Iron deficiency anemia is a common complication of chronic kidney disease (CKD). CKD patients suffer from both absolute and functional iron deficiency. Absolute iron deficiency is defined by severely reduced or absent iron stores, while functional iron deficiency is defined by adequate iron stores but insufficient iron availability for incorporation into erythroid precursors. This is due to increased levels of hepcidin. Anemia in CKD is associated with an increased risk of morbidity and mortality. The association between anemia and mortality may be related to the severity of anemia. All CKD patients should be screened for anemia during the initial evaluation for CKD. Criteria used to define iron deficiency are different among CKD compared to normal renal function. Among CKD patients, absolute iron deficiency is defined when the transferrin saturation (TSAT) is ≤20% and the serum ferritin concentration is ≤100 ng/mL among predialysis and peritoneal dialysis patients or ≤200 ng/mL among hemodialysis patients. Functional iron deficiency, also known as iron-restricted erythropoiesis, is characterized by TSAT ≤20% and elevated ferritin levels. Iron supplementation is recommended for all CKD patients with anemia. There is general agreement according to guidelines that intravenous (i.v.) iron supplementation is the preferred method for CKD patients on dialysis (CKD stage 5D) and either i.v. or oral iron is recommended for patients with CKD ND (CKD stages 3–5). In this review we discuss the evidence base for these recommendations.

Objectives: To assess the effect of quinolone prophylaxis following chemotherapy for malignancies on the emergence of resistant bacteria in neutropenic patients. Methods: Systematic review and meta-analysis of randomized controlled trials comparing quinolone prophylaxis with placebo or no intervention, or another antibiotic, for the prevention of bacterial infections in afebrile neutropenic patients. The Cochrane Library, PubMed, Embase, conference proceedings and references were searched. Two reviewers independently applied selection criteria, carried out quality assessment and extracted the data. Relative risks (RR) with 95% confidence intervals (CIs) were estimated and pooled. Primary outcomes were rates of colonization and infection by quinolone-resistant bacteria. Results: The search yielded 56 trials, 22 compared quinolones with placebo or no intervention. Data on colonization by resistant organisms could be extracted from 27 trials (48%). When compared with placebo or no intervention, there was a statistically non-significant increase in colonization with organisms resistant to quinolones (RR 1.68; 95% CI 0.71–4.00). There was no difference in the number of patients developing infections caused by resistant pathogens (RR 1.04; 95% CI 0.73–1.50). In trials comparing quinolones with trimethoprim/sulfamethoxazole, there were fewer incidents of colonization by bacteria resistant to the prophylactic agent in the quinolone arm than in the trimethoprim/sulfamethoxazole arm (RR 0.49; 95% CI 0.37–0.66). Data on baseline resistance of colonizing isolates, resistance development and cross-resistance to β-lactam antibiotics were too scarce to analyse. Conclusions: Patients treated with quinolones have a non-significant increase in colonization by quinolone-resistant bacteria. There is no difference in the number of infections caused by pathogens resistant to quinolones. As quinolone prophylaxis reduces the risk of death in neutropenic patients, the risk associated with colonization and infections caused by quinolone-resistant organisms does not outweigh the gain. Future trials should focus on better documentation of infections caused by resistant organisms.

Posttransplantation anemia (PTA) is common among kidney transplant patients. Early PTA is usually defined as anemia which develops up to 6 months after transplantation, and late PTA is defined as anemia which develops after 6 months. There are multiple causes, with iron deficiency being the major contributor. The occurrence of late PTA has been associated with impaired graft function. Early PTA has been shown to be a predictor of late PTA. PTA is associated with reduced mortality, reduced graft survival, and a decline in GFR. The association with mortality is related to the severity of the anemia and to specific causes of anemia. Treatment of PTA should probably begin as soon as possible after kidney transplantation. The optimal target hemoglobin level in kidney transplant recipients with anemia is higher than recommended in chronic kidney disease and should probably be up to 12.5–13 g/dL. In order to achieve this target, appropriate treatment with erythropoiesis-stimulating agents (ESA) and iron is indicated.