A new character on the scene of cardiorenal syndrome

Renal dysfunction is related to increased arterial stiffness and left ventricular (LV) hypertrophy, which are two important risk factors for cardiovascular events. In addition, arterial

stiffness and LV mass have been linked to each other and to early signs of renal damage, such as microalbuminuria.1 Arterial stiffness has a strong influence on the kidney because of the

distinctive structure of the renal microcirculation. Certain tissues, such as the brain, heart, skin and skeletal muscle tissues, contain precapillary arterioles and metarterioles that

disperse the majority of the mean and pulsatile energy content of the advancing pressure and flow waveform before it reaches the capillary. In contrast, glomerular capillaries are located

between afferent and efferent arterioles. Because efferent arteriolar resistance is physiologically greater than afferent resistance, the mean and pulsatile pressures in the glomerulus are

relatively elevated. This high hydrostatic pressure ensures the maintenance of an elevated glomerular filtration fraction, which is normally ∼20% of renal plasma flow, but exposes the

glomerular capillary to potentially harmful pulsatile pressures if arterial stiffness and pulse pressure are high. Moreover, the myogenic tone of the afferent arteriole is influenced by

pressure pulsatility.2 Therefore, if the pulse pressure becomes greater than the mean pressure, renal vascular resistance will rise, and renal blood flow will fall. The pathophysiology that

links aortic stiffness to cardiovascular morbidity and mortality in hypertensive subjects may be associated with the reduced compliance of the large arteries that modifies the timing of wave

reflections and thus determines ventricular load. The net effect of these hemodynamic changes may be ischemia, particularly in the subendocardium, which, if chronic, is associated with

interstitial fibrosis and the development of heart failure.3 Chen _et al._4 have found that a left ventricular ejection fraction lower than 40% and an increased brachial-ankle pulse wave

velocity were independently associated with declines in renal function and progression to a renal end point. In our opinion, these findings are relevant because they support the hypothesis

that increased arterial stiffness is one of the mechanisms involved in the cross talk between the kidneys and the heart. Thus, as suggested by Chen _et al._, cardiorenal syndrome may be

renamed as cardiovascular renal syndrome. According to the pathophysiology mentioned above, the treatment of arterial stiffness could be useful for improving the prognosis in patients with

cardiorenal syndrome. REFERENCES * Cirillo M, Stellato D, Laurenzi M, Panarelli W, Zanchetti A, De Santo NG . Pulse pressure and isolated systolic hypertension: association with

microalbuminuria. The GUBBIO Study Collaborative Research Group. _Kidney Int_ 2000; 58: 1211–1218. Article  CAS  PubMed  Google Scholar  * Loutzenhiser R, Bidani A, Chilton L . Renal

myogenic response: kinetic attributes and physiological role. _Circ Res_ 2002; 90: 1316–1324. Article  CAS  PubMed  Google Scholar  * Mitchell GF, Hwang SJ, Vasan RS, Larson MG, Pencina MJ,

Hamburg NM, Vita JA, Levy D, Benjamin EJ . Arterial stiffness and cardiovascular events: the Framingham Heart Study. _Circulation_ 2010; 121: 505–511. Article  PubMed  PubMed Central  Google

Scholar  * Chen S-C, Lin T-H, Hsu P-C, Chang J-M, Lee C-S, Tsai W-C, Su H-M, Voon W-C, Chen H-C . Impaired left ventricular systolic function and increased brachial-ankle pulse-wave

velocity are independently associated with rapid renal function progression. _Hypertens Res_ 2011; 34: 1052–1058. Article  PubMed  Google Scholar  Download references AUTHOR INFORMATION

AUTHORS AND AFFILIATIONS * Department of Cardiology, Second University of Study of Naples, Naples, Italy Francesco Natale, Emanuela Lo Priore, Luigi Aronne, Alessandro Siciliano, Maria

Credendino, Chiara Cirillo, Chiara Granato, Paolo Calabrò, Maria Giovanna Russo & Raffaele Calabrò Authors * Francesco Natale View author publications You can also search for this author

inPubMed Google Scholar * Emanuela Lo Priore View author publications You can also search for this author inPubMed Google Scholar * Luigi Aronne View author publications You can also search

for this author inPubMed Google Scholar * Alessandro Siciliano View author publications You can also search for this author inPubMed Google Scholar * Maria Credendino View author

publications You can also search for this author inPubMed Google Scholar * Chiara Cirillo View author publications You can also search for this author inPubMed Google Scholar * Chiara

Granato View author publications You can also search for this author inPubMed Google Scholar * Paolo Calabrò View author publications You can also search for this author inPubMed Google

Scholar * Maria Giovanna Russo View author publications You can also search for this author inPubMed Google Scholar * Raffaele Calabrò View author publications You can also search for this

author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to Francesco Natale. ETHICS DECLARATIONS COMPETING INTERESTS The authors declare no conflict of interest. RIGHTS AND

PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Natale, F., Lo Priore, E., Aronne, L. _et al._ A new character on the scene of cardiorenal syndrome. _Hypertens Res_

34, 996 (2011). https://doi.org/10.1038/hr.2011.93 Download citation * Published: 21 July 2011 * Issue Date: September 2011 * DOI: https://doi.org/10.1038/hr.2011.93 SHARE THIS ARTICLE

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