Iron is the most common nutrient deficiency globally, affecting nearly 2 billion people. It may cause long-term neurocognitive impairments and behavioral deficits in premature and low-birthweight neonates. Reticulocyte hemoglobin (Ret-He) is a reliable, valid, low-cost, and minimally invasive phlebotomy laboratory test for assessing iron status and guiding iron dosing.

Background: Patients with chronic kidney disease (CKD) undergoing hemodialysis commonly present multiple comorbidities and require complex medication regimens. Polypharmacy increases the risk of clinically relevant drug interactions that may compromise treatment safety and effectiveness. Objective: To estimate the prevalence of potential drug interactions among patients with CKD undergoing hemodialysis and classify these interactions according to clinical risk and mechanism of action. Methods: A cross-sectional study was conducted with patients undergoing hemodialysis at a dialysis clinic in Southern Santa Catarina, Brazil. Potential drug interactions were identified using the Medscape and Drugs.com databases and classified according to severity (major, moderate, or minor) and mechanism of action. Results: A total of 151 patients were included. Potential drug interactions were identified in all participants (973 interactions; mean 6.4 per patient). Of these, 234 (24.0%) were classified as major, 545 (56.0%) as moderate, and 194 (19.9%) as minor. The most frequent major interactions involved furosemide + losartan (n = 8) and acetylsalicylic acid + clopidogrel (n = 6). Among moderate interactions, the most common were sevelamer + calcium carbonate (n = 14) and losartan + amlodipine (n = 12). The most frequent minor interactions involved epoetin alfa + acetylsalicylic acid (n = 14) and epoetin alfa + calcium carbonate (n = 10). Pharmacodynamic interactions predominated, mainly involving additive effects of cardiovascular medications. Conclusions: Potential drug interactions were highly prevalent among patients undergoing hemodialysis, with moderate-severity interactions predominating. Routine screening for potential drug interactions may support safer prescribing, optimize pharmacotherapy, and strengthen multidisciplinary medication management in this high-risk population.

VEXAS (vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic) syndrome is a recently described autoinflammatory disorder caused by somatic UBA1 mutations in hematopoietic stem and progenitor cells. It typically presents in older males with treatment-refractory systemic inflammation and hematologic abnormalities. We report a case of a 92-year-old male who presented with auricular chondritis and other systemic symptoms, including inflammatory arthritis, conjunctivitis, and a diffuse rash. Laboratory evaluation revealed macrocytic anemia and elevated inflammatory markers, with largely negative autoimmune serologies aside from a mildly elevated rheumatoid factor. Bone marrow analysis showed cytoplasmic vacuolization of myeloid and erythroid precursors, and genetic testing identified a UBA1 p.Met41Thr pathogenic variant, confirming the diagnosis of VEXAS syndrome. Treatment with oral prednisone, monthly tocilizumab infusions, and supportive epoetin alfa-epbx led to significant clinical improvement. This case underscores the importance of considering VEXAS syndrome in elderly male patients presenting with unexplained systemic inflammation, chondritis, and cytopenias, and highlights the critical roles of early recognition, multidisciplinary evaluation, and timely genetic testing in diagnosis and management.

