Opportunities to improve the management of anemia in peritoneal dialysis patients: lessons from a national study in routine clinical practice.

Background: Current guidelines establish the same hemoglobin (Hb) and iron biomarkers targets for hemodialysis (HD) and peritoneal dialysis (PD) in patients receiving erythropoiesis-stimulating agents (ESAs) even though patients having PD are usually younger, more active and less comorbid. Unfortunately, specific renal anemia [anemia in chronic kidney disease (aCKD)] trials or observational studies on PD are scanty. The aims of this study were to describe current aCKD management, goals and adherence to clinical guidelines, identifying opportunities for healthcare improvement in PD patients. Methods: This was a retrospective, nationwide, multicentre study including patients from 19 PD units. The nephrologists collected baseline data, demographics, comorbidities and data related to anemia management (laboratory values, previously prescribed treatments and subsequent adjustments) from electronic medical records. The European adaptation of KDIGO guidelines was the reference for definitions, drug prescriptions and targets. Results: A total of 343 patients (mean age 62.9 years, 61.2% male) were included; 72.9% were receiving ESAs and 33.2% iron therapy [20.7% intravenously (IV)]. Eighty-two patients were receiving ESA without iron therapy, despite 53 of them having an indication according to the European Renal Best Practice guidelines. After laboratory results, iron therapy was only started in 15% of patients. Among ESA-treated patients, 51.9% had an optimal control [hemoglobin (Hb) 10-12 g/dL] and 28.3% between 12-12.9 g/dL. Seventeen patients achieved Hb >13 g/dL, and 12 of them remained on ESA after overshooting. Only three patients had Hb <10 g/dL without ESAs. Seven patients (2%) met criteria for ESA resistance (epoetin dose >300 IU/kg/week). The highest tertile of erythropoietin resistance index (>6.3 UI/kg/week/g/dL) was associated with iron deficiency and low albumin corrected by renal replacement therapy vintage and hospital admissions in the previous 3 months. Conclusion: Iron therapy continues to be underused (especially IV). Low albumin, iron deficiency and prior events explain most of the ESA hyporesponsiveness. Hb targets are titrated to/above the upper limits. Thus, several missed opportunities for adequate prescriptions and adherence to guidelines were identified.

Glomerulopatías C3. Una nueva perspectiva en enfermedades glomerulares / C3 Glomerulopathies. A new perspective on glomerular diseases

El término glomerulonefritis membranoproliferativa denota un patrón general de daño glomerular fácilmente reconocido por microscopía óptica. Con estudios adiciones de microscopía electrónica e inmunofluorescencia, la clasificación en subgrupos es posible. El estudio por microscopía electrónica resuelve las diferencias según la localización de los depósitos electrodensos, mientras que la inmunofluorescencia detecta la composición de los depósitos electrodensos. La glomerulopatía C3 es una entidad descrita de forma reciente, una glomerulonefritis proliferativa (normalmente, pero no siempre), con un patrón de glomerulonefritis membranoproliferativa en la microscopía óptica y con depósitos de C3 aislados en el estudio de inmunofluorescencia, implicando una hiperactividad de la vía alternativa del complemento. La evaluación de un paciente con glomerulopatía C3 debe centrarse en la cascada del complemento, en la desregulación de la vía alternativa del complemento y en la cascada terminal del complemento. Aunque no hay actualmente tratamientos específicos para las glomerulopatías C3, una mejor comprensión de la patogénesis sentaría las bases para el posible uso de drogas anticomplemento como terapia de elección, como el eculizumab. En la presente revisión, se resume la patogenia de las glomerulopatías C3, centrándonos en el papel del complemento, las series de casos recientemente publicados y las opciones terapéuticas hasta el momento actual (AU)

Membranoproliferative glomerulonephritis (MPGN) denotes a general pattern of glomerular injury that is easily recognized by light microscopy. With additional studies, MPGN subgrouping is possible. For example, electron microscopy resolves differences in electron-dense deposition location, while immunofluorescence typically detects the composition of electron-dense deposits. A C3 glomerulopathy (C3G) is a recently described entity, a proliferative glomerulonephritis (usually but not always), with a MPGN pattern on light microscopy, with C3 staining alone on inmunoflouresencie, implicating hyperactivity of the alternative complement pathway. The evaluation of C3G should focus on the complement cascade, as dysregulation of the alternative pathway and terminal complement cascade underlies pathogenesis. Although there are no specific treatments currently available for C3G, a better understanding of their pathogenesis would set the stage for the possible use of anti-complement drugs, as eculizumab. In this review, we summarise the pathogenesis of the C3 glomerulopathies, focusing on the role of complement, the patient cohorts recently reported and options of treatment up to the current moment (AU)

C3 glomerulopathies. A new perspective on glomerular diseases.

Membranoproliferative glomerulonephritis denotes a general pattern of glomerular injury that is easily recognised by light microscopy. With additional studies, MPGN subgrouping is possible. For example, electron microscopy resolves differences in electron-dense deposition location, while immunofluorescence typically detects the composition of electron-dense deposits. A C3 glomerulopathy (C3G) is a recently described entity, a proliferative glomerulonephritis (usually but not always), with a MPGN pattern on light microscopy, with C3 staining alone on immunofluorescence, implicating hyperactivity of the alternative complement pathway. The evaluation of C3G in a patient should focus on the complement cascade, as deregulation of the alternative pathway and terminal complement cascade underlies pathogenesis. Although there are no specific treatments currently available for C3G, a better understanding of their pathogenesis would set the stage for the possible use of anti-complement drugs, as eculizumab. In this review, we summarise the pathogenesis of the C3 glomerulopathies, focusing on the role of complement, the patient cohorts recently reported and options of treatment up to the current moment.

Cholesterol atheroembolism and combined treatment with steroids and iloprost.

Cholesterol atheroembolism (CAE) is a systemic disorder whose incidence has increased in recent decades and that presents high morbidity and mortality. Although several therapeutic alternatives have been reported, there is no consensus about the best treatment for this disease. In this paper we report the case of a patient with CAE with skin, bowel and kidney involvement who presented a good response to combined therapy with steroids and prostaglandin analogues. Although there are no conclusive studies, we recommend this therapeutic alternative in the management of CAE with organic failure.