title: High-density lipoprotein in uremic patients: metabolism, impairment, and therapy.
abstract: Several studies have shown that HDL has altered antioxidant and anti-inflammatory effects in chronic uremia, either by the reduction in its antioxidant enzymes or by the impairment of their activity. Systemic oxidative stress, which is highly prevalent in chronic kidney disease (CKD) patients, has been shown to decrease antioxidant and anti-inflammatory effects of HDL and even transform it into a pro-oxidant and pro-inflammatory agent. For this reason, we believe that the propensity for accelerated cardiovascular disease in CKD is facilitated by a few key features of this disease, namely, oxidative stress, inflammation, hypertension, and disorders of lipid metabolism. In a nutshell, oxidative stress and inflammation enhance atherosclerosis leading to increased cardiovascular mortality and morbidity in this population. In this detailed review, we highlight the current knowledge on HDL dysfunction and impairment in chronic kidney disease as well as the available therapy.
authors: Department of Cardiology, Dartmouth-Hitchcock Medical Center, One Medical Center Drive, Lebanon, NH, 03756-0001, USA, khoueiry_gm@hotmail.com.
authors: Georges
authors: G
authors: Khoueiry
authors: Mokhtar
authors: M
authors: Abdallah
authors: Faisal
authors: F
authors: Saiful
authors: Nidal
authors: N
authors: Abi Rafeh
authors: Muhammad
authors: M
authors: Raza
authors: Tariq
authors: T
authors: Bhat
authors: Suzanne
authors: S
authors: El-Sayegh
authors: Kamyar
authors: K
authors: Kalantar-Zadeh
authors: James
authors: J
authors: Lafferty
mesh_terms: D000081:Acetamides; D000085:Acetates / Q000627:therapeutic use; D000101:Acetyl-CoA C-Acetyltransferase / Q000037:antagonists & inhibitors; D000893:Anti-Inflammatory Agents; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D000975:Antioxidants; D016632:Apolipoprotein A-I / Q000627:therapeutic use; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology; D002784:Cholesterol / Q000378:metabolism; D053480:Cholesterol Ester Transfer Proteins / Q000037:antagonists & inhibitors; D050171:Dyslipidemias / Q000188:drug therapy*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008075:Lipoproteins, HDL / Q000378:metabolism*; D009525:Niacin / Q000627:therapeutic use; D047493:PPAR alpha / Q000819:agonists; D011804:Quinolines / Q000627:therapeutic use; D051436:Renal Insufficiency, Chronic / Q000150:complications / Q000378:metabolism*; D013449:Sulfonamides; D013451:Sulfonic Acids / Q000627:therapeutic use; D014511:Uremia / Q000097:blood* / Q000209:etiology
chemical_list: D000081:Acetamides; D000085:Acetates; D000893:Anti-Inflammatory Agents; D000924:Anticholesteremic Agents; D000975:Antioxidants; D016632:Apolipoprotein A-I; C506642:CETP protein, human; D053480:Cholesterol Ester Transfer Proteins; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D008075:Lipoproteins, HDL; D047493:PPAR alpha; D011804:Quinolines; D013449:Sulfonamides; D013451:Sulfonic Acids; D009525:Niacin; C423185:avasimibe; C483909:torcetrapib; D002784:Cholesterol; D000101:Acetyl-CoA C-Acetyltransferase