title: Hyperlipidemia and transplantation: etiologic factors and therapy.
abstract: Hyperlipidemia is a well-recognized complication of renal transplantation. In long-term survivors of renal transplantation, cardiovascular disease accounts for the majority of patient deaths. In the cyclosporine era, cardiovascular disease has surpassed infection as the number one cause of death. Risk factors in the transplant population for hyperlipidemia include age, male sex, diabetes, prednisone dose, graft impairment, obesity, and antihypertensive therapy. Recently, cyclosporine has been implicated as an aggravating factor in the development of hyperlipidemia after transplantation, although its role has been controversial. Because renal transplant recipients have other significant risk factors for the development of coronary artery disease, the amelioration of hyperlipidemia may improve long-term patient survival. Because most late deaths occur in patients with a functioning graft, long-term graft survival could also be improved. The role of corticosteroids in the development of hyperlipidemia is well established. Recent studies employing corticosteroid withdrawal after transplantation have shown a marked reduction in cholesterol despite the use of cyclosporine. Data on corticosteroid withdrawal in living related transplants at our center show a significant reduction in total cholesterol after steroid withdrawal. Data from heart transplant recipients under corticosteroid-free protocols show a similar reduction in total cholesterol. Other treatments for hyperlipidemia include diet and cholesterol-lowering agents, such as Mevacor (lovastatin; Merck Sharp & Dohme, West Point, PA). The efficacy of lowering cholesterol in this high-risk population is unknown.
authors.affiliation: Department of Medicine, University of Wisconsin School of Medicine, Madison.
authors.forename: J D
authors.initials: JD
authors.lastname: Pirsch
authors.forename: A M
authors.initials: AM
authors.lastname: D'Alessandro
authors.forename: H W
authors.initials: HW
authors.lastname: Sollinger
authors.forename: S J
authors.initials: SJ
authors.lastname: Knechtle
authors.forename: A
authors.initials: A
authors.lastname: Reed
authors.forename: M
authors.initials: M
authors.lastname: Kalayoglu
authors.forename: F O
authors.initials: FO
authors.lastname: Belzer
mesh_terms: D000305:Adrenal Cortex Hormones / Q000009:adverse effects; D000959:Antihypertensive Agents / Q000009:adverse effects; D003327:Coronary Disease / Q000209:etiology / Q000517:prevention & control; D004232:Diuretics / Q000009:adverse effects; D015248:Gemfibrozil / Q000627:therapeutic use; D006801:Humans; D006949:Hyperlipidemias / Q000178:diet therapy / Q000188:drug therapy / Q000209:etiology*; D007166:Immunosuppressive Agents / Q000009:adverse effects; D007676:Kidney Failure, Chronic / Q000097:blood / Q000601:surgery*; D016030:Kidney Transplantation; D050356:Lipid Metabolism; D008071:Lipoprotein Lipase / Q000172:deficiency; D008148:Lovastatin / Q000627:therapeutic use; D011183:Postoperative Complications / Q000209:etiology*; D012307:Risk Factors
chemical_list: D000305:Adrenal Cortex Hormones; D000959:Antihypertensive Agents; D004232:Diuretics; D007166:Immunosuppressive Agents; D008148:Lovastatin; D008071:Lipoprotein Lipase; D015248:Gemfibrozil