Nephrology Division, Internal Medicine Department, Hospital General Juan Cardona, c/ Pardo Bazán s/n, 15406 Ferrol, Spain.
Rev Cardiovasc Med. 2020 Mar 30;21(1):41-56. doi: 10.31083/j.rcm.2020.01.5102.
The curve that describes the relationship between glomerular filtration rate (GFR) and cardiovascular risk is U-shaped, indicating that both reduced GFR (kidney failure) and elevated GFR (glomerular hyperfiltration) are equivalent cardiovascular risk factors. The elevated cardiovascular risk associated with abnormal GFR is not explained by standard cardiovascular risk factors. The relationship between GFR and all-cause mortality follows a similar pattern, so that altered GFR (either low or high) increases the risk for overall mortality. Glomerular hyperfiltration is an adaptive process that arises under conditions that demand improved kidney excretory capacity, such as animal protein ingestion and kidney failure. Unlike vegetable protein, animal protein consumption increases dietary acid load and requires an elevation of the GFR to restore acid-base balance. The loss of functioning nephrons in diseased kidneys requires a compensatory increase of the GFR in the nephrons that remain working to enhance whole-kidney GFR. A major factor that raises GFR is the pancreatic hormone glucagon. Glucagon infusion and endogenous glucagon release increase GFR in healthy subjects and patients with kidney failure. In addition to its kidney hemodynamic effect, glucagon causes insulin resistance. Like hyperglucagonemia, insulin resistance develops across the entire spectrum of abnormal GFR, from glomerular hyperfiltration to advanced kidney disease. Insulin resistance is associated with subclinical vascular injury in the general population and patients with diabetes and kidney failure, being a strong cardiovascular risk factor in these population groups. Animal protein consumption activates glucagon secretion and promotes insulin resistance, having a detrimental effect on cardiovascular disease and renal outcomes.
描述肾小球滤过率（GFR）与心血管风险之间关系的曲线呈 U 形，表明 GFR 降低（肾衰竭）和升高（肾小球高滤过）都是同等的心血管危险因素。与异常 GFR 相关的升高的心血管风险不能用标准的心血管危险因素来解释。GFR 与全因死亡率之间的关系也呈现出类似的模式，因此 GFR 的改变（无论是低还是高）都会增加总体死亡率的风险。肾小球高滤过是一种适应性过程，发生在需要提高肾脏排泄能力的情况下，如动物蛋白摄入和肾衰竭。与植物蛋白不同，动物蛋白的摄入会增加饮食中的酸负荷，需要提高 GFR 来恢复酸碱平衡。患病肾脏中功能丧失的肾单位需要剩余工作的肾单位代偿性增加 GFR，以增强整个肾脏的 GFR。提高 GFR 的一个主要因素是胰腺激素胰高血糖素。胰高血糖素输注和内源性胰高血糖素释放会增加健康受试者和肾衰竭患者的 GFR。除了其对肾脏血流动力学的影响外，胰高血糖素还会引起胰岛素抵抗。与高胰高血糖血症一样，胰岛素抵抗也会发生在整个异常 GFR 谱中，从肾小球高滤过到晚期肾病。胰岛素抵抗与普通人群和糖尿病及肾衰竭患者的亚临床血管损伤有关，是这些人群的一个强烈心血管危险因素。动物蛋白摄入会激活胰高血糖素分泌并促进胰岛素抵抗，对心血管疾病和肾脏结局产生不利影响。
