Correlation Of The Aldosterone And Chronic Allograft Nephropathy

Objective:We explore the correlation of the aldosterone and Chronic Allograft Nephropathythrough studying the tendency of the serum aldosterone levels and seeing theeffectiveness which the aldosterone antagonist is used to treat the proteinuria in patientswith the CAN. It would present the direction and theoretic evidences to delay theprogression of the CAN in order to improve the long-term survival in renal transplantpatients.Methods:1. Studying the serum aldosterone levels in the CANMethods: Renal allograft biopsy was performed in all of the renal allograftrecipients with the proteinuria or the increased serum creatinine level who came into ourhospital from March2011to January2012. Among them28cases were diagnosed aschronic allograft nephropathy based on the pathological observation.5cases of thetransplant recipients were collected as the control group. They were made thesequencing renal allograft biopsy and their pathologic manifestation were normal. The subjects were not asked to use the drug impacting on the secretion of aldosteronemore than2weeks. we gain the serum aldosterone, the serum potassium and serumcreatinine level. The estimated glomerular filtration rate (eGFR) is learned accordingthe formula of CKD-EPI. And the24hours urine protein excretion was measuredamong the28cases. According the pathologic condition from the allograft biopsy, the28cases which were eventually diagnosed as the CAN were divided into the threegroups: mild (I Group),7cases; moderate (Ⅱ Group),9cases; severe (III Group),12cases. The relationship is presented an analysis among the serum aldosterone, theglomerular filtration rate, the24hours urine protein excretion and renal allograft biopsyin the CAN through making the statistical analysis.Result:1. The higher the allograft pathological grade is, the less the glomerular filtration ratebecome (F=51.358，P＜0.01). And the higher the allograft pathological grade is, themore the24hours urine protein excretion become (F=15.39, P＜0.01). Compare withthe control group, the serum aldosterone levels obviously raise in the CAN (F=7.059，P＜0.01). The serum aldosterone levels in III Group are significantly higher than those inI Group and Ⅱ Group （0.259±0.057vs.0.203±0.017;0.259±0.057vs.0.187±0.073),the serum aldosterone levels in Ⅱ Group are higher than those in I Group (0.203±0.017vs.0.187±0.073).2. Along with the descent of eGFR and the ascent of the24hoursurine protein excretion in the CAN, the serum aldosterone levels also present thetendency of progressive elevation. In the most of cases, the serum aldosterone levels arehigher negatively correlated with the eGFR (r=﹣0.726, P＜0.01). And the serumaldosterone levels are higher positively correlated with the24hours urine proteinexcretion (r=0.78, P＜0.01).2. Clinical applications about the aldosterone receptor antagonists in patients withthe CANMethods:50patients with the CAN who were in our hospital from January2012toNovember2013were elected in this study and then randomly divided into the twogroups. The treatment group (25cases) was treated with Valsartan (80mg/d) and Spironolactone (20mg/d). And the control group (25cases) was treated only withValsartan (80mg/d). The level of serum potassium (K+), systolic bloodpressurediastolic blood pressure, the estimated glomerular filtration rate (GFR) and the24hours urine protein excretion were monitoring after the3and6months of therapy.We make statistical analysis.Result:1. after the treatment, the level of systolic blood pressure and the diastolicblood pressure are not statistical significance between the two group (P＞0.05). theeGFR were observed to slightly decrease both two groups after the3and6months oftreatment, but no statistical significance were observed. The serum potassium levelswere observed to a little increase in the treatment group after3and6months oftreatment. There was no statistical significance were observed as compared to the samegroup before the treatment and the control group after the same period of treatment.There was not hyperkalemia during the treatment.2. After3and6months oftreatment,24hours urine protein excretion were decreased in the treatment group(T=16.22, P＜0.05; T=21.22, P＜0.05). But in the control group,24hours urine proteinexcretion which was observed after3months of the treatment was no statisticalsignificance(T=1.29, P=0.21＞0.05). After6months of treatment,24hours urineprotein excretion was markedly decreased in the control group(T=7.04，P＜0.05). Thequantitative of24hours urine protein excretion in the treatment group after6months ofthe treatment was significantly lower than that of the control group （T=21.84，P＜0.05）.Conclusion:The first study shows that there is a positive correlation between the serumaldosterone levels and24hours urine protein excretion, and there is a negativecorrelation between the serum aldosterone levels and the glomerular filtration rate in theCAN. Compared to the control group, the serum aldosterone level is significantelevation. And the higher the allograft pathological grade is, the more this tend is. Thesecond study signs that the levels of24hours urine protein excretion was markedly decreased by using the aldosterone antagonist in the CAN. Aldosterone may play animportant role in the CAN. They both indicate the aldosterone might be involved in thepathogenesis of the CAN and be one of the influential factor. The aldosterone may be apotential therapeutic target.