title: Renal transplantation and red blood cell sodium transport: role of prednisone treatment.
abstract: This study assesses the role of prednisone and endogenous digoxin-like immunoreactivity (EDLI) in the increased Na+ pump activity in renal allograft patients. Red blood cell (RBC) Na+ transport activities and plasma concentrations of EDLI were measured in ten controls and ten renal allograft recipients (5 hypertensive) while undergoing treatment with cyclosporin, prednisone, and azathioprine, and also after prednisone withdrawal. As compared to controls, prednisone-treated patients showed an increased Na+ pump activity (0.323/h vs 0.571, P less than 0.05) and decreased RBC Na+ concentration (6.69 mM vs 4.99, P less than 0.05). They also showed a decrease in the activity of cotransport, countertransport, and passive Na+ efflux (0.02/h vs 0.005, P less than 0.05; 207 mumol/l vs 35, P less than 0.05; 0.02/h vs 0.005 respectively, P less than 0.05). After prednisone withdrawal, normotensive and hypertensive patients showed RBC Na+ transport system activities and RBC Na+ concentration similar to those of controls. EDLI was not detected in controls or in patients. We conclude that prednisone treatment increased the Na+ pump activity, and decreased the RBC Na+ concentration. Moreover, it induced a decrease in the activity of secondary RBC Na+ transport systems. This study provides no evidence for a modulatory role of EDLI in the RBC Na+ pump activity. Neither parameters can be presumed to be a marker of hypertension in these patients.
authors.affiliation: Department of Nephrology, Fundación Jiménez Díaz-Consejo Superior de Investigaciones Científicas, Madrid, Spain.
authors.forename: R J
authors.initials: RJ
authors.lastname: Bosch
authors.forename: N
authors.initials: N
authors.lastname: Hernando
authors.forename: J J
authors.initials: JJ
authors.lastname: Plaza
authors.forename: S
authors.initials: S
authors.lastname: Casado
authors.forename: J M
authors.initials: JM
authors.lastname: Lopez-Novoa
mesh_terms: D000328:Adult; D001693:Biological Transport, Active; D001794:Blood Pressure / Q000187:drug effects; D001798:Blood Proteins / Q000502:physiology; D002298:Cardenolides; D004077:Digoxin; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism; D005260:Female; D006801:Humans; D016030:Kidney Transplantation / Q000502:physiology*; D008094:Lithium / Q000097:blood; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood; D011241:Prednisone / Q000494:pharmacology*; D012503:Saponins; D012964:Sodium / Q000097:blood*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors / Q000097:blood
chemical_list: D001798:Blood Proteins; D002298:Cardenolides; D012503:Saponins; C034504:digoxin-like factors; D004077:Digoxin; D008094:Lithium; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium; D011241:Prednisone