Weinrauch L A, Kennedy F P, Gleason R E, Keough J, D'Elia J A
Department of Medicine of Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Am J Hypertens. 1998 Mar;11(3 Pt 1):302-8. doi: 10.1016/s0895-7061(97)00472-x.
The objective of this study was to test the relationship between neurologic and microvascular complications of type 1 diabetes mellitus. It was hypothesized that the mechanisms operative in autonomic dysfunction seen in diabetic patients with microangiopathy play a role in the rapidity of progression to renal failure. Twenty-six type 1 diabetic patients with proteinuria were studied with computerized monitoring of heart rate variation during timed ventilation, assumption of upright posture, and Valsalva maneuver and with 24-h ambulatory blood pressure monitoring at baseline. Renal function was evaluated over the ensuing 12 months of intensive insulin therapy. Blood pressure was treated so as to achieve consistent 24-h readings < 140/90 mm Hg. Angiotensin converting enzyme inhibitors were the preferred antihypertensive agents. Serial serum creatinine concentrations were compared using repeated measures analysis of variance. Over 12 months there were no significant serum creatinine changes for any autonomic test group with normal results at baseline. Groups with abnormal autonomic results at baseline demonstrated statistically significant increases in serum creatinine over 12 months compared to their baseline. Of the tests, Valsalva separated groups of patients with similar degrees of baseline renal impairment. Each of the sympathetic plus Valsalva combinations demonstrated a significant difference in progression of serum creatinine increase over 12 months. In each instance, if both sympathetic and Valsalva results were abnormal, there was a statistically significant increase in serum creatinine over 12 months when compared to groups in which one or both test results were normal. There is a relationship between autonomic function and the progression of renal dysfunction. The inability to vary the heart rate to a Valsalva maneuver identifies a degree of parasympathetic dysfunction that permits unopposed sympathetic tone, heralding more rapid renal destruction. A simple inexpensive bedside laboratory test discerned a relatively low-risk group of diabetic patients with proteinuria that demonstrated no deterioration in renal function over 12 months. When the Valsalva maneuver was markedly abnormal the presence of a mean arterial pressure > 100 mm Hg was associated with a greater likelihood of rapid renal deterioration. This group at higher risk of renal deterioration should undergo aggressive lowering of mean arterial blood pressure to < 95 mm Hg.
本研究的目的是检验1型糖尿病神经病变与微血管并发症之间的关系。研究假设是，在患有微血管病变的糖尿病患者中，自主神经功能障碍的作用机制在进展至肾衰竭的速度方面发挥作用。对26例有蛋白尿的1型糖尿病患者进行了研究，在定时通气、体位由平卧位变为直立位以及瓦尔萨尔瓦动作期间通过计算机监测心率变化，并在基线时进行24小时动态血压监测。在随后12个月的强化胰岛素治疗期间评估肾功能。治疗血压以实现24小时读数持续<140/90 mmHg。血管紧张素转换酶抑制剂是首选的抗高血压药物。使用重复测量方差分析比较系列血清肌酐浓度。在12个月期间，基线时自主神经测试结果正常的任何组血清肌酐均无显著变化。基线时自主神经结果异常的组在12个月期间血清肌酐较其基线有统计学显著升高。在这些测试中，瓦尔萨尔瓦动作区分了基线肾功能损害程度相似的患者组。交感神经加瓦尔萨尔瓦动作的每种组合在12个月期间血清肌酐升高的进展方面均显示出显著差异。在每种情况下，如果交感神经和瓦尔萨尔瓦动作的结果均异常，与一项或两项测试结果正常的组相比，1个月期间血清肌酐有统计学显著升高。自主神经功能与肾功能障碍的进展之间存在关联。对瓦尔萨尔瓦动作不能改变心率表明存在一定程度的副交感神经功能障碍，使得交感神经张力无对抗，预示着肾脏破坏更快。一项简单廉价的床边实验室检查识别出一组蛋白尿糖尿病患者，其风险相对较低，在12个月期间肾功能无恶化。当瓦尔萨尔瓦动作明显异常时，平均动脉压>mmHg与肾脏快速恶化的可能性更大相关。这组肾脏恶化风险较高的患者应积极将平均动脉血压降至<95 mmHg。
