ABSTRACT
Intradialytic hypotension is a major complication during hemodialysis session, associated with increased risk of cardiovascular events and mortality. Its pathophysiology is believed to be multifactorial and remains not well elucidated. The aim of this study is to put forward new mechanisms behind the development of intradialytic hypotension. The study included sixty-five subjects on chronic hemodialysis, divided into two groups: intradialytic hypotensive (n=12) and normotensive (n=53), according to the variation of systolic blood pressure between post-dialysis and pre-dialysis measurements. Renin and angiotensin converting enzyme I plasma concentrations increased in both groups but more likely in normotensive group. Aldosterone plasma concentration is increased in the normotensive group while it decreased in the intradialytic hypotension group. Plasma endothelin concentrations showed higher values in intradialytic hypotension group. Post-dialysis asymmetric dimethylarginine and angiotensin converting enzyme 2 plasma concentrations were significantly higher in intradialytic hypotension group as compared to normotensive one. Collectrin plasma concentrations were significantly lower in intradialytic hypotension group. Finally, post-dialysis vascular endothelial growth factor C plasma concentration significantly increased in intradialytic hypotension group. In conclusion, endothelial dysfunction characterized by a lower level of vasoactive molecule seems to play a critical role in intradialytic hypotension development.
Subject(s)
Blood Pressure , Endothelium, Vascular/physiopathology , Hypotension/etiology , Kidney Diseases/therapy , Renal Dialysis/adverse effects , Aged , Aged, 80 and over , Aldosterone/blood , Angiotensin-Converting Enzyme 2 , Arginine/analogs & derivatives , Arginine/blood , Biomarkers/blood , Endothelin-1/blood , Endothelium, Vascular/metabolism , Female , Humans , Hypotension/blood , Hypotension/physiopathology , Kidney Diseases/blood , Kidney Diseases/physiopathology , Male , Membrane Glycoproteins/blood , Middle Aged , Peptidyl-Dipeptidase A/blood , Renin/blood , Time Factors , Vascular Endothelial Growth Factor C/bloodSubject(s)
Cyclosporine/pharmacokinetics , Drug Monitoring/methods , Immunosuppressive Agents/pharmacokinetics , Kidney Transplantation/immunology , Lymphocyte Count , Lymphocytes/immunology , Biopsy , Cyclosporine/therapeutic use , Graft Rejection/epidemiology , Graft Rejection/pathology , Humans , Immunosuppressive Agents/therapeutic use , Kidney Transplantation/pathology , Lymphocytes/drug effects , Reproducibility of ResultsSubject(s)
Azathioprine/therapeutic use , Blood Transfusion , Cyclosporine/therapeutic use , Immunosuppressive Agents/therapeutic use , Kidney Transplantation/immunology , Prednisolone/therapeutic use , Tissue Donors , Age Factors , Chi-Square Distribution , Creatinine/blood , Drug Therapy, Combination , Female , Follow-Up Studies , Graft Rejection/epidemiology , Graft Rejection/prevention & control , Histocompatibility Testing , Humans , Incidence , Male , Time Factors , Treatment OutcomeABSTRACT
Nephrogenic ascites is a complex problem with a poorly understood pathophysiology. We report the case of a patient with nephrogenic ascites and concomitant secondary hyperparathyroidism who was resistant to the usual treatment but had a complete resolution after subtotal parathyroidectomy. We believe that secondary hyperparathyroidism might be implicated in the pathogenesis of nephrogenic ascites.
