title: Cyclosporin A impairs the nocturnal blood pressure fall in renal transplant recipients.
abstract: In renal transplant recipients, hypertension and a diminished nocturnal blood pressure fall are frequently found. To investigate whether this diminished nocturnal blood pressure fall is related to the use of cyclosporin A or to other factors, such as the use of glucocorticoids, we measured 24-hour ambulatory blood pressure in 18 renal transplant recipients both before and 16 weeks after conversion from cyclosporin A to azathioprine. Renal blood flow and glomerular filtration rate were estimated from 131I-hippurate and 125I-iothalamate clearances, respectively, and plasma concentrations of renin, atrial natriuretic peptide, norepinephrine, prostaglandin E2, and thromboxane B2 were determined. During cyclosporin A treatment, mean 24-hour blood pressure was 117 +/- 3 mm Hg, and the nocturnal fall in blood pressure was 4 +/- 9 mm Hg. A nondipping diurnal blood pressure pattern was present in 13 patients. After conversion to azathioprine, mean 24-hour blood pressure decreased to 109 +/- 3 mm Hg (P < .001), the nocturnal fall increased to 9 +/- 6 mm Hg, and the number of patients with a nondipping diurnal blood pressure pattern decreased to 9. The nocturnal fall in heart rate (17 +/- 10 beats per minute) during cyclosporin A did not change after conversion. Body weight and plasma concentrations of norepinephrine and renin did not change. Plasma concentrations of prostaglandin E2 and thromboxane B2 decreased after conversion, as did plasma atrial natriuretic peptide. Renal blood flow and glomerular filtration rate increased after conversion. In conclusion, cyclosporin A appears to be involved in the disturbance of the circadian blood pressure rhythm in renal transplant recipients. Although the precise mechanism is unclear. the elevated plasma atrial natriuretic peptide and slightly suppressed plasma renin concentrations suggest that intravascular volume expansion may contribute to the observed hemodynamic alterations.
authors.affiliation: Department of Internal Medicine I, University Hospital Dijkzigt, Rotterdam, Netherlands.
authors.forename: M A
authors.initials: MA
authors.lastname: van den Dorpel
authors.forename: A H
authors.initials: AH
authors.lastname: van den Meiracker
authors.forename: T W
authors.initials: TW
authors.lastname: Lameris
authors.forename: F
authors.initials: F
authors.lastname: Boomsma
authors.forename: M
authors.initials: M
authors.lastname: Levi
authors.forename: A J
authors.initials: AJ
authors.lastname: Man in 't Veld
authors.forename: W
authors.initials: W
authors.lastname: Weimar
authors.forename: M A
authors.initials: MA
authors.lastname: Schalekamp
mesh_terms: D000328:Adult; D001379:Azathioprine / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects*; D002940:Circadian Rhythm; D016572:Cyclosporine / Q000494:pharmacology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology*; D016030:Kidney Transplantation / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D009638:Norepinephrine / Q000097:blood; D011184:Postoperative Period; D012083:Renin / Q000097:blood
chemical_list: D007166:Immunosuppressive Agents; D016572:Cyclosporine; D012083:Renin; D001379:Azathioprine; D009638:Norepinephrine