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      Síndrome cardiorrenal: fisiopatologia e tratamento Translated title: Cardio-renal syndrome: pathophysiology and treatment

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          Abstract

          A doença renal crônica (DRC) é um dos principais problemas de saúde pública mundial. A anemia é um frequente achado na DRC, afetando aproximadamente 90% dos pacientes. A relação entre anemia e doença cardiovascular já é bastante estabelecida e resulta de alterações na estrutura do ventrículo esquerdo e sua função. A anemia per se pode induzir significante morbidade cardíaca na ausência de doença renal e é um fator de risco independente para complicações cardíacas em paciente com insuficiência renal. O presente artigo de revisão avalia as inter-relações entre anemia, insuficiência cardíaca e doença renal, incluídas recentemente na chamada síndrome da anemia cardiorrenal.

          Translated abstract

          Chronic kidney disease (CKD) is one of the most important problems of public health, worldwide. Anemia is frequent in CKD, affecting approximately 90% of patients. The relationship between anemia and cardiovascular disease is well established and is due to alterations in left ventricular structure and function. Anemia per se can lead to significant cardiac morbidity in the absence of renal disease and is an independent risk factor for cardiac complication in the patient with renal insufficiency. The present review evaluates the inter-relations between anemia, heart failure and renal disease, which were recently included in the so-called cardio-renal anemia syndrome.

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          Most cited references 63

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          The cardiomyopathy of overload: an unnatural growth response in the hypertrophied heart.

           David A Katz (1994)
          Heart failure is a progressive condition with a 5-year survival of less than 50%. This poor prognosis, which can be reproduced by overloading the hearts of experimental animals, may reflect molecular abnormalities caused when overload stimulates adult cardiac myocytes to undergo hypertrophy. Because these terminally differentiated cells have little or no capacity to divide, hypertrophy represents an unnatural growth response; however, the mechanism by which overload shortens survival remains speculative. Modification of this unnatural growth response by converting enzyme inhibitors and nitrates, which have growth inhibitory as well as vasodilator effects, may contribute to the ability of these drugs to improve prognosis in patients with heart failure.
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            Reversal of Anemia by Erythropoietin Therapy Retards the Progression of Chronic Renal Failure, Especially in Nondiabetic Patients

            Therapy with human recombinant erythropoietin (EPO) has been accepted as effective for renal anemia in dialysis patients. However, studies in rats have shown that correcting anemia with EPO may affect the progression of renal dysfunction. In humans, however, the effect of EPO on residual renal function is a matter of controversy. We, therefore, investigated whether the long-term administration of EPO to predialysis patients influences residual renal function. Anemic patients at the predialysis stage with a serum creatinine (Cr) concentration ranging from 2 to 4 (average 2.9) mg/dl and a hematocrit (Ht) of less than 30% were randomly assigned to two groups which consisted of anemic patients not treated with EPO (group I, untreated anemic controls, n = 31) and anemic patients treated with EPO (group II, treated anemics, n = 42). Patients with nonsevere or moderate anemia (Ht > 30%) with a Cr ranging from 2 to 4 (average 2.6) mg/dl were also recruited as nonanemic controls (group III, untreated nonanemic controls, n = 35). Blood pressure was controlled to the same degree among the three groups by combined treatment with calcium antagonists and angiotensin-converting enzyme inhibitors. All patients were kept strictly on a low-protein (0.6 g/kg/day) and a low-salt (7 g/day) diet. The degree of control of dietary protein and blood pressure and the frequency of angiotensin-converting enzyme inhibitor administration were comparable among the three groups. The primary end point for each patient was a doubling of the baseline Cr which yielded cumulative renal survival rates which were plotted against time. Ht rose significantly from 27.0 ± 2.3 to 32.1 ± 3.2% in group II (n = 42, p < 0.001) with a rate of increase of 0.4 ± 0.06%/week. However, it declined from 27.9 ± 1.8 to 25.3 ± 1.9% in group I (n = 31, p < 0.001) and from 35.9 ± 3.5 to 32.2 ± 3.9% in group III (n = 35, p < 0.001). Cr doubled in 26 patients (84%) in group I as compared with 22 (52%) in group II and 21 (60%) in group III. The cumulative renal survival rates in groups II and III were significantly better than that in group I: p = 0.0003 (group I vs. group II) and p = 0.0024 (group I vs. group III). However, there was no difference in the renal survival rate between groups II and III (p = 0.3111). The better survival rate obtained in group II was attributable to the better survival rate for the nondiabetic patients in this group. The present study suggests that anemia, per se, is a factor in the progression of end-stage renal failure and that reversal of anemia by EPO can retard the progression of renal failure, especially in nondiabetic patiens, provided that blood pressure control, rate of increase in Ht, and dietary protein restriction are appropriate.
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              The role of inflammation in the anaemia of end-stage renal disease.

               P Stenvinkel (2000)
              Chronic inflammation is a common feature of end-stage renal disease (ESRD) that is gaining increasing attention as a major cause of morbidity and mortality. It is well established that ESRD per se carries a heightened risk of inflammatory disorders and other co-morbid conditions, but it should also be pointed out that dialysis treatment per se can bring additional risk factors for inflammation, such as impure dialysate or bio-incompatible membranes. Inflammation has recently been associated with atherosclerosis and malnutrition in ESRD, and this link has led to the development of the malnutrition, inflammation, atherosclerosis (MIA) hypothesis. This describes a syndrome whereby raised levels of pro-inflammatory cytokines (such as IL-1, IL-6 and TNF-alpha) are a common link between malnutrition, inflammation and atherosclerosis. Also, anaemia appears to be an important element linking elevated cytokine levels with poor patient outcomes. Several mechanisms for cytokine-induced anaemia have been proposed, including intestinal bleeding, impaired iron metabolism and suppression of bone marrow erythropoiesis and erythropoietin production. These effects suggest that pro-inflammatory cytokines may also be an important cause of lack of response to recombinant human erythropoietin (rh-Epo) therapy. In the light of this putative role of pro-inflammatory cytokines, anti-cytokine agents may prove useful to optimize efficacy of rh-Epo in anaemic chronic renal failure patients. Other potential therapeutic strategies include minimizing exposure to causes of inflammation from various co-morbid conditions, such as persistent infections and chronic heart failure.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                ramb
                Revista da Associação Médica Brasileira
                Rev. Assoc. Med. Bras.
                Associação Médica Brasileira (São Paulo )
                1806-9282
                2009
                : 55
                : 1
                : 89-94
                Affiliations
                [1 ] Universidade Federal do Ceará Brazil
                [2 ] Universidade Federal do Ceará Brazil
                [3 ] Universidade Federal do Ceará Brazil
                Article
                S0104-42302009000100022
                10.1590/S0104-42302009000100022
                Product
                Product Information: website
                Categories
                MEDICINE, GENERAL & INTERNAL

                Internal medicine

                Insuficiência renal, Heart failure, Renal failure, Anemia, Insuficiência cardíaca

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