| Hypertension is a commonly encountered disease in clinicalpractice. It's pathogenesis is not explicit yet. Many animal modelexperiment in recent years have indicated that kidney plays animportant role in the occurrence of primary hypertension. The core ofthis role is the obstacle of the regulation to natrium. The normalbalance-regulation mecanism of natrium can be in disturbence, whichwill cause the occurrence of hypertention. The strong blood pressureand abnormity of renal hemodynamics lead indirectly to the damageof renal parenchyma, including the ischemia and sclerosis ofglomerulus and the injure of renal tubule-interstitium. The renaldamage of hypertensive patients may become serious in pace with thedegree and long course of hypertension.The study indicates that clinical manifestation appears when thecourse of hypertension last for more than five years, blood pressuregoes up continuously, there is widespread vitreous degeneration inreno-arteriole, there are pachynsis and fibrosis in the media ofinterlobular, there is ischemia of glomerulus and renal tubule, there arelocalized thickness is capinary wall and shrinkage in capillary loopsand there are focal atrophy of tubule and thickness and cleavage ofbasement membrance. The earlier period of hypertensive renal diseaseis out the attension, and can't be easily detected by routine check.Though the doctors notice the possibicity of hypertensive renal disease,most are satisfied with the results of routine examination, and haven'tpay enough attention to the patients of no symptom and negativelaboratory report, and lose the opportunity of earlier diagnosis andtreatment. When the wrinary protein. Blood creatinine and ureanitrogen rise, the ill condition has get to a high degree. The sensitiveexamine method of earlier primary hypertensive renal disease includeurinary micero-albumin, β2-microglobulin and NAG. Most urinarymicro-albumin can't go through filtration membrance in normalcondition because it's negative charge and the charge-electing obstacleof the filtration membrance. Recent research show that the increasedNa+/Li+ reverting of hypertensive patients can cause the disturbanceof renal hemodynamics self-regulation, the hyperper fusion ofglomerulus, the decreased charge of filtration membrance and themore urinary micro-albumin. Material and method The forty-two cases of hypertensive renal disease are electedfrom the three hundred and six cases of primary hypertensive patientsadmitted from 1999.1 to 2004.1 in our hospital. Of that male 28 cases,female 24 cases, age change from 41 to 76, average age 63.4 years old.Retrospective analysis is taken to the clinical data of the 52 cases andthe datum is analysed by statistics method and u test. Result:1 ,There is significant difference (P<0.01) between thehypertensive patients whose disease course is less than 5 years andchange from 5 years to 9 years and between the patients whose diseasecourse change from 10 years to 19 years and is more than 20 years.There is no significant difference (P>0.05) between the patients whosecourse change from 5 years to 9 years and change from 10 years to 19years. 2,There is no specific clinical manifestation 3 ,Kidney has no change on sonography of the stage 1hypertensive patients To stage 2 hypertension, Kidney don't shrinksignificantly, the renal parenchyma don't become thin, but medullabecome large, the echo becomes strong on parenchyma and the limitbetween parenchyma and collecting system is clear in most cases. Tostage 3 hypertenson, in sonography, renal capsule is not smooth,kidney shrink, renal cortex becomes thin, medulla become small, theecho becomes strong from parenchyma, the limit between parenchymaand the collecting system is not clear. 4,If the blood pressure can be well controlled, most patients willbecome better. conclusion: 1,If the course of hypertension is extended, the degree becomeserious, the renal damage is aggravated. 2,Ultrosonic examination can't be used as the earlier diagnose...
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