Nowicki M, Kokot F, Surdacki A
Department of Nephrology, Silesian University School of Medicine, Katowice, Poland.
Nephrol Dial Transplant. 1998 Oct;13(10):2566-71. doi: 10.1093/ndt/13.10.2566.
Patients with renal failure are characterized by impaired insulin-mediated glucose uptake. Insulin plays a major role in the maintenance of phosphate homeostasis but it remains to be determined whether in uraemia insulin-dependent renal and extrarenal phosphate disposal is also affected.
The effect of hyperinsulinaemia on serum concentrations of phosphate, ionized calcium and intact PTH as well as renal excretion of calcium and phosphate was studied under euglycaemic conditions (glucose clamp technique) in patients with advanced renal failure and in healthy subjects. Fifteen patients with renal failure (mean serum creatinine 917 micromol/l) and 12 control subjects were included. All subjects underwent a 3-h euglycaemic clamp with constant infusion of insulin (50 mU/m2/min) following a priming bolus. The urine was collected for 3 h before and throughout the clamp.
The tissue insulin sensitivity (M/I) was lower in patients with renal failure than in control subjects (5.3+/-2.4 vs 6.7+/-1.8mg/kg/min per mU/ml, P= 0.001) but the phosphate lowering action of insulin was larger in patients with renal failure than in control subjects. Urinary calcium excretion increased (P < 0.05) and phosphate excretion did not change during the clamp in both groups. Despite a decrease of serum ionized calcium in the group of patients with renal failure and no change in the control group, plasma PTH fell significantly in both groups but this effect was still significant after 180 min only in the renal failure group. A significant correlation was observed between changes in serum phosphate and PTH induced by hyperinsulinaemia (r = 0.48, P < 0.01 )
Phosphate-lowering effect of insulin is well preserved in severe renal failure despite the resistance to insulin-stimulated glucose uptake. The decrease of serum PTH observed during hyperinsulinaemia appears to be independent of serum ionized calcium.
肾衰竭患者的特征是胰岛素介导的葡萄糖摄取受损。胰岛素在维持磷酸盐稳态中起主要作用，但尿毒症中胰岛素依赖的肾脏和肾外磷酸盐处理是否也受影响仍有待确定。
在正常血糖条件下（葡萄糖钳夹技术），研究了高胰岛素血症对晚期肾衰竭患者和健康受试者血清磷酸盐、离子钙和完整甲状旁腺激素（PTH）浓度以及肾脏钙和磷酸盐排泄的影响。纳入了15例肾衰竭患者（平均血清肌酐917微摩尔/升）和12例对照受试者。所有受试者在给予首剂负荷量后，进行3小时的正常血糖钳夹，并持续输注胰岛素（50毫单位/平方米/分钟）。在钳夹前3小时及整个钳夹过程中收集尿液。
肾衰竭患者的组织胰岛素敏感性（M/I）低于对照受试者（5.3±2.4对6.7±1.8毫克/千克/分钟每毫单位/毫升，P = 0.001），但胰岛素的降磷作用在肾衰竭患者中比对照受试者更大。两组在钳夹期间尿钙排泄增加（P < 0.05），而磷酸盐排泄未改变。尽管肾衰竭组血清离子钙降低，对照组无变化，但两组血浆PTH均显著下降，但仅在肾衰竭组180分钟后这种作用仍显著。高胰岛素血症引起的血清磷酸盐和PTH变化之间存在显著相关性（r = 0.48，P < 0.01）。
尽管对胰岛素刺激的葡萄糖摄取存在抵抗，但胰岛素的降磷作用在严重肾衰竭中仍得到很好的保留。高胰岛素血症期间观察到的血清PTH降低似乎与血清离子钙无关。
