臨牀透析 Vol.21 No.9(17)


特集名 尿毒症・慢性透析にみられる合併症と関連する諸物質
題名 脂質代謝障害
発刊年月 2005年 08月
著者 上野 高浩 日本大学医学部内科学講座腎臓内分泌部門
【 要旨 】 慢性腎不全においては動脈硬化性疾患が多く,その死因に大きな割合を占めている.脂質代謝異常は動脈硬化性疾患と密接に関連し,慢性腎不全患者においてもその管理の重要性が高まっている.慢性腎不全患者においてもっともよくみられる脂質代謝異常は高中性脂肪血症と低HDL (高比重リポ蛋白) 血症であり,両者は合併することが多い.さらに,慢性腎不全患者は酸化ストレスが亢進した状態にあることが知られており,リポ蛋白の酸化変性は動脈硬化をさらに進展させると考えられる.抗酸化作用をもつものとしては,L-カルニチン,α-トコフェロール,アスコルビン酸が慢性腎不全における投与により良好な成績が報告されており,尿毒症では酸化ストレスを抑制する物質の欠乏が,脂質代謝障害を引き起こす有力なものとして捉えられる.酸化ストレスに関わる物質の検討も必要である.
Theme The Various Uremic Symptomes and their Causative Substances
Title Dyslipidemia in renal failure
Author Takahiro Ueno Division of Nephrology and Endocrinology, Department of Medicine, Nihon University School of Medicine
[ Summary ] It is well known that atherosclerotic diseases are major causes of mortality in patients with chronic renal failure (CRF). They are caused by numerous factors, defined as risk factors. One of these factors, dyslipidemia, is often observed in patients with CRF. The prominent features of uremic dyslipidemia are an increased levels of plasma triglycerides and a reduction in HDL cholesterol.
On the other hand, CRF is associated with oxidative stress that promotes production of reactive oxygen species. In patients undergoing maintenance hemodialysis treatment, this condition is usually present with plasma carnitine insufficiency. This is due to accumulations of metabolic intermediates combined with impaired carnitine biosynthesis, reduced protein intake and increased removal via hemodialysis. Several studies have indicated that L-cartinine supplementation may be of some benefit in the prevention of atherosclerosis.
For reduction of oxdative stress, high doseage supplementation with α-tocopherol also has been shown to reduce cardiovascular risk in studies of hemodialysis patients with preexisting cardiovascular disease.
Moreover, it is essential to study the supposed mechanisms of uremic dyslipidemia, since optimal treatment is essential for the prevention or delay of cardiovascular complications in patients with CRF.
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