Economic Evaluation of Ferric Carboxymaltose for the Management of Hemodialysis Patients with Iron Deficiency Anemia in Italy.

INTRODUCTION: Patients with chronic kidney disease on hemodialysis (HD) are at high risk of developing both iron deficiency and iron deficiency anemia (IDA). The administration of intravenous iron therefore represents the standard of care for the management of anemia in this patient setting. METHODS: A retrospective cohort of 38 HD patients in Italy was analyzed to assess the clinical and economic implications of switching from intravenous ferric gluconate (FG) to ferric carboxymaltose (FCM) on achievement of adequate hemoglobin (Hb) values and iron balance. The total observational period for each patient was 12 months, 6 months before and 6 months after switching to iron FCM. The pharmacoeconomic analysis considered the hospital perspective and the consumption of iron, blood transfusions and erythropoiesis-stimulating agents (ESAs), including healthcare personnel time. RESULTS: Switching from FG to FCM in dialysis adult patients with IDA allows a cost reduction per patient/month in the range €14-46, considering the use of biosimilar ESA or originator ESA, respectively. The percentage of patients with Hb target values increased from 63% to 82%, considering the entire observation period. In addition, other clinical parameters (ferritin, transferrin saturation, erythropoietin resistance index) improved after switching from FG to FCM. CONCLUSION: FCM in HD patients was shown to provide a favorable efficacy profile over FG, with a lower cost per patient, mainly driven by a consistent reduction of ESA consumption. FUNDING: Vifor Pharma Italia Srl.

Predictors of estimated GFR decline in patients with type 2 diabetes and preserved kidney function.

BACKGROUND AND OBJECTIVES: This study examined predictors of the annual decline in estimated GFR (eGFR) in patients with type 2 diabetes and preserved kidney function. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In a prospective, observational cohort study, 1682 individuals with type 2 diabetes and baseline eGFR ≥60 ml/min per 1.73 m(2) (as estimated by the Chronic Kidney Disease Epidemiology Collaboration equation) were followed for 10 years. Linear regression was used to estimate participants' changes in eGFR over time. RESULTS: During follow-up, 263 (15.6%) individuals had a rapid eGFR decline defined as >4.0% per year. Average eGFR decline was -5.8 ± 3 and -0.6 ± 2 ml/min per 1.73 m(2) per year in rapid decliners and nondecliners, respectively. Compared with normotensive, normoalbuminuric patients (-0.2 ± 0.2 ml/min per 1.73 m(2) per year), those with hypertension (-1.0 ± 0.1 ml/min per 1.73 m(2) per year), hemoglobin A(1c)≥7% (-1.0 ± 0.1 ml/min per 1.73 m(2) per year), longer diabetes duration (-1.0 ± 0.1 ml/min per 1.73 m(2) per year), obesity (-1.2 ± 0.1 ml/min per 1.73 m(2) per year), insulin treatment (-1.5 ± 0.1 ml/min per 1.73 m(2) per year), microalbuminuria (-1.3 ± 0.2 ml/min per 1.73 m(2) per year), or macroalbuminuria (-2.7 ± 0.4 ml/min per 1.73 m(2) per year) had significantly faster age-adjusted annual eGFR declines. Multivariable linear regression analyses revealed that albuminuria (P<0.001) was the strongest predictor of annual eGFR decline. Other independent predictors of annual eGFR decline were older age, hypertension, insulin treatment, and lower baseline eGFR. CONCLUSIONS: Annual eGFR decline is predicted by multiple modifiable risk factors in patients with type 2 diabetes and preserved kidney function.

Serum uric acid levels and incident chronic kidney disease in patients with type 2 diabetes and preserved kidney function.