Timely recognition and monitoring of chronic kidney disease (CKD) is critical for improving patient outcomes. Non-coding RNAs (ncRNAs) are implicated in CKD pathophysiology. However, their clinical translation, particularly in patients on maintenance hemodialysis (MHD), and their association with erythropoiesis-stimulating agent (ESA) resistance remain under-investigated. This case-control study evaluated the signature of serum circ_DLGAP4, lncRNA KCNQ1OT1, and their targets miR-9/SOX7 in CKD across various stages, including MHD, and the clinical significance of their integration in diagnosis, staging, and ESA resistance. Overall, 180 individuals: 60 controls, 60 non-hemodialysis (non-HD) CKD G2-G4 patients, and 60 MHD patients with CKD G5, were enrolled. ncRNAs and SOX7 were measured using RT-qPCR and ELISA, respectively. Bioinformatics analysis revealed the interaction network of the investigated markers and their involvement in CKD pathophysiology. Serum circ_DLGAP4, KCNQ1OT1, and miR-9 were upregulated in CKD patients, with or without MHD, while SOX7 was downregulated in MHD patients compared to controls. circ_DLGAP4 and SOX7 were lower, and miR-9 was higher in MHD versus non-HD patients. circ_DLGAP4 and SOX7 were differentially expressed across CKD categories/stages. ROC analysis revealed diagnostic utility for circ_DLGAP4, KCNQ1OT1, and miR-9 and prognostic potential for circ_DLGAP4, miR-9, and SOX7. In multivariate analysis, KCNQ1OT1 was independently associated with CKD detection in non-HD patients. The circ_DLGAP4/SOX7 panel independently predicted CKD progression to MHD with high accuracy [Area under the curve (AUC) = 0.93, 95% confidence interval (CI) = 0.8823-0.9754]. We developed a simple nomogram for easier application in CKD progression prediction (AUC = 0.938, 95% CI = 0.8959-0.9808). circ_DLGAP4, miR-9, and SOX7 showed correlations with eGFR. miR-9 was associated with the ESA resistance index in MHD patients receiving epoetin alfa, independent of BMI. Conclusively, this study introduces serum KCNQ1OT1 as a potential candidate biomarker for CKD diagnosis, circ_DLGAP4/SOX7 as a novel panel useful for assessing CKD progression using a nomogram, and miR-9 as a potential candidate ESA resistance biomarker in MHD. Trial registration number: NCT07037953, date of registration: 10-6-2025.

Erythropoiesis-stimulating agents (ESAs) are essential in managing anemia associated with chronic kidney disease (CKD). Although iron deficiency and inflammation are the most frequent causes of ESA hyporesponsiveness, a rare but serious complication is pure red cell aplasia (PRCA) caused by anti-EPO antibodies. This condition results in severe anemia and requires discontinuation of ESA therapy. Roxadustat, a hypoxia-inducible factor prolyl hydroxylase inhibitor, has recently emerged as a promising therapeutic alternative. We report the case of a 72-year-old woman with stage G3bA1 CKD who initially responded to epoetin alfa but developed progressive anemia 11 months later, reaching a hemoglobin level of 5.6 g/dL despite dose escalation. Bone marrow biopsy showed absence of erythroid precursors, and anti-EPO antibodies were detected, confirming PRCA. ESA therapy was stopped, and roxadustat was initiated. Within 7 weeks, the patient achieved transfusion independence with stable hemoglobin levels. Follow-up marrow biopsy demonstrated erythroid recovery, and anti-EPO antibodies became undetectable. ESA-induced PRCA has been linked to subcutaneous administration, formulation changes, and genetic predisposition. Standard treatment includes ESA withdrawal and immunosuppression, although outcomes vary. Roxadustat may restore erythropoiesis without additional immunosuppression, providing both hematologic and immunologic benefit. Further studies are needed to validate its role in this context.

Paroxysmal cold hemoglobinuria (PCH) is a rare form of complement-mediated hemolytic anemia in children. It is typically triggered by viral infections and mediated by Donath-Landsteiner antibodies, which induce intravascular hemolysis upon cold exposure. We reviewed the clinical course, laboratory findings, and management of a pediatric adenovirus-associated PCH to highlight diagnostic and therapeutic considerations. The eight-year-old previously healthy, unimmunized female patient presented with acute hemolytic anemia following a febrile viral illness. She developed jaundice and severe anemia with reticulocytosis, hyperbilirubinemia, and elevated lactate dehydrogenase (LDH). The direct antiglobulin test (DAT) was positive for complement (C3) but negative for immunoglobulin G (IgG). Blood bank evaluation revealed a positive Donath-Landsteiner antibody, confirming PCH. Treatment included normothermia, intravenous methylprednisolone, intravenous immunoglobulin (IVIG), epoetin alfa, folic acid, and empiric azithromycin. The patient's clinical condition stabilized with gradual hematologic recovery and resolution of symptoms. This case identifies adenovirus as a potential trigger for PCH in children and emphasizes the importance of early recognition, laboratory confirmation, and supportive management.