Caffeine intake by patients with autosomal dominant polycystic kidney disease

Because caffeine may induce cyst and kidney enlargement in autosomal dominant polycystic kidney disease (ADPKD), we evaluated caffeine intake and renal volume using renal ultrasound in ADPKD patients. Caffeine intake was estimated by the average of 24-h dietary recalls obtained on 3 nonconsecutive days in 102 ADPKD patients (68 females, 34 males; 39 ± 12 years) and compared to that of 102 healthy volunteers (74 females, 28 males; 38 ± 14 years). The awareness of the need for caffeine restriction was assessed. Clinical and laboratory data were obtained from the medical records of the patients. Mean caffeine intake was significantly lower in ADPKD patients versus controls (86 vs 134 mg/day), and 63% of the ADPKD patients had been previously aware of caffeine restriction. Caffeine intake did not correlate with renal volume in ADPKD patients. There were no significant differences between the renal volumes of patients in the highest and lowest tertiles of caffeine consumption. Finally, age-adjusted multiple linear regression revealed that renal volume was associated with hypertension, chronic kidney disease stage 3 and the time since diagnosis, but not with caffeine intake. The present small cross-sectional study indicated a low level of caffeine consumption by ADPKD patients when compared to healthy volunteers, which was most likely due to prior awareness of the need for caffeine restriction. Within the range of caffeine intake observed by ADPKD patients in this study (0-471 mg/day), the renal volume was not directly associated with caffeine intake.

Malformación de la placa ductal en el desarrollo de la fibrosis hepática congénita. Un estudio inmunohistoquímico / Importance of the ductal plate malformation in the development of congenital hepatic fibrosis. An inmunohistochemical study

La fibrosis hepática congénita es una enfermedad autosómica recesiva caracterizada histológicamente por la presencia de tejido fibroconectivo en los espacios porta con numerosos conductos biliares de mediano calibre. Éste es un estudio inmunofenotípico de la placa ductal y su participación en la génesis de la fibrosis hepática congénita . Se estudiaron cuatro casos postmortem con diagnóstico histopatológico de fibrosis hepática congénita y cortes histológicos de hígados de embriones de ocho, nueve y 10 semanas de gestación. Se obtuvieron cortes histológicos y se utilizaron reacciones de inmunohistoquímica (citoqueratina 7, 8, 18, 19 y laminina). Los hepatocitos primitivos que rodean las ramas de la vena porta, muestran reactividad para citoqueratinas 7, 8, 18, 19 y laminina. La falta de remodelación de la placa ductal resulta en persistencia de conductos biliares embrionarios; estas anormalidades de la placa ductal pueden ser responsables de enfermedades congénitas de los conductos biliares intrahepáticos donde se incluye la fibrosis hepática congénita. Los resultados obtenidos demuestran que las células que forman placas ductales son positivas para citoqueratinas 8, 18, 19 y laminina a partir de la semana ocho de gestación y persiste su positividad en conductos biliares en la fibrosis hepática congénita. Estos hallazgos apoyan la hipótesis del desarrollo de la fibrosis hepática congénita por persistencia de la placa ductal.