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• W2113120657 abstract "The interplay between the heart and the kidneys has received widespread attention in recent years. A novel five-class definition of cardiorenal syndromes has been proposed. The ability of two markers of cardiac dysfunction to predict progression of primary kidney disease, described by Dieplinger and his co-workers, highlights the prognostic importance of the chronic cardiorenal (types 2 and 4) syndromes. The interplay between the heart and the kidneys has received widespread attention in recent years. A novel five-class definition of cardiorenal syndromes has been proposed. The ability of two markers of cardiac dysfunction to predict progression of primary kidney disease, described by Dieplinger and his co-workers, highlights the prognostic importance of the chronic cardiorenal (types 2 and 4) syndromes. In 2002 the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (KDOQI) Work Group defined chronic kidney disease (CKD) as the 3-month presence of proteinuria or a persistently lowered glomerular filtration rate (GFR) regardless of the underlying pathology. According to this definition, almost 20 million adults in the United States have CKD, and yet another 20 million are considered at risk for developing CKD. Because of its growing prevalence and its high socioeconomic burden, CKD has recently been termed the ‘silent epidemic.’ The course of CKD is marked by secondary complications such as bone disease and anemia as well as a considerably increased risk for cardiovascular disease and, in a minority of patients, the progression to end-stage renal disease. Age, background cardiovascular risk, and the etiology of kidney disease have all been described as impacting the progression of the disease independent of baseline CKD stage. A recent study by O'Hare et al. convincingly demonstrated the flaws of a purely GFR-based approach to CKD patients by showing a tenfold increase in the ratio of necessary to unnecessary vascular access surgery in elderly patients.1.O'Hare A.M. Bertenthal D. Walter L.C. et al.When to refer patients with chronic kidney disease for vascular access surgery: should age be a consideration?.Kidney Int. 2007; 71: 555-561Abstract Full Text Full Text PDF PubMed Scopus (111) Google Scholar A GFR-independent marker of disease progression would help clinicians to tailor therapy and intervention and to base their decisions on the individual patient's risk. Dieplinger et al.2.Dieplinger B. Mueller T. Kollerits B. et al.Pro-A-type natriuretic peptide and pro-adrenomedullin predict progression of chronic kidney disease: the MMKD Study.Kidney Int. 2009; 75 (xxx): xxxAbstract Full Text Full Text PDF Scopus (60) Google Scholar (this issue) describe the ability of pro-A-type natriuretic peptide and pro-adrenomedullin to predict disease progression in patients with nondiabetic kidney disease enrolled in the Mild to Moderate Kidney Disease (MMKD) Study. A-type natriuretic peptide (ANP) is a cardiac peptide with potent natriuretic, vasodilator, and diuretic actions. ANP stems from the enzymatic cleavage of its precursor proANP, which is significantly more stable than the active breakdown product. The co-released, inactive N-terminal split product is subject to further enzymatic fragmentation, leaving the midregional breakdown product MR-proANP as a stable and readily measurable parameter of circulating ANP levels. ANP is primarily secreted from the cardiac atria in response to volume overload and myocyte stretch. Increased levels of ANP have been observed in heart failure, left ventricular dysfunction, coronary artery disease, and renal failure. Adrenomedullin (ADM) is also a potent natriuretic and vasodilatory peptide. It has a short half-life and is derived from the cleavage of a larger precursor molecule, proADM. MR-proADM is stable at room temperature and can be measured by a sandwich immunoassay. MR-proADM directly reflects circulating adrenomedullin levels. Increased adrenomedullin levels have been observed in disorders associated with hypervolemia, such as heart failure, myocardial infarction, and ESRD under hemodialysis. Pathologically increased adrenomedullin levels were recently shown to reflect the degree of underlying cardiac dysfunction.3.Cheung B.M. Li C.Y. Wong L.Y. Adrenomedullin: its role in the cardiovascular system.Semin Vasc Med. 2004; 4: 129-134Crossref PubMed Scopus (24) Google Scholar, 4.Yoshihara F. Ernst A. Morgenthaler N.G. et al.Midregional proadrenomedullin reflects cardiac dysfunction in haemodialysis patients with cardiovascular disease.Nephrol Dial Transplant. 2007; 22: 2263-2268Crossref PubMed Scopus (15) Google Scholar While adrenomedullin has been detected in multiple tissues, disease-induced secretion appears to stem from biventricular cardiac dilation5.Yoshihara F. Nishikimi T. Horio T. et al.Ventricular adrenomedullin concentration is a sensitive biochemical marker for volume and pressure overload in rats.Am J Physiol Heart Circ Physiol. 2000; 278: H633-H642PubMed Google Scholar and increased vascular shear stress.6.Chun T.H. Itoh H. Ogawa Y. et al.Shear stress augments expression of C-type natriuretic peptide and adrenomedullin.Hypertension. 