Rodicio J L
Nephrology Department, Hospital 12 de Octubre, Universidad Complutense, Madrid, Spain.
J Hypertens Suppl. 1996 Sep;14(2):S69-75; discussion S75-6. doi: 10.1097/00004872-199609002-00014.
To review the beneficial effect on renal function of antihypertensive treatment in patients with essential hypertension.
Several prospective, randomized trials have demonstrated that blood pressure control reduces the incidence of stroke and coronary heart disease mortality but end-stage renal disease secondary to essential hypertension has increased by 16-26% during the last decade. This apparent discordance can be explained by the reduction in brain and heart mortality, so that a greater proportion of renal damage is produced, or by a failure of antihypertensive drugs to protect the kidney as efficiently as other organs. MECHANISMS OF RENAL DAMAGE IN ESSENTIAL HYPERTENSION: Two mechanisms have been proposed. One hypothesis is that renal ischemia affects different kidney zones by producing periglomerular fibrosis, intimal amplification with hyaline deposits and reduction of the vessel lumen. The second hypothesis proposes that the elevation of intraglomerular pressure observed with secondary glomerular sclerosis is regulated by afferent-efferent arteriolar vasoconstriction or vasodilation. PARAMETERS FOR MEASURING RENAL FUNCTION: Creatinine clearance is the most appropriate method to measure glomerular filtration rate in routine clinical practice. Serum creatinine is not elevated until renal function is reduced below 50 ml/ min. The Cockcroft formula has been proposed in order to calculate creatinine clearance from plasma creatinine levels. Microalbuminuria and proteinuria are two other parameters that can be used to measure renal damage. ANTIHYPERTENSIVE TREATMENT: Antihypertensive therapy with concomitant control of blood pressure reduces protein excretion and the hypertension-induced deterioration in renal function. Angiotensin converting enzyme (ACE) inhibitors and calcium antagonists have shown good renal protection, and a combination of these two types of drugs may improve results and reduce side effects.
In the past decade, end-stage renal disease secondary to essential hypertension is increased despite a clear reduction in stroke and coronary heart disease mortality resulting from blood pressure control. Measurements of creatinine clearance, serum creatinine in advanced renal failure, microalbuminuria and proteinuria are adequate indicators of renal damage. Blood pressure control with any class of drugs reduces the progression of renal failure and proteinuria, but ACE inhibitors and calcium antagonists seem to provide better renal protection; ACE inhibitors have a greater antiproteinuric effect. The combination of these two types of drugs might further reduce renal damage and side effects.
回顾原发性高血压患者降压治疗对肾功能的有益影响。
多项前瞻性随机试验表明,血压控制可降低中风发病率和冠心病死亡率,但在过去十年中,原发性高血压继发的终末期肾病增加了16% - 26%。这种明显的不一致可以通过脑和心脏死亡率的降低来解释,从而导致更大比例的肾损害,或者通过降压药物不能像保护其他器官那样有效地保护肾脏来解释。原发性高血压肾损害的机制:提出了两种机制。一种假说是肾缺血通过产生肾小球周围纤维化、内膜增厚伴透明样沉积和血管腔狭窄影响不同的肾区。第二种假说提出,继发性肾小球硬化时观察到的肾小球内压升高是由入球小动脉和出球小动脉的血管收缩或扩张调节的。评估肾功能的参数:肌酐清除率是常规临床实践中测量肾小球滤过率的最合适方法。直到肾功能降低到50毫升/分钟以下,血清肌酐才会升高。已提出Cockcroft公式以便根据血浆肌酐水平计算肌酐清除率。微量白蛋白尿和蛋白尿是另外两个可用于评估肾损害的参数。降压治疗:伴随血压控制的降压治疗可减少蛋白尿排泄以及高血压引起的肾功能恶化。血管紧张素转换酶(ACE)抑制剂和钙拮抗剂已显示出良好的肾脏保护作用,这两种药物联合使用可能会改善疗效并减少副作用。
在过去十年中,尽管血压控制使中风和冠心病死亡率明显降低,但原发性高血压继发的终末期肾病仍有所增加。肌酐清除率、晚期肾衰竭时的血清肌酐、微量白蛋白尿和蛋白尿的测量是肾损害的适当指标。使用任何一类药物控制血压均可减缓肾衰竭进展和减少蛋白尿,但ACE抑制剂和钙拮抗剂似乎提供更好的肾脏保护作用;ACE抑制剂具有更大的抗蛋白尿作用。这两种药物联合使用可能会进一步减少肾损害和副作用。