Raimondi C, Castiglioni A, Allergri L, Bocchi B, Orsini S, Vinci S, Savazzi G M
Istituto di Clinica medica e Nefrologia, Università, Parma.
Recenti Prog Med. 1990 Dec;81(12):782-7.
This paper synthesizes the pathogenic steps of arterial hypertension in diabetes mellitus: hyperosmolarity due to the hyperglycemia and increased sodic tubular reabsorption accounting for the expansion of the extracellular volume with hypervolemia; abnormalities of the ionic membrane pumps leading to abnormal intracellular calcium distribution, thereby inducing an increased vascular tone; atypical vasomotor reactivity to cathecolamines; modifications of the renin-angiotension-aldosterone system. The pathophysiological derangements by which hypertension could induce nephropathy are examined: the vasodilatation which can be detected from the onset of diabetes, may be a determinant in the transmission of systemic hypertension to the glomerular microcirculation with resulting enhancement of the hydrostatic transglomerular pressure gradient (i.c. the major factor producing glomerular injury), glomerular plasmatic flow and filtration rate. The nephron hyperfiltration increases the movement of plasmatic proteins across the glomerular capillary wall with subsequent mesangial hyperactivity and sclerosis. Antihypertensive treatment in diabetes follows general guidelines and it should be instituted even in the case of microhypertension being facilitated in this setting the appearance of microalbuminuria i.e. the starting point of nephropathy. Even if experimental studies are to favor ACE inhibitors as the first-line drugs for abating glomerular hypertension by mitigation of the direct effect of angiotensin II on the efferent arteriolar tone, clinical observations suggest that, regardless of type of treatment, the normalization of systemic arterial pressure, by reversing glomerular hypertension may be effective in preventing diabetic nephropathy.
高血糖导致的高渗状态以及肾小管钠重吸收增加，引起细胞外液量扩张和血容量过多；离子膜泵异常导致细胞内钙分布异常，从而引起血管张力增加；对儿茶酚胺的非典型血管运动反应；肾素 - 血管紧张素 - 醛固酮系统的改变。文中还探讨了高血压诱发肾病的病理生理紊乱：糖尿病发病时即可检测到的血管舒张，可能是系统性高血压传递至肾小球微循环的决定因素，进而导致肾小球跨膜静水压梯度（即造成肾小球损伤的主要因素）、肾小球血浆流量和滤过率增加。肾单位高滤过增加了血浆蛋白穿过肾小球毛细血管壁的移动，随后导致系膜增生和硬化。糖尿病患者的降压治疗遵循一般原则，即使是轻度高血压也应进行治疗，因为这会促使微量白蛋白尿的出现，而微量白蛋白尿是肾病的起始点。尽管实验研究倾向于将血管紧张素转换酶（ACE）抑制剂作为减轻血管紧张素 II 对出球小动脉张力直接影响从而降低肾小球高血压的一线药物，但临床观察表明，无论采用何种治疗方式，通过逆转肾小球高血压使系统性动脉血压恢复正常，可能对预防糖尿病肾病有效。
