Mogensen C E, Schmitz A, Christensen C K
Medical Department M, Second University Clinic of Internal Medicine, Kommunehospitalet, Aarhus, Denmark.
Diabetes Metab Rev. 1988 Aug;4(5):453-83. doi: 10.1002/dmr.5610040504.
Hyperfiltration is a very characteristic feature in insulin-dependent diabetes. Hyperfiltration is to some extent associated with long-term glycemic control but the correlation is not very strong. Long-term hyperfiltration may play a role in the genesis of late diabetic nephropathy, but it is difficult to distinguish effects of hyperfiltration per se from effects of poor metabolic control. Long-term hyperfiltration without diabetes does not produce nephropathy. It is hypothesized that IDDM patients who do not show considerable hyperfiltration in spite of poor metabolic control may be those who are to some extent protected against late diabetic nephropathy, but other mechanisms may also be involved in the renal protection of these patients, who survive long-term diabetes without nephropathy. On the other hand, those with poor metabolic control combined with hyperfiltration are likely to develop nephropathy. In addition, it is suggested that the metabolic aberrations in diabetes, with the subsequent changes in the biochemistry of the glomerular wall, are permissive and absolutely required for the development of diabetic nephropathy. Of note, diabetic glomerulopathy in NIDDM occurs without significant hyperfiltration and extreme hyperfiltration in the one-kidney-model (without diabetes) does not produce nephropathy. Nonglycemic modalities of intervention, resulting in reduced hyperfiltration, e.g., low-protein diet or administration of somatostatin analogues, deserves interest as new potential ways of preventing or postponing diabetic nephropathy. Also intervention with aldose-reductase inhibitors may be an important therapeutic modality for those patients in whom good metabolic control is not obtainable. It is now well-established that antihypertensive treatment, including ACE-inhibition, reduces rate of decline in GFR in patients with already established nephropathy. In addition, protein excretion is diminished in IDDM patients with incipient diabetic nephropathy by antihypertensive treatment where GFR is well-preserved during treatment. No data are available for NIDDM.
超滤是胰岛素依赖型糖尿病的一个非常典型的特征。超滤在一定程度上与长期血糖控制相关，但这种相关性不是很强。长期超滤可能在晚期糖尿病肾病的发生中起作用，但很难将超滤本身的影响与代谢控制不佳的影响区分开来。没有糖尿病的长期超滤不会导致肾病。据推测，尽管代谢控制不佳但未表现出明显超滤的胰岛素依赖型糖尿病患者可能在一定程度上受到保护，不易发生晚期糖尿病肾病，但其他机制可能也参与了这些长期患糖尿病而无肾病患者的肾脏保护。另一方面，代谢控制不佳且合并超滤的患者很可能会发展为肾病。此外，有人提出糖尿病中的代谢异常以及随后肾小球壁生物化学的变化，对于糖尿病肾病的发生是允许的且绝对必要的。值得注意的是，非胰岛素依赖型糖尿病中的糖尿病肾小球病变在没有明显超滤的情况下发生，而单肾模型（无糖尿病）中的极端超滤不会导致肾病。导致超滤减少的非血糖干预方式，例如低蛋白饮食或给予生长抑素类似物，作为预防或延缓糖尿病肾病的新潜在方法值得关注。对于那些无法实现良好代谢控制的患者，醛糖还原酶抑制剂的干预也可能是一种重要的治疗方式。现在已经明确，包括血管紧张素转换酶抑制剂在内的降压治疗可降低已患肾病患者的肾小球滤过率下降速度。此外，在治疗期间肾小球滤过率保持良好的情况下，降压治疗可减少早期糖尿病肾病的胰岛素依赖型糖尿病患者的蛋白尿排泄。非胰岛素依赖型糖尿病尚无相关数据。