OBJECTIVE: Recent studies have suggested an association between hyperuricemia and adverse renal outcomes in nondiabetic populations. Data on the relationship between hyperuricemia and the risk of incident chronic kidney disease (CKD) in type 2 diabetic patients with normal or near-normal kidney function are lacking. We determined whether baseline serum uric acid levels predict the subsequent development of CKD in patients with type 2 diabetes. RESEARCH DESIGN AND METHODS: We followed 1,449 type 2 diabetic patients with normal kidney function and without overt proteinuria for 5 years for the occurrence of incident CKD (defined as overt proteinuria or estimated glomerular filtration rate [eGFR] <60 mL/min/1.73 m(2)). RESULTS: During a 5-year follow-up period, 194 (13.4%) patients developed incident CKD. The cumulative incidence of CKD was significantly greater in patients with hyperuricemia than in those without hyperuricemia (29.5 vs. 11.4%, P < 0.001). In univariate logistic regression analysis, the presence of hyperuricemia roughly doubled the risk of developing CKD (odds ratio [OR] 2.55 [95% CI 1.71-3.85], P < 0.001). After adjusting for age, sex, BMI, smoking status, diabetes duration, systolic blood pressure, antihypertensive treatment, insulin therapy, HbA(1c), eGFR, and albuminuria, hyperuricemia was associated with an increased risk of incident CKD (adjusted OR 2.10 [1.16-3.76], P < 0.01). In continuous analyses, a 1-SD increment in the serum uric acid level was significantly associated with a 21% increased risk of CKD. CONCLUSIONS: In type 2 diabetic individuals with preserved kidney function, hyperuricemia seems to be an independent risk factor for the development of incident CKD.

Treating elderly people with diabetes and stages 3 and 4 chronic kidney disease.

Dedicated European and US clinical guidelines for type 2 diabetes in the elderly have been released, but they do not specifically address the issue of advanced chronic kidney disease (CKD) in older patients with diabetes. General clinical guidelines have been published on the treatment of patients with diabetic nephropathy (DN), but these address the issue of how to prevent progression and treat advanced DN without distinguishing between different age groups. Elderly patients with diabetes and stages 3 to 4 CKD have particular needs that differ from those of younger patients with the same conditions. This is mainly due to their frailty and shorter life expectancy. Differently tailored therapeutic strategies are needed, which may have less stringent targets; and the use of common drugs should be critically evaluated. The management agenda (metabolic control, low-protein diet, controlling BP, preventing progression of advanced DN, preventing cardiovascular outcomes) for these patients is discussed in light of the limits and perspectives of current guidelines. Intensive, simultaneous management of all items on the agenda may not be feasible for a proportion of older patients, and clinicians may have to give priority to reducing some risk factors rather than others, choosing between different therapies.

Anaemia in diabetic renal failure: is there a role for early erythropoietin treatment in preventing cardiovascular mortality?

The mortality rate in diabetics with chronic kidney disease (CKD) is seven times higher than end-stage renal disease mainly because of cardiac causes. Anaemia may have a relevant role in the pathogenesis of cardiovascular (CV) disease in CKD. Anaemia occurs at an earlier stage of CKD in diabetic individuals than in those with other causes of CKD. Observational findings support the unfavourable influence of anaemia on mortality in CKD patients, and the combination of anaemia and CKD in diabetics identifies a group with a particularly high mortality risk. While the effect of erythropoietin on these patients' quality of life is known, its impact on mortality and CV risk is uncertain. The recent Anaemia Correction in Diabetes (ACORD) trial in diabetic CKD patients, which targeted haemoglobin levels of 13-15 mg/dl, disclosed no statistically significant favourable or adverse effects on mortality or morbidity over the 2-year follow-up, while other studies endeavouring to nearly normalize haemoglobin have reportedly proved risky. Even if anaemia is causally involved, the pathogenesis of CV disease in diabetics with CKD is so complex that addressing just one factor (anaemia) may not suffice to prevent CV risk, and normalizing haemoglobin levels may even be harmful.

Primary cutaneous plasmacytoma after rejection of a transplanted kidney: case report and review of the literature.

Immunosuppressed organ allograft recipients are at risk of developing lymphomas and lymphoproliferative disorders as a consequence of immunosuppressive therapy and long-term antigenic stimulation from both the graft and possible viral infections. No more than 4% of the malignant tumors detected in organ recipients are plasmacytomas. Primary cutaneous plasmacytoma is a rare type of cutaneous B-cell lymphoma arising primarily in the skin. It is derived from clonally expanded plasma cells with various degrees of maturation and atypia. We report the occurrence of a solitary cutaneous plasmacytoma in a 56-year-old male patient undergoing hemodialysis after rejection of a grafted kidney. The diagnosis was made a few months after the kidney had been surgically removed. A thorough examination showed no evidence of systemic disease. Skin lesions were successfully treated with local radiotherapy. After 2 years of follow-up there were no local or systemic recurrences.