included generalized tonic-clonic seizures lasting for 5.4 +/- 1 days, n:8. Focal seizures were present in the remaining patients. Dilated cardiomyopathy was present in 6 children. Eight children suffered hemorrhagic colitis. Nine patients survived. Within one year of the injury, neurological sequelae, Glasgow outcome scale (GOS) 3 and 4, were present in two patients, chronic renal failure in one patient. We suggest that early introduction of this protocol could benefit D+ HUS patients with hemodynamic instability and neurological dysfunction at onset. Further studies are likely to elucidate the mechanisms involved in this early adverse clinical presentation of D+ HUS patients.

La respuesta inflamatoria de la célula endotelial se incluye en el desarrollo del daño vascular observado en la infección por Escherichia coli enterohemorrágica que deviene en Síndrome Urémico Hemolítico (SUH). Se evaluó en forma prospectiva, entre 1999 y 2003, la respuesta a un tratamiento no convencional, en doce pacientes, edad 2.8 ± 0.6 años, que desarrollaron SUH con presencia de diarrea sanguinolenta (SUH D+) y evidencia serológica de toxina Shiga, los cuales en fase inicial presentaron parámetros hemodinámicoscompatibles con shock séptico y compromiso neurológico grave. El protocolo incluyó transfusión de plasmafresco, pulsos de metilprednisolona (10mg/k/día) por tres días consecutivos y plasmaféresis por cinco días, iniciados en las primeras 48 horas. Los doce pacientes ingresaron en terapia intensiva, presentando unapuntuación de riesgo de mortalidad pediátrica (PRISM): 18 ± 2, con requerimiento de diálisis por 17.4 ± 4 días, asistencia ventilatoria mecánica por 10 ± 1días y soporte temprano con drogas inotrópicas por un período de10.5 ± 1 días. La disfunción neurológica se presentó con convulsiones tónico-clónicas generalizadas por 5.4 ±1 días en 8 pacientes y con convulsiones focalizadas en los restantes. Seis pacientes desarrollaron miocardiopatíadilatada y 8 presentaron colitis hemorrágica. Sobrevivieron a la etapa aguda de la enfermedad 9 pacientes. Alfinalizar el primer año de seguimiento, dos de ellos presentaban secuelas neurológicas (escala de seguimientode Glasgow; GOS 3 y 4 respectivamente) y uno, fallo renal crónico. La introducción temprana de este protocolo podría beneficiar a pacientes con SUH D+ con inestabilidad hemodinámica grave y disfunción neurológica al inicio. Los mecanismos involucrados en esta temprana presentación clínica adversa de SUH D+ permanecen aún sin dilucidar.

Effect of glandular kallikrein on distal bicarbonate transport. Role of basolateral Cl-/HCO3- exchanger and vacuolar H(+)-ATPase

The luminal membrane of collecting duct cells, specially the intercalated cells, is normally exposed to active kallikrein. This is due to the specific localization of renal kallikrein in the connecting tubule cells. We have previously reported inhibition of distal bicarbonate secretion by renal kallikrein. The present study was performed to evaluate the participation of basolateral Cl-/HCO3- exchanger and luminal H(+)-ATPase activity of cortical collecting duct segments (CCD) in the mechanism involved in the inhibition of bicarbonate secretion induced by the enzyme. The effect of orthograde injections of 1 microgram/ml (250 U/6.3 mg) pig pancreatic kallikrein, in the absence and presence of 1 mM DIDS (stilbene-disulfonic acid) in the renal tubule system, was evaluated. Urine fractions were collected after two-minutes stop-flow. Changes in the urine fraction (Fr) related to those in free-flow urine samples (Ff) were related to the respective polyfructosan (Inutest) ratio. Renal kallikrein activity (Fr:Ff kallikrein/Fr:Ff polyfructosan) increased significantly in the first 120 microliters urine fraction collected after glandular 1 microgram/ml kallikrein, P < 0.05, (first stop-flow) and after glandular 1 microgram/ml kallikrein plus 1 mM. DIDS P < 0.05 (second stop flow). Bicarbonate secretion rate (Fr:Ff HCO3-/Fr:Ff polyfructosan) of collecting ducts was significantly reduced in the first 120 microliters urine fraction collected, related to control, during the first and second stop-flow periods. No difference was shown in bicarbonate excretion between the first 120 microliters urine fractions collected after administration of glandular kallikrein and glandular kallikrein plus DIDS. To measure H(+)-ATPase activity, rat microdissected cortical collector tubules (CCD) were incubated in the presence of increasing glandular kallikrein doses (A: 93, B: 187 and C: 375 mU/200 microL) in the presence of ouabain (4 microM) and omeprazole (100 microM) to inhibit Na(+)-K(+)-ATPase and H(+)-K(+)-ATPase, respectively. In CCD, bafilomycin-sensitive H(+)-ATPase activity (pmol/mm/min) after increasing kallikrein doses did not differ significantly from control...

Inmunidad celular en sindrome nefrotico a cambios minimos. / Cellular immunity with minimal changes in nephrotic syndrome

Varios autores han referido la probable participacion de la inmunidad mediada por celulas en la fisiopatogenia del sindrome nefrotico a cambios minimos (SNCM). El objeto de esta comunicacion fue estudiar cuantitativamente la inmunidad celular y establecer su posible participacion en SNCM. Nuestras observaciones sugieren una disminucion de las celulas T circulantes en SNCM con respecto a los ninos del grupo control. Esta disminucion puede estar dada por un bloqueo del receptor para eritrocitos de carnero a nivel de la membrana linfocitaria por factores sericos o por una reducion real de celulas T circulantes

Tratamiento local de quemaduras con rifamicina en metodo expuesto. / Local treatment of burns with rifamycin by non-occlusive method

Se describen los resultados obtenidos en el tratamiento de 25 pacientes quemados, usando el metodo expuesto con rifamicina. Los resultados fueron de buenos a excelentes en cuanto a morbimortalidad. No se presentan casos de intolerancia al medicamento