This study confirms the renal morphology of MeN: chronic glomerular and tubulointerstitial damage with glomerulosclerosis and chronic glomerular ischemia. Follow-up data show that eGFRs, on average, deteriorated.

No abstract

The purpose of the present study was to evaluate the potential of the Na+/H+ exchange inhibitor cariporide to protect the lung from injury after cardiopulmonary bypass (CPB). In a randomized placebo-controlled study, 16 pigs were subjected to CPB for 75 min. Administration of vehicle or cariporide (bolus 180 mg, 40 mg/hour) began 30 min pre-CPB and was continued throughout the protocol. The alveolo-arterial O2-gradient (AaDO2), the pulmonary shunt (Qs/Qt), the compliance (Cpl), haemodynamic variables and glycerol and water content in lung tissue were measured 10 min before and up to 180 min post-CPB. All animals in the control versus 75% in the cariporide group survived the experiment. At 5 and 60 min post-CPB, the mean AaDO2 and at 5, 60 and 180 min post-CPB, the mean pulmonary vascular resistance index were higher in the cariporide group (p < 0.05), respectively. More lung water accumulation was found in the cariporide group (p < 0.05). Mean Cpl decreased; the Qs/ Qt and glycerol in lung tissue increased without significant intergroup difference. In this model, the inhibitor of the Na+/H+ antiporter showed no protective effect on lung injury after CPB and might even have harmful effects on pulmonary vascular tone and function.

We observed no effect of i. v. cariporide on LV function or myocardial damage after cardioplegic arrest. Our data suggest that cariporide is washed out of the myocardium by repeated application of crystalloid cardioplegia. Thus, the mode of delivery also appears to be critical for cardioprotection with NHE-inhibitors.

Se presenta el caso de un hombre adulto con fenómeno de Raynaud secundario y refractario al manejo médico asociado a vasculitis cutánea, que previamente venía recibiendo interferón beta para tratamiento de esclerosis múltiple. La agresividad del proceso requiere la interrupción de la medicación, la utilización de vasodilatadores, inhibidores de endotelina 1, simpatectomía bilateral por video toracoscópia, aplicación de toxina botulínica peri-arterial interdigital en manos y terapia inmunosupresora con corticoide a altas dosis y ciclofosfamida obteniendo detención del proceso isquémico, pero con pérdida anatómica asociada.