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Pathological Features Of Benign Hypertensive Nephrosclerosis And Clinical-Pathological Correlations

Posted on:2013-01-16Degree:MasterType:Thesis
Country:ChinaCandidate:J KouFull Text:PDF
GTID:2234330374966275Subject:Internal Medicine
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Background and Objective: Prevalence of primary hypertensive is increasingworldwide year by year. Hypertensive nephropathy is a common cause leading to endstage renal disease. The pathological feature of hypertensive nephropathy is benignhypertensive nephrosclerosis. Since the majorities of this disease were diagnosed byclinical evidences and were lack of renal biopsy, clinical pathological correlations ofhypertensive nephropathy are limited both in domestic and abroad. The roles of bloodpressure and other clinical and laboratory parameters on renal pathology are stillcontroversial. The pathogenesis of benign hypertensive nephrosclerosis is not yet clear.This study analyzed the patients with benign hypertensive nephrosclerosis proved byrenal biopsy. Clinical and pathological features were collected. Correlations betweenclinical indicators and pathological changes were analyzed. The relationship betweenbenign renal arteriolosclerosis and other renal pathologic changes were investigated.This study aims to summarize the characteristics of patients with benign hypertensivenephrosclerosis.Methods: According to the strict inclusion criteria,48patients diagnosesed asbenign hypertensive nephrosclerosis proved by renal biopsy were retrospectivelyanalyzed from1995to2011in our hospital, detailed clinical indicators were recordedand biopsy slides were re-analyzed. Clinical data includes age,gender, smoking history,drinking history, family history of hypertension, blood pressure when admission, bodymass index, renal ultrasound and the main laboratory examination index, includingblood routine examination, urine routine examination, serum biochemistry,immunological tests, coagulation index, blood glucose, blood lipids, blood uric acid, glomerular filtration rate (eGFR) and other metabolic parameters, renal tubular functiontests, eGFR is estimated by the application of CKD-EPI equation. Pathologicalparameters,including glomerular area, glomerular density and glomerularlesions(ischemia wrinkled glomeruli, hypertrophic glomeruli, focal segmental scleroticglomeruli, solidified glomeruli, obsolescent glomeruli), tubulointerstitial lesions(including interstitial inflammatory cell infiltration, interstitial fibrosis and tubularatrophy), and arterioles lesions (hyalinization, the endomysium hypertrophy), lumenwall diameter ratio and of arterioles stenosis percentage were used to evaluate thedegree of arterioles stenosis. Record the way the medication using, and get theoutcomes of the patients by follow-up.We analysis the clinical and pathological features,the correlation between the renal vascular lesions and glomerular, tubulointerstitiallesions, use logistic regression analysis and survival analysis, SPSS17.0software isused to take all statistical analysis.Result:48patients were included,10women,38men, all patients aged46.56±9.59years old,25patients has family history of hypertension. Blood pressure aregrouped according to the Chinese Hypertension Prevention Guide, arterioles stenosisproportion (P=0.021) and glomerular density (P=0.045) are significantly differentamong the groups, with further study, systolic blood pressure showed significantpositive relation with arterioles stenosis proportion (r=0.35, P=0.02), glomerulardensity (r=0.375, P=0.009), tubulointerstitial lesions degree (r=0.295, P=0.04), andsignificant negative relation with eGFR (r=-0.333, P=0.021); mean arterial bloodpressure showed significant positive correlation with arterioles stenosis proportion (r=0.3, P=0.04), glomerular density (r=0.315, P=0.031); pulse pressure showedsignificant positive correlation with glomerular density (r=.301, P=0.04)andsignificant negative relation with eGFR (r=-0.432, P=0.002). Other clinical indicatorshave little effect to arterioles, glomerular and tubulointerstitial pathological parameters,the odds ratio of the indicators is small,0.9~1.2. Proteinuria is an independent riskfactor to global sclerosis. The tubulointerstitial lesions degree is an independent risk factor to eGFR decline (<60ml/min/1.73square meters)and the odds ratio was1.99. Thefollow-up data suggests that clinical and pathological indicators, medication using hadinfluence to prognosis, while alcohol drinking is a risk factor to poor prognostic (P=0.03). Analysis for the pathological features showed that the percentage of arteriolesstenosis caused by endomysium hypertrophy is22.85%, and the percentage of arterioleshyalinization is19.17%. Ischemic lesions is the most common type of glomerularlesions, take up32.88%(including obsolescent glomeruli,20.20%, ischemic wrinkledglomeruli,12.68%), solidified glomeruli take up only8.41%. Arterioles stenosis aresignificantly positive correlated to the percentage of lesion glomeruli, ischemicglomeruli and tubulointerstitial lesions degree. Percentage of arterioles hyalinization didnot affect glomerular and tubulointerstitial lesions. Glomerular lesions andtubulointerstitial lesions was positively correlated, but glomerular lesions may happenprecede tubulointerstitial lesions.Conclusion: Blood pressure level of the patients with benign hypertensivenephrosclerosis, especially systolic blood pressure,is the most important factor to therenal pathology and renal function. Ischemic lesions are the most common types ofglomeruli lesions, arterioles stenosis (not hyalinization)caused by the endomysiumhypertrophy affect glomerular and tubulointerstitial lesions. Glomerular lesions mayhappen precede to tubulointerstitial lesions. Proteinuria is an independent risk factor forglobal sclerosis.Alcohol drinking is risk factors to the poor prognosis. It suggested thatblood pressure control, reduction of proteinuria and alcohol withdrawal are importantmeans of prevention and treatment of hypertensive nephropathy.
Keywords/Search Tags:Benign hypertensive nephrosclerosis, endomysium hypertrophy, hyalinization, ischemic, tubulointerstitial
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