The Effects Of Smoking On Intact Parathyroid Hormone And Left Ventricular Remodeling In The End Stage Renal Disease Patients

Objective: Foreign studies have shown that smoking patients had higherlevels of intact parathyroid hormone (iPTH) in the end stage renal diseasepatients and smoking was positively correlated with iPTH; iPTH promotedleft ventricular hypertrophy(LVH). Smoking increased the mortality ofcardiovascular diseases. This study observed the effects of smoking on intactparathyroid hormone and left ventricular remodeling in the end stage renaldisease patients.Methods:1139cases which were non-dialysis end-stage renal disease of chronicglomerulonephritis were sequence selected.85cases were men and54caseswere women, age (45.1±15.0) years, and eGFR was (CKD-EPI equation,8.38±2.24) ml.min-1.1.73m^-2. The standard of excluding:1Using drugs thataffected iPTH,2Acute renal injury,3Idiohyperparathyroidism,4Diabetes,5Sleep apnea syndrome,6Obesity (BMI>28Kg／m²)).2Clinical observed parameters: Indicators of thickness of interventricularseptum (IVS), leftventricular posterior wall thickness (LVPW), left ventricularend diastolic diameter (LV) and ejection fraction (EF) were examined by theSiemens Sequoia512two-dimensional color Doppler echocardiography. Weasked and recorded the daily cigarette consumption, the smoking age, age,blood pressure, duration of hypertension, body mass index (BMI), durationof kidney disease and the use of ACEI∕ARB, and collected iPTH,hemoglobin, fasting glucose, high density lipoprotein, triglycerides, sodium,calcium, phosphorus, creatinine, uric acid and other laboratory parameters.3I analyzed relationships among iPTH level and the LVMI and otherclinical indicators in end-stage renal disease patients.4Clinical indicators which were normal distributed datas used mean± standard deviation. Normal distribution data of two independent samples usedt test. Multiple independent samples of the normal distribution data werecompared using analysis of variance, and between groups using the Post Hoctest. Non-normally distributed datas were analyzed using Wilcoxon test.counting data used the X²test. The relations of iPTH, LVMI and correlatedclinical parameters used Spearman single-factor analysis. I used analysis ofLogistic regression to exclude influencing factors. Applying SPSS13.0statistical software to analyze datas. P<0.05represented statisticallysignificant difference.Results:1The comparison of clinical parameters in smoking and nonsmokinggroups.Nonsmoking group had102cases, and48cases were men,54cases werewomen; smoking group had37cases which were men. There were nodifferences in calcium, phosphorus, age, MAP, the compliance rate oftreatment of hypertension, kidney disease duration and hemoglobin in the twogroups (p>0.05). There were differences in iPTH, LVMI, duration ofhypertension, uric acid and urinary protein quantity in the two groups, whileHDL in the smoking group was lower than that of in the nonsmoking group(p<0.05). The rate of hypertension prevalence was90.66%in the smokinggroup (34/37) and80.39%(82/102) in the nonsmoking group. The rates ofhypertension prevalence was different (p <0.05).2LVMI and iPTH in the heavy smoking group were higher than that ofin lignt somking group.Light smoking group had21cases, and heavy smoking group had16cases. There were no differences in age, prevalence of hypertension andcompliance rate, duration of hypertension, kidney disease duration,hemoglobin, uric acid, HDL and urinary protein quantity (P=0.14⁰.92, P>0.05). LVMI and iPTH in heavy smoking group were higher than those in thelight smoking group, the difference was statistically significant (p <0.05).3The comparison of clinical parameters in LVH and non-LVH groups. 111cases were left ventricular hypertrophy in139patients and theincidence of left ventricular hypertrophy was79.86%. Age, diastolic bloodpressure, MAP, duration of hypertension, hemoglobin, calcium, phosphorus,height (sex ratio between the two groups had no difference), HDL and urinaryprotein quantity had no significant difference between the two groups (P>0.05). iPTH, smoking rate and systolic blood pressure in left ventricularhypertrophy group were higher than non-LVH group and the rate of ACEI/ARB drugs were less than non-LVH group (P <0.05).4The correlations of iPTH, LVMI with clinical parameters.iPTH had positive correlations with smoking, phosphorus, BUN, Scr andUA (r=0.17⁰.37, p <0.05), and had negative correlations with Hb and Ca(r=-0.25^-0.40, p <0.05). LVMI had positive correlations with smoking,iPTH systolic blood pressure, serum phosphate, BUN, Scr and UA (r=0.21⁰.33, p <0.05), LVMI had no correlation with MAP, diastolic blood pressureand Hb.5The correlations of smoking with iPTH and LVMI after correcting therelative parameters.The risk of iPTH increased in smokers was1.85times than that ofnonsmokers after correcting calcium, phosphorus, BUN, Scr and UA usingLogistic regression analysis(95%CI：1.08—3.16); The risk of left ventricularhypertrophy in smokers was1.74times than that of nonsmokers and patientswhose iPTH were higher was2.97times than those iPTH were normal aftercorrecting age, height, systolic blood pressure, phosphorus, iPTH, BUN, Scrand UA using Logistic regression analysis(95%CI：1.04—3.12).Conclusion:smoking further elevated serum iPTH and promoted left ventricularhypertrophy in the end stage renal disease patients.