title: Hypertension in cyclosporine-treated renal transplant recipients is sodium dependent.
abstract: OBJECTIVE
  Physicians increasingly prescribe cyclosporine as an immunosuppressive agent for both organ-transplant and non-organ-transplant recipients. Investigators have reported a high incidence of drug-induced hypertension even when clinical nephrotoxicity was not present. We wanted to determine the reason.
  
  
  METHODS
  A comparison was made of hypertension in 15 cyclosporine-treated transplant recipients with that in a similar group of 15 azathioprine-treated transplant recipients.
  
  
  RESULTS
  Hypertension in the cyclosporine group responded differently from that seen in the azathioprine group and from previously described forms of post-transplantation hypertension. Hypertensive cyclosporine-treated patients show a sodium acquisitive renal state that responds to sodium restriction. Unlike rat models, which suggest cyclosporine-induced stimulation of the renin-angiotensin system, or previous forms of post-transplant hypertension in humans, plasma renin levels were not elevated and blood pressure did not respond to a test dose of captopril.
  
  
  CONCLUSIONS
  Hypertension in cyclosporine-treated patients is an iatrogenic form of hypertension that may be associated with an early, subtle, renal defect in sodium excretion, a genesis of hypertension that is consistent with Guyton's view of essential hypertension.
mesh_terms: D000328:Adult; D001379:Azathioprine / Q000009:adverse effects; D003524:Cyclosporins / Q000009:adverse effects*; D004039:Diet, Sodium-Restricted; D005260:Female; D006801:Humans; D006973:Hypertension / Q000139:chemically induced* / Q000378:metabolism; D016030:Kidney Transplantation; D008297:Male; D010953:Plasma Volume / Q000187:drug effects; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D003524:Cyclosporins; D012964:Sodium; D001379:Azathioprine