Hutchison F N
Division of Nephrology, Medical University of South Carolina, Charleston.
Miner Electrolyte Metab. 1993;19(3):127-36.
Hyperlipidemia in the nephrotic syndrome is the result of abnormalities in both synthesis and catabolism of lipids and lipoproteins. The etiology of nephrotic hyperlipidemia has not been established, but both abnormal glomerular permeability to plasma proteins and reduced serum oncotic pressure may contribute. Although standard hypolipemic drugs are effective in nephrotic patients, therapies such as dietary protein restriction and angiotensin-converting enzyme inhibitors which reduce proteinuria and increase serum oncotic pressure ameliorate hyperlipidemia as well. Hyperlipidemia may also induce proteinuric renal disease in normal animals and worsen renal injury in a variety of animal models of kidney disease. Conversely, treatment of hyperlipidemia prevents renal injury and lessens proteinuria. Potential mechanisms by which hyperlipidemia may cause renal injury include inflammatory and immunologically mediated injury and alteration of glomerular paracrine function.
肾病综合征中的高脂血症是脂质和脂蛋白合成与分解代谢异常的结果。肾病性高脂血症的病因尚未明确，但肾小球对血浆蛋白的通透性异常和血清胶体渗透压降低可能都起了作用。虽然标准的降血脂药物对肾病患者有效，但诸如限制饮食蛋白质摄入和使用血管紧张素转换酶抑制剂等能减少蛋白尿并提高血清胶体渗透压的疗法，也能改善高脂血症。高脂血症在正常动物中也可能诱发蛋白尿性肾病，并使各种肾病动物模型中的肾损伤恶化。相反，治疗高脂血症可预防肾损伤并减轻蛋白尿。高脂血症可能导致肾损伤的潜在机制包括炎症和免疫介导的损伤以及肾小球旁分泌功能的改变。
