Causes of Chronic Kidney Disease and Their Associations with Cardiovascular Risk and Disease in a Sub-Saharan Low-Income Population.

Introduction: The causes of chronic kidney disease (CKD) in people living in Sub-Saharan Africa await identification. Also, whether cardiovascular risk and disease extent differ among patients with different CKD etiologies is uncertain. Methods: In this prospective cross-sectional study, we examined the presumed causes of chronic kidney disease (CKD) and their relationships with cardiovascular risk and disease in 743 consecutive patients from a sub-Saharan low-income population. Results: Hypertensive nephropathy (HNP) (60.2%), diabetic nephropathy (DNP) (24.4%), HIV associated CKD (20.0%) and glomerular disease (13.6%) comprised the major CKD etiologies upon enrolment at the hospital nephrology clinic. Pulse pressure was larger in patients with concurrent HNP and DNP than in those with HNP only (p<0.001). Pulse pressure and systolic blood pressure were larger in HNP or/and DNP patients than those with HIV associated CKD and glomerular disease (p=0.04 to <0.001). Cardiovascular disease was more prevalent in patients with HNP and concurrent HNP and DNP than those from other etiologic categories (p<0.05). HNP and DNP were associated with pulsatile pressures (pulse pressure and systolic blood pressure) independent of one another (p<0.01). In adjusted product of coefficient mediation analysis, mean arterial or distending pressure accounted fully for the potential impact of HNP on pulsatile pressures (103.9-115.7%) but not for that of DNP on the respective pressures (-2.0%-(-)7.5%). Conclusion: HNP is by far the most prevalent presumed cause of CKD in this African population. Cardiovascular risk and disease differ markedly across CKD etiological categories.

The relative potential contribution of volume load and vascular mechanisms to hypertension in non-dialysis and dialysis chronic kidney disease patients.

Background: Hypertension is highly prevalent and particularly difficult to treat adequately in patients with chronic kidney disease (CKD). The relative contribution of volume overload and vascular mechanisms to blood pressure measures in CKD and whether these effects differ in non-dialysis compared to dialysis patients is unknown. Methods: We determined the potential impact of volume load (stroke volume) and vascular mechanisms (inverse of total arterial compliance (inv TAC) and systemic vascular resistance (SVR)) on mean and brachial and aortic systolic blood pressures in 67 non-dialysis and 48 dialysis chronic kidney disease (CKD) patients. Relationships were determined in confounder adjusted regression models. Results: Stroke volume (p value = 0.003) was more strongly associated with mean arterial pressure than SVR (p value = 0.9) (p value for difference = 0.03). When stroke volume and SVR were entered in the same regression model (model R2 = 0.324), they contributed equally to the variation in mean arterial pressure (p value for difference = 0.5). Stroke volume (p value ≤ 0.002) and inv TAC (p value ≤ 0.001) contributed equally to the variation in systolic pressures (p value for difference ≥ 0.9). When stroke volume and inv TAC were entered in the same regression model (model R2 = 0.752 to 0.765), they contributed equally to the variation in systolic blood pressures (p value for difference = 0.7). Stroke volume, TAC and SVR were similar (p value ≥ 0.5) and associated to the same extent with blood pressure measures in non-dialysis and dialysis CKD patients (p value for difference ≥ 0.1). In receiver operator characteristic curve analysis, elevated systolic blood pressure was determined by stroke volume (p value = 0.005) and inv TAC (p value = 0.03) but not SVR (p value = 0.8). The calculated power of the study was 0.999 based on α = 0.05. Conclusions: The present investigation suggests that both volume load and vascular mechanisms should be considered in the management of hypertension among patients with CKD. The extent and relative potential impact of volume load and vascular mechanisms on blood pressure measures are as large in non-dialysis compared to dialysis CKD patients.

Associations of Traditionally Determined Left Ventricular Mass Indices and Hemodynamic and Non-Hemodynamic Components of Cardiac Remodeling with Diastolic and Systolic Function in Patients with Chronic Kidney Disease.

We aimed to evaluate the extent to which different left ventricular mass parameters are associated with left ventricular function in chronic kidney disease (CKD) patients. We compared the associations between traditionally determined left ventricular mass indices (LVMIs) and hemodynamic (predicted LVMIs) and non-hemodynamic remodeling parameters with left ventricular function in patients with CKD; non-hemodynamic remodeling was represented by inappropriate left ventricular mass and inappropriate excess LVMIs (traditionally determined LVMIs-predicted LVMIs). Non-hemodynamic left ventricular remodeling parameters were strongly associated with impaired left ventricular systolic function (p < 0.001), whereas hemodynamic left ventricular remodeling was also related strongly (p < 0.001) but directly to left ventricular systolic function. Independent of one another, hemodynamic and non-hemodynamic left ventricular remodeling had associations in opposite directions to left ventricular systolic function and was associated directly with traditionally determined left ventricular mas indices (p < 0.001 for all relationships). Non-hemodynamic cardiac remodeling parameters discriminated more effectively than traditionally determined LVMIs between patients with and without reduced ejection fraction (p < 0.04 for comparison). Left ventricular mass parameters were unrelated to impaired diastolic function in patients with CKD. Traditionally determined LVMIs are less strongly associated with impaired systolic function than non-hemodynamic remodeling parameters (p < 0.04-0.01 for comparisons) because they represent both adaptive or compensatory and non-hemodynamic cardiac remodeling.