Response to Macrocirculation Meets Microcirculation
We thank Papachristou and Baumann1 for their interest in our article2 and their insightful comments. We agree that determining the direction of causality between change in aortic stiffness and change in renal function is difficult to establish and that iatrogenic changes are possible confounders. However, none of our prospective observational cohort were using calcineurin inhibitors or cyclophosphamide. Nevertheless, changes in antihypertensive drugs can lead to alteration in glomerular filtration rate. Antihypertensive medication in this group was managed by the primary care physician and nephrologist with the aim of achieving United Kingdom Renal Association targets.3
Sixty-five percent of all patients were taking either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. This proportion was not significantly different between the groups (χ2=0.212; P=0.645). Sixteen of 23 of those who reached the end point of ≥25% decline in renal function or dialysis were receiving renin-angiotensin system blockade in comparison to 71 of 110 in the group who did not reach the end point. Five of 23 patients in the progressor group started renin-angiotensin system blockade during the study period, whereas in the <25% decline group 12 of 110 started renin-angiotensin system blockade (χ2=2.001; P=0.172). These data suggest that this drug class is unlikely to have affected the results.
We fully accept the confounding potential posed by the subgroup for whom aortic pulse wave velocity measurement was not possible. However, in this group of 13 patients, only 1 reached the renal end point. Aortic pulse wave velocity is determined by many factors, including medication, distending pressure, and comorbidities, and, therefore, there will be obligatory covariance between many potential variables. Thus, it is reassuring that when aortic pulse wave velocity was entered into a regression model with other variables, significance was retained. If this model is reconstructed using solely data from the 120 patients for whom aortic pulse wave velocity measurements were available, the same parameters are retained in a model with R2=0.12 and P=0.02.
Like Papachristou and Baumann, we eagerly anticipate other studies that will help us explore this intriguing relationship.
Papachristou E, Baumann M. Macrocirculation meets microcirculation. Hypertension. 2010; 56: e171.
Ford ML, Tomlinson LA, Chapman TP, Rajkumar C, Holt SG. Aortic stiffness is independently associated with rate of renal function decline in chronic kidney disease stages 3 and 4. Hypertension. 2010; 55: 1110–1115.