1997; 29: 1296-1302Crossref PubMed Scopus (167) Google Scholar During the 7-year follow-up period covered in the MMKD Study, the combined end point of a doubling of serum creatinine or disease progression to ESRD requiring renal replacement therapy was reached in 65 of 177 patients. In accordance with previous studies, Dieplinger et al.2.Dieplinger B. Mueller T. Kollerits B. et al.Pro-A-type natriuretic peptide and pro-adrenomedullin predict progression of chronic kidney disease: the MMKD Study.Kidney Int. 2009; 75 (xxx): xxxAbstract Full Text Full Text PDF Scopus (60) Google Scholar found patients reaching this end point to be older and to display higher levels of proteinuria and lower GFR. Additionally, the authors reported higher levels of MR-proANP and MR-proADM in progressors. The predictive accuracy of these novel biomarkers was equal to the predictive potential of baseline GFR values (AUCMR-proANP=0.810, AUCMR-proADM=0.876, AUCGFR=0.838). Remarkably, MR-proANP and MR-proADM retained high diagnostic accuracy even after the adjustment for the most common cofactors for disease progression: age, sex, GFR, and proteinuria. These results suggest that MR-proANP and MR-proADM, two reliable markers of cardiac dysfunction, could help clinicians to estimate the pace of disease progression, even in patients with equal GFR and proteinuria levels. This study extends and corroborates similar findings from the same cohort for NT-proBNP, a quantitative marker of cardiac stress that is released predominantly by the cardiac ventricles. BNP and NT-proBNP are co-secreted and, under non-stressed conditions, are found only in atrial granules. In response to stress, however, BNP and NT-proBNP are synthesized, stored, and released mainly from ventricular myocardium. The primary stimulus for BNP and NT-proBNP formation seems to be end-diastolic wall stress. One important limitation, which was appropriately acknowledged by the authors, is the lack of detailed functional and structural cardiac assessment (for example, echocardiography) and therefore the inability to elucidate whether MR-proANP and MR-proADM were associated with CKD progression independently of the presence of structural and/or functional cardiac disease or whether clinically undetected cardiac disease at least to some extent triggered the deterioration of renal function. The interplay between the heart and the kidneys has received widespread attention in recent years (Figure 1). Initially, the ‘cardiorenal syndrome’ has generally been considered to be driven by a failing heart causing a secondary deterioration of kidney function. In this setting, impaired kidney function has convincingly been shown to be associated with a significantly reduced patient survival. This simplistic and unidirectional view has recently been challenged after accelerated cardiac atherosclerosis, left ventricular hypertrophy and remodeling, and myocardial microangiopathy were observed in primary kidney diseases.7.Berl T. Henrich W. Kidney-heart interactions: epidemiology, pathogenesis, and treatment.Clin J Am Soc Nephrol. 2006; 1: 8-18Crossref PubMed Scopus (178) Google Scholar To accommodate these important kidney–heart interactions, a novel five-classed definition of cardiorenal syndromes (CRS) has been proposed.8.Ronco C. House A.A. Haapio M. Cardiorenal syndrome: refining the definition of a complex symbiosis gone wrong.Intensive Care Med. 2008; 34: 957-962Crossref PubMed Scopus (169) Google Scholar In this classification, types 1 and 2 represent the acute and chronic forms of the ‘classic’ cardiorenal syndrome, in which decreased cardiac function induces a progressive and potentially permanent decline in kidney function. Similarly, types 3 and 4 represent the acute and chronic forms of the ‘renocardiac’ syndrome, in which primary kidney disease induces acute (for example, heart failure, arrhythmia) or chronic (for example, hypertrophy, coronary atherosclerosis) cardiac disorders. An additional type 5 includes systemic diseases such as sepsis, amyloidosis, and systemic lupus erythematosus that are able to induce cardiac as well as renal dysfunction. Hence, the ability of two markers of cardiac dysfunction to predict progression of primary kidney disease, described by Dieplinger and his co-workers,2.Dieplinger B. Mueller T. Kollerits B. et al.Pro-A-type natriuretic peptide and pro-adrenomedullin predict progression of chronic kidney disease: the MMKD Study.Kidney Int. 2009; 75 (xxx): xxxAbstract Full Text Full Text PDF Scopus (60) Google Scholar highlights the prognostic importance of the chronic cardiorenal syndromes (CRS types 2 and 4). Unfortunately, this obvious pathophysiological link between CKD and cardiac dysfunction is confronted by a significant underprescription of cardiovascular disease-modifying pharmacotherapy in CKD patients. A recent, alarming study investigating patients after acute myocardial infarction found less than 50% of all CKD patients to be treated with a combination of aspirin, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins.9.Berger A.K. Duval S. Krumholz H.M. Aspirin, beta-blocker, and angiotensin-converting enzyme inhibitor therapy in patients with end-stage renal disease and an acute myocardial infarction.J Am Coll Cardiol. 2003; 42: 201-208Abstract Full Text Full Text PDF PubMed Scopus (256) Google Scholar Only the minority of CKD patients receiving standard combination drug therapy experienced 30-day survival similar to that of non-CKD patients. This lack of guideline-conforming therapy is generally caused by concerns over increasing creatinine levels and potential nephrotoxicity. However, a short-term, ACE inhibitor-associated increase in serum creatinine was found to reflect successful nephroprotection in patients with renal insufficiency by a large metaanalysis.10.Bakris G.L. Weir M.R. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: is this a cause for concern?.Arch Intern Med. 2000; 160: 685-693Crossref PubMed Google Scholar While research activities in the cardiorenal syndromes are only beginning to grow and consensus definitions are only being discussed, clinicians may presently not be able to stop the vicious cycle of declining renal and cardiac function but can nevertheless significantly slow down its progression. Treating the shared risk factors by adequately lowering blood pressure and sufficiently blocking the renin–angiotensin system as well as by controlling diabetes mellitus, treating dyslipidemia, and advocating smoking cessation remains of pivotal importance. We as clinicians need to consider and attempt to use these powerful tools in all our CRS patients. The authors declared no competing interests. Correction to Predicting progression in nondiabetic kidney disease: the importance of cardiorenal interactionsKidney InternationalVol. 76Issue 1PreviewCorrection to: Kidney International (2009) 75, 253–255. doi:10.1038/ki.2008.591 Full-Text PDF Open Archive" @default.
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