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Cardio-renal anemia syndrome. Third part: TherapyIn the previous sections of this chapter the clinical, epidemiological, pathophysiological and diagnostic aspects of cardiorenal anemia syndrome (CRAS) were treated. In this third and final component of the review the updates on the therapeutic aspects will be addressed. Erythropoiesis-stimulating agents (ESAs) and adjuvant iron therapy represent the primary treatment for anemia in CRS. The latest randomized trials for the treatment of iron deficiency in CRAS using intravenous (i.v.) Fe, have shown an improvement in symptoms, functional capacity and quality of life. These beneficial effects were independent of the presence of anemia. Furthermore, treatment with i.v. Fe can reduce the hospitalization rate due to the worsening of CHF. Oral iron is available at a lower cost than i.v. Fe, but its use did not translate into beneficial effects in CHF patients with iron deficiency (ID). The use of ESAs has been recently debated; the latest interventional study seems to demonstrate a neutral or negative effect in the active arm with darbepoetin treatment. These findings contrast with previous single-blind studies and meta-analyses, which showed an improvement in quality of life, left ventricular systolic function, and exercise tolerance following ESA therapy. In this review we discuss interventional studies in patients with CRAS and the potential role of ESA in this setting. [ABSTRACT FROM AUTHOR]

In Part One of this two-part series, the clinical and epidemiological aspects of the cardiorenal anemia syndrome (CRAS) were discussed. Anemia is a complication frequently associated with chronic heart failure (CHF) and chronic kidney disease (CKD).Part Two of this review focuses on the diagnostic elements of anemia in cardiorenal syndrome (CRS). Bone marrow biopsy remains the gold standard for the assessment of iron (Fe) stores. However, many other laboratory tests are available, both biochemical and hematological, that are less invasive, more practical and useful for the diagnosis and gradation of iron deficiency (ID). Biochemical tests are based on Fe metabolism and allow the identification of ID before the onset of anemia. Hematologic examinations, on the other hand, based on the morphologic characteristics of the red blood cells are more readily available. New tests are currently available for ID diagnosis before anemia is present. All of these tests are used to determine the type and cause of anemia in a patient with CRS. Unfortunately, there is no single test capable of establishing the diagnosis of ID with or without anemia, but it is necessary to resort to a combination of assessments adapted to the patient’s specific clinical situation. Indeed, every assessment aimed at evaluating the iron profile expresses a different aspect of each compartment of the total body Fe (deposit, transport, metabolic-functional, etc.).Using the various available tests improves diagnostic specificity and enhances differential diagnosis. [ABSTRACT FROM AUTHOR]

Anemia is a common complication associated with congestive heart failure (CHF) and chronic kidney disease (CKD), and is often reported as a component of the cardiorenal syndrome (CRS). The triad anemia, CHF and CKD has adverse prognostic implications that have led to the reformulation of the syndrome with the term "cardiorenal anemia syndrome" (CRAS). However, there is insufficient agreement about the definition of anemia in the CHF patient, probably due to the heterogeneity of the clinical criteria and the diversity of the patient populations in different studies. The evolution of drug therapy and technology (such as resynchronization of the left ventricle) has not stopped the increase in its incidence nor the associated health system costs. Unfortunately, the current guidelines do not provide specific recommendations for the adequate management of anemia in the cardiorenal patient. The pathophysiological mechanisms at the origin of anemia in CRS are complex and numerous. On the cardiovascular side the most important mechanisms are activation of the sympathetic and renin-angiotensin-aldosterone systems, antidiuretic hormone, and hemodilution, while those associated with CKD include reduction of the endogenous production of erythropoietin, chronic microinflammation, and iron deficiency. Consequently, anemia could represent a new clinical and therapeutic biomarker in CRS. A more comprehensive, 360-degree view, which stratifies the etiological, clinical and pathophysiological aspects, could significantly contribute to improving the prognosis of CRS patients. [ABSTRACT FROM AUTHOR]

Anemia is a frequent complication in chronic kidney disease (CKD), and it is often accompanied by various clinical symptoms. The primary cause of anemia in CKD patients is the reduction in the erythropoietin production, which results in a decrease of signaling molecule that stimulates red blood cell production. Other possible causes of anemia in CKD include iron deficiency, inflammation, and the accumulation of uremic toxin. This chapter focuses the discussion on the strategy of the management of anemia in patients with CKD. Erythropoiesis-stimulating agents (ESAs) and adjuvant iron therapy represent the primary treatment for anemia in chronic kidney disease. The introduction of ESAs into clinical practice was a success goal, mediating an increase in hemoglobin concentrations without the risk for recurrent blood transfusions and improving quality of life substantially., (Copyright by Società Italiana di Nefrologia SIN, Rome, Italy.)

Background: A significant proportion of patients undergoing radical nephrectomy (RN) for clear-cell renal cell carcinoma (RCC) develop chronic kidney disease (CKD) within a few years following surgery. Chronic kidney disease has important health, social and economic impact and no predictive biomarkers are currently available. MicroRNAs (miRs) are small non-coding RNAs implicated in several pathological processes., Methods: Primary objective of our study was to define miRs whose deregulation is predictive of CKD in patients treated with RN. Ribonucleic acid from formalin-fixed paraffin embedded renal parenchyma (cortex and medulla isolated separately) situated >3 cm from the matching RCC was tested for miR expression using nCounter NanoString technology in 71 consecutive patients treated with RN for RCC. Validation was performed by RT-PCR and in situ hybridisation. End point was post-RN CKD measured 12 months post-operatively. Multivariable logistic regression and decision curve analysis were used to test the statistical and clinical impact of predictors of CKD., Results: The overexpression of miR-193b-3p was associated with high risk of developing CKD in patients undergoing RN for RCC and emerged as an independent predictor of CKD. The addition of miR-193b-3p to a predictive model based on clinical variables (including sex and estimated glomerular filtration rate) increased the sensitivity of the predictive model from 81 to 88%. In situ hybridisation showed that miR-193b-3p overexpression was associated with tubule-interstitial inflammation and fibrosis in patients with no clinical or biochemical evidence of pre-RN nephropathy., Conclusions: miR-193b-3p might represent a useful biomarker to tailor and implement surveillance strategies for patients at high risk of developing CKD following RN.