الفهرس 
Chronic Kidney Disease (CKD)Only 14 pages are availabe for public view
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Abstract
CKD is recognized as a strong risk factor for cardiovascular events and all-cause mortality, and thus presents a worldwide public health problem.
The principles of CKD management to reduce CVD risks are based on the achievement of adequate dialysis outcomes, with particular emphasis on the manage¬ment of fluid levels and blood pressure and regulation of the calcium–phosphorus–parathyroid hormone complex and levels of vitamin D. Although adaptive changes in the heart and vasculature begin in predialysis CKD, the dialysis procedure itself accelerates the progression of CVD, as shown in almost all pediatric studies.
CKD patients are often asymptomatic, and thus, a laboratory measurement of kidney function is required. In practice, serum creatinine is the most widely used endogenous marker of glomerular filtration (GFR).
Identifying serum biomarkers that are useful in profiling cardiovascular risk and enabling stratification of early mortality and cardiovascular risk is an important goal in the treatment of patients with end-stage renal disease (ESRD).
In our cross-sectional work; we conducted a study on 86 patients who are following up in the pediatric nephrology department, Children’s hospital, Ain Shams University hospitals with different stages of CKD (from stage 1 to stage 5 based on 24-hour creatinine clearance). We measured both serum Cystatin C and BNP to assess their values as markers for the early detection of functional and structural cardiac changes detected by echocardiography in CKD patients with different stages.
In the current study, CKD stage 1 represented 18.6 % (16/86) of the study group, stage 2 represented 5.8% (5/86), stage 3 represented 26.7% (23/86), stage 4 represented 26.7% (23/86) and stage 5 represented 22.1% (19/86) of the study group. All patients had normal systolic functions.
We found that there was a significant correlation between CKD and left ventricular mass z score (p value 0.019).
Additionally, we found that CKD staging was related to cardiac volumes. There was a significant correlation between CKD stage and left atrial volume index (LAVI) (p-value 0.003), left ventricular end diastolic volume index (LVEDVI) (p-value 0.033), left ventricular end systolic volume index (LVESVI) (p-value 0.042), as well as LVEDD Z score (p-value 0.028) and LVPWd (p-value 0.045)
Also, there was a significant correlation between CKD stage and early diastolic velocity of the septal mitral annulus (e′) (p value <0.001), ratio of early transmitral flow velocity to early diastolic mitral annulus velocity (E/e′) (p value 0.005), denoting diastolic dysfunction with advancement of the CKD stage.
There was no significant correlation between Cystatin C and CKD stage among the study group (p-value 0.919).
We found that there was no significant correlation between Cystatin C and left atrial volume index (LAV) (p-value 0.37), left ventricular end diastolic volume index (LVEDVI) (p-value 0.76) or left ventricular end systolic volume index (LVESVI) (p-value 0.57).
Cystatin C was not significant correlating with early transmitral flow (E-wave) and a late flow with atrial contraction (A wave) (E/A ratio) (p-value 0.9), ratio of early transmitral flow velocity to early diastolic mitral annulus velocity (E/e′) (p-value 0.52) nor the deceleration time of the E-wave (Dct) (p-value 0.73). Also, there was no significant correlation between Cystatin C and left atrial dimension (LAD) Z score (p-value 0.63), LVEDD Z score (p-value 0.41) and relative wall thickness (p-value 0.18). Additionally, there was no significant correlation between Cystatin C and left ventricular mass (LVM) Z score (p-value 0.23). This means that Cystatin C did not correlate with neither cardiac dimensions nor cardiac functions in CKD patients.
Moreover, we found no significant correlation between Cystatin C and BNP (p value 0.482).
Regarding BNP; the median value of BNP in our study was 1000 (pg/ml) with interquartile range from 420 to 1900. This means that most of our patients had high BNP level.
Regarding cardiac volumes and dimensions we did not find any significant correlation between BNP and left atrial dimension (LAD) Z score (p-value 0.68), left atrial volume index (LAVI) (p-value 0.58) , LVEDD Z score (p-value 0.344), left ventricular end diastolic volume index (LVEDVI) (p-value 0.12), left ventricular end systolic volume index (LVESVI) (p-value 0.35), relative wall thickness (RWT) (p-value 0.88), nor left ventricular mass (LVM) Z score (p-value 0.086).
There was no significant correlation between BNP and left ventricular ejection fraction (LVEF) (p-value 0.7), early transmitral flow (E-wave) and a late flow with atrial contraction (A wave) (E/A ratio) (p-value 0.46), deceleration time of the E-wave (Dct) (p-value 0.063), early diastolic velocity of the septal mitral annulus (e′) (p-value 0.3) or LVPWd (p-value 0.238). This means that BNP did not correlate with neither cardiac dimensions nor cardiac functions in CKD patients.