Aortic pulsatility and cardio-renal syndrome: renal heamodyamics and the microvasculature

Izzard, Ashley S.

doi: 10.1097/HJH.0000000000000266
Editorial Commentaries

Institute of Cardiovascular Sciences, University of Manchester, Manchester, UK

Correspondence to Ashley S. Izzard, PhD, Institute of Cardiovascular Sciences, Core Technology Facility (3rd Floor), University of Manchester, 46 Grafton St, Manchester M13 9NT, UK. Tel: +44 161 275 1227; fax: +44 161 275 1183; e-mail:

Article Outline

Although cardio-renal syndrome has been considered to be a bidirectional pathological link between chronic kidney disease (CKD) and cardiac complications, increased central (aortic) pulsatile haemodynamics may be an additional common underlying pathogenic mechanism, and in the current issue of the Journal, Hashimoto and Ito [1] provide evidence to support this possibility. Central haemodynamics, estimated glomerular filtration rate (eGFR), and standard parameters were measured in a group of patients with hypertension along with B-type natriuretic peptide (BNP) and urinary albumin/creatinine ratio (UACR), biomarkers for cardiac and renal damage, respectively. BNP levels were positively and negatively correlated with UACR and eGFR, respectively, and pulse pressure (PP) showed the strongest correlation with BNP out of the central haemodynamic parameters measured. In the absence of haemodynamic parameters, notably PP and pulse wave velocity (PWV), albuminuria was an independent predictor of a BNP elevation, but not when PP and/or PWV were included in the multivariate logistic analysis model; on the contrary, lower eGFR predicted higher BNP levels in all models. The data are indicative of a shared common mechanism in the context of (micro) albuminuria and raised BNP levels, namely increased aortic PP, whereas the association between reduced eGFR and BNP is mediated by a separate mechanism (possibly volume expansion). The authors’ suggest aortic PP as a possible therapeutic target because it is a common exacerbating factor for both renal and cardiac complications [1].

In this study, positive correlations were observed between plasma BNP and aortic PWV and augmentation index, in addition to aortic PP, and this is in agreement with other studies [2,3]. Although in the discussion, the authors’ relate plasma BNP levels to left-ventricular hypertrophy, the latter seems to be more strongly related to aortic systolic pressure rather than aortic PP [4,5].

Studies using a rat model of CKD, the Fawn Hooded rat, suggest that glomerular hypertension is a major causative factor [6]. A study in normotensive humans demonstrated that wave reflection (including augmentation index) was associated with signs of increased glomerular pressure, namely increased filtration fraction and UACR [7]. In a previous study, Hashimoto and Ito [8] demonstrated that increased aortic PP is closely related to changes in renal haemodymanics, namely the renal resistive index, in patients with hypertension, which the authors considered to be the mechanism responsible for microalbuminuria. However, it is uncertain if and how increased aortic PP increases glomerular pressure or whether glomerular pressure and/or flow pulsatility is a major determinant of UACR. Do increases in aortic pulsatility (aortic banding) cause CKD in animal models? Also, in the context of increased aortic pulsatility, what, if any, is the role of impaired myogenic properties of the afferent arteriole? Impaired myogenic properties of the afferent arteriole are thought to be a key determinant of hypertensive renal injury [9], and impaired myogenic properties of proximal renal arteries have been observed in the Fawn Hooded rat prior to advanced kidney failure [10]. Given the concept of cross-talk between large and small arteries [11], perhaps a shared underlying pathology may also exist.

Back to Top | Article Outline


Conflicts of interest

There are no conflicts of interest.

Back to Top | Article Outline


1. Hashimoto J, Ito S. Central pulse pressure links microalbuminuria with plasma B-type natriuretic peptide elevation: causal implication for cardiorenal syndrome in hypertension. J Hypertens 2014; 32:1665–1671.
2. Dawson A, Davies JI, Morris D, Struthers AD. B-type natriuretric peptide is associated with both augmentation index and left ventricular mass in diabetic patients without heart failure. Am J Hypertens 2005; 18:1586–1591.
3. Chatzis D, Tsioufis C, Tsiachris D, Taxiarchou E, Lalos S, Kyriakides Z, et al. Brain natriuretic peptide as an integrator of cardiovascular stiffening in hypertension. Int J Cardiol 2010; 141:291–296.
4. Roman MJ, Okin PM, Kizer JR, Lee ET, Howard BV, Devereux RB. Relations of central and brachial blood pressure to left ventricular hypertrophy and geometry: the Strong Heart Study. J Hypertens 2010; 28:384–388.
5. Roman MJ, Devereux RB. Association of central and peripheral blood pressures with intermediate cardiovascular phenotypes. Hypertension 2014; 63:1148–1153.
6. Simons JL, Provoost AP, Anderson S, Troy JL, Rennke HG, Sandstrom DJ, Brenner BM. Pathogenesis of glomerular injury in the Fawn Hooded rat: early glomerular hypertension predicts glomerular sclerosis. J Am Nephrol 1993; 3:1775–1782.
7. Fesler P, du Cailar G, Ribstein J, Mimran A. Glomerular hemodynamics and arterial function in normal individuals. J Hypertens 2010; 28:2462–2467.
8. Hashimoto J, Ito S. Central pulse pressure and aortic stiffness determine renal hemodynamics: pathophysiological implication for microalbuminuria in hypertension. Hypertension 2011; 58:839–846.
9. Bidani AK, Griffin KA, Williamson G, Wang X, Loutzenhiser R. Protective importance of the myogenic response in the renal circulation. Hypertension 2009; 54:393–398.
10. Ochodnicky P, Henning RH, Buikema HJ, de Zeeuw D, Provoost AP, van Dokkum RP. Renal vascular dysfunction precedes the development of renal damage in the hypertesnsive Fawn Hooded rat. Am J Physiol 2010; 298:F625–F633.
11. Laurent S, Briet M, Boutouyrie P. Large and small artery cross-talk and recent morbidity-mortality trials in hypertension. Hypertension 2009; 54:388–392.
© 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins