The role of the kidney in heart failure.
Renal dysfunction is common in patients with heart failure and is associated with high morbidity and mortality. Cardiac and renal dysfunction may worsen each other through multiple mechanisms such as fluid overload and increased venous pressure, hypo-perfusion, neurohormonal and inflammatory activation, and concomitant treatment. The interaction between cardiac and renal dysfunction may be critical for disease progression and prognosis. Renal dysfunction is conventionally defined by a reduced glomerular filtration rate, calculated from serum creatinine levels. This definition has limitations as serum creatinine is dependent on age, gender, muscle mass, volume status, and renal haemodynamics. Changes in serum creatinine related to treatment with diuretics or angiotensin-converting enzyme inhibitors are not necessarily associated with worse outcomes. New biomarkers might be of additional value to detect an early deterioration in renal function and to improve the prognostic assessment, but they need further validation. Thus, the evaluation of renal function in patients with heart failure is important as it may reflect their haemodynamic status and provide a better prognostic assessment. The prevention of renal dysfunction with new therapies might also improve outcomes although strong evidence is still lacking.
Institute of Cardiology, University of Brescia, c/o Spedali Civili di Brescia, Piazzale Spedali Civili 1, Brescia, Italy. metramarco@libero.it
Marco
M
Metra
Gad
G
Cotter
Mihai
M
Gheorghiade
Livio
L
Dei Cas
Adriaan A
AA
Voors
D000118:Acetylglucosaminidase / Q000378:metabolism; D058186:Acute Kidney Injury / Q000209:etiology / Q000503:physiopathology; D000209:Acute-Phase Proteins / Q000378:metabolism; D000419:Albuminuria / Q000209:etiology / Q000503:physiopathology; D000740:Anemia / Q000209:etiology; D015415:Biomarkers / Q000378:metabolism; D001806:Blood Urea Nitrogen; D059347:Cardio-Renal Syndrome / Q000209:etiology / Q000503:physiopathology*; D003404:Creatinine / Q000378:metabolism; D055316:Cystatin C / Q000378:metabolism; D005919:Glomerular Filtration Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D000072596:Hepatitis A Virus Cellular Receptor 1; D006801:Humans; D020382:Interleukin-18; D007668:Kidney / Q000294:innervation; D007676:Kidney Failure, Chronic / Q000209:etiology* / Q000503:physiopathology; D000071068:Lipocalin-2; D054834:Lipocalins / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D011379:Prognosis; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D011991:Receptors, Virus / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology
D000209:Acute-Phase Proteins; D015415:Biomarkers; D055316:Cystatin C; C491143:HAVCR1 protein, human; D000072596:Hepatitis A Virus Cellular Receptor 1; D020382:Interleukin-18; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D008562:Membrane Glycoproteins; D011518:Proto-Oncogene Proteins; D011991:Receptors, Virus; D003404:Creatinine; D000118:Acetylglucosaminidase