Renin–angiotensin system (RAS) inhibitors — including angiotensin-converting–enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs) — slow the progression of mild or moderate chronic kidney disease. However, the results of some studies have suggested that the discontinuation of RAS inhibitors in patients with advanced chronic kidney disease may increase the estimated glomerular filtration rate (eGFR) or slow its decline.

Before the introduction of erythropoiesis-stimulating agents (ESAs) in 1989, repeated transfusions given to patients with end-stage renal disease caused iron overload, and the need for supplemental iron was rare. However, with the widespread introduction of ESAs, it was recognized that supplemental iron was necessary to optimize hemoglobin response and allow reduction of the ESA dose for economic reasons and recent concerns about ESA safety. Iron supplementation was also found to be more efficacious via intravenous compared to oral administration, and the use of intravenous iron has escalated in recent years. The safety of various iron compounds has been of theoretical concern due to their potential to induce iron overload, oxidative stress, hypersensitivity reactions, and a permissive environment for infectious processes. Therefore, an expert group was convened to assess the benefits and risks of parenteral iron, and to provide strategies for its optimal use while mitigating the risk for acute reactions and other adverse effects.

Aims To determine the prevalence and incidence of renal dysfunction (RD) in patients with chronic heart failure (CHF), to identify contributory factors and predictors of worsening renal function (WRF), and to explore the relationship between RD and mortality. Methods and results Prospective data on 1216 patients with CHF were analysed. The glomerular filtration rate (GFR) was used to determine renal function, and WRF was defined as an increase in serum creatinine of >26.5 µmol/L (>0.3 mg/dL). The prevalence of RD defined as a GFR of 9 mmol/L. Two hundred and sixty-three (21.6%) patients died, and baseline RD and WRF both predicted a higher mortality (P<0.001), whereas an improvement in renal function over the first 6 months predicted a lower mortality (hazard ratio 0.8, 95% confidence interval 0.6–1.0). Conclusion In ambulatory patients with CHF, RD is common, commonly deteriorates over a relatively short period of time, is unlikely to recover substantially, and augurs a poor prognosis.

Background—: We evaluated the effect of the selective mineralocorticoid receptor antagonist eplerenone on renal function and the interaction between changes in renal function and subsequent cardiovascular outcomes in patients with heart failure and left ventricular systolic dysfunction after an acute myocardial infarction in the Eplerenone Post–Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS). Methods and Results—: Serial changes in estimated glomerular filtration rate (eGFR) were available in 5792 patients during a 24-month follow-up. Patients assigned to eplerenone had a decline in eGFR with an adjusted mean difference of −1.4±0.3 mL · min ⁻¹ · 1.73 m ⁻² compared with placebo ( P 20% in the first month, 16.9% and 14.7% in the eplerenone and placebo groups, respectively (odds ratio, 1.15; 95% confidence interval, 1.02–1.30; P =0.017). In multivariate analyses, determinants of this early decline in eGFR were female sex, age ≥65 years, smoking, left ventricular ejection fraction 20% was associated with worse cardiovascular outcomes independently of baseline eGFR and of the use of eplerenone, which retained its prognostic benefits even under these circumstances. Conclusions—: In patients with heart failure after acute myocardial infarction and receiving standard medical care, an early decline in eGFR is not uncommon and is associated with poor long-term outcome. Eplerenone induced a moderately more frequent early decline in eGFR, which did not affect its clinical benefit on cardiovascular outcomes.

OBJECTIVE: To examine the effect of intravenous iron and erythropoietin-stimulating agents (ESAs) on glycemic control and A1C of patients with diabetes and chronic kidney disease (CKD). RESEARCH DESIGN AND METHODS: This was a prospective study of patients with type 2 diabetes and CKD stage IIIB or IV undergoing intravenous iron (group A) and/or ESA (group B). Full blood profiles were determined over the study period. Glycemic control was monitored using A1C, seven-point daily glucose three times weekly, and continuous glucose monitoring (CGM). RESULTS: There were 15 patients in both group A and group B. Mean A1C (95% CI) values fell in both groups (7.40% [6.60–8.19] to 6.96% [6.27–7.25], P < 0.01, with intravenous iron and 7.31% [6.42–8.54] to 6.63% [6.03–7.36], P = 0.013, ESA). There was no change in mean blood glucose in group A (9.55 mmol/l [8.20–10.90] vs. 9.71 mmol/l [8.29–11.13], P = 0.07) and in group B (8.72 mmol/l [7.31–10.12] vs. 8.78 mmol/l [7.47–9.99], P = 0.61) over the study period. Hemoglobin and hematocrit values significantly increased following both treatments. There was no linear relationship found between the change in A1C values and the rise of hemoglobin following either treatment. CONCLUSIONS: Both iron and ESA cause a significant fall in A1C values without a change to glycemic control in patients with diabetes and CKD. At the present time, regular capillary glucose measurements and the concurrent use of CGM remain the best alternative measurements of glycemic control in this patient group.

Overall survival in 1095 patients with severe acute renal failure (ARF) between 1984 and 1995 was 59.5%. Of these, 107 (16.2%) remained dependent on long-term dialysis. The frequency of end-stage renal failure (ESRF) in survivors of ARF varied between 3% and 41% according to the cause of ARF, being highest in those with acute renal parenchymal disease (in whom survival was also among the highest at 84%) and lowest in ARF due to obstetrics and trauma. Patients failing to regain adequate renal function did not appear to differ on clinical grounds from survivors who became dialysisindependent. Survival in those requiring long-term dialysis was less good than for other patients with ESRF, partly due to excess mortality in those for whom vascular disease or surgery was the precipitating cause of ARF. Six patients recovered sufficient renal function to become independent of dialysis after 3–18 months on regular dialysis therapy (6–21 months after onset of ARF). ESRF resulting from ARF is more frequent than previously reported. This increase may be due to a changing case-mix, increasing age of patients (and hence reduced capacity for renal recovery), and an increase in aggressive surgery for patients with advanced vascular disease. This presents a significant and increasing problem, with implications for both clinical management and the provision of dialysis services.