PubMed Health⌕ Search

Biomedical subjects

Gina-Marie Barletta

Publications and source records attributed to Gina-Marie Barletta.

4 recordsLinked to original sources

Medication errors and patient complications with continuous renal replacement therapy.

Continuous renal replacement therapy (CRRT) is commonly used for renal support in the intensive care unit. While the risk of medication errors in the intensive care unit has been described, errors related specifically to CRRT are unknown. The purpose of this study is to characterize medication errors related to CRRT and compare medication errors that occur with manually compounded solutions versus commercially available solutions. We surveyed three separate internet-based, pediatric list serves that are commonly used for communications for programs utilizing CRRT. Data regarding CRRT practices and medication errors were recorded. Medication errors were graded for degree of severity and compared between programs using manually compounded dialysis solutions versus commercially available dialysis solutions. In a survey with 31 program responses, 18 reported medication errors. Two of the 18 were related to heparin compounding, while 16/18 were due to solution compounding errors. Half of the medication errors were classified as causing harm, two of which were fatal. All medication errors were reported by programs that manually compounded their dialysis solutions. Medication errors related to CRRT are associated with a high degree of severity, including death. Industry-based, commercially available solutions can decrease the occurrence of medication errors due to CRRT.

Child↗

Acute renal failure in children and infants.

PURPOSE OF REVIEW: This review provides an overview of various topics related to acute renal failure and summarizes the results of recent advancements of particular significance in the care of children with acute renal failure. RECENT FINDINGS: Over the past two decades, the treatment and prognosis of children with acute renal failure has notably shifted owing to advances in continuous treatment modalities, improvements in vascular access, and increased acknowledgment and understanding of the importance of optimizing nutritional support. SUMMARY: After discussing the various causes of acute renal failure in children and infants, this review focuses on recent advancements in the management of acute renal failure, including acute dialysis modalities and continuous renal replacement therapy.

Acute Kidney Injury↗

Use of mycophenolate mofetil in steroid-dependent and -resistant nephrotic syndrome.

Cyclosporin (Cs-A) is an effective treatment for difficult cases of nephrotic syndrome (NS), but its use can be complicated by renal toxicity and a high incidence of relapses after withdrawal. We reviewed the charts of 10 Cs-A-dependent patients and 4 patients with steroid-dependent nephrotic syndrome (SDNS) not previously treated with Cs-A therapy. All patients had persistent NS, even after prior treatment with oral cyclophosphamide. Of 10 patients treated with Cs-A, 4 had surveillance renal biopsies consistent with Cs-A toxicity, and 8 of 10 had interstitial fibrosis prior to mycophenolate mofetil (MMF). Patients were treated with MMF, at 1,200 mg/m(2) per day, in an attempt to allow weaning of Cs-A and/or steroid therapy, and reduce the frequency of relapses. Overall, a significant decrease in frequency of relapses was noted after initiation of MMF therapy. In addition, 5 patients were weaned off Cs-A by 1-2 years of follow-up. One patient was weaned off Cs-A and MMF, and remained in complete remission. However, the subgroup of patients with frequently relapsing SDNS not treated with Cs-A appeared to have a reduction in the number of relapses while on MMF that did not reach statistical significance. Two patients with intractable steroid-resistant NS continued to relapse repeatedly on MMF and Cs-A therapy. We conclude that in this small, single-center, uncontrolled experience, MMF therapy in patients with Cs-A-dependent NS appears to be effective in reducing Cs-A exposure. In addition, MMF appears to significantly decrease the frequency of relapses in this patient population. Further controlled studies are warranted to better define the potential efficacy and side effects of long-term MMF therapy in this setting.

Anti-Inflammatory Agents, Non-Steroidal↗

Nephrin and Neph1 co-localize at the podocyte foot process intercellular junction and form cis hetero-oligomers.

Glomerular visceral epithelial cells (podocytes) appear to play a central role in maintaining the selective filtration barrier of the renal glomerulus. While the immunoglobulin superfamily member Nephrin was proposed to act as a cell adhesion molecule at the podocyte intercellular junction necessary for maintaining glomerular perm selectivity, the Nephrin ligand has not been identified. The existence of a new subfamily of Nephrin-like molecules including Neph1 was recently described. Genetic deletion of Nephrin or Neph1 resulted in similar phenotypes of podocyte foot process effacement and proteinuria. The subcellular localization of Neph1 and the possibility that Nephrin and Neph1 interact was investigated. Polyclonal antiserum for Neph1 was raised and characterized. Neph1 migrated as a 90-kDa protein on SDS-PAGE under reducing conditions. Neph1 was identified in a glomerular and podocyte-specific distribution in adult rat kidney. Like Nephrin and Podocin, Neph1 was enriched in Triton X-100 detergent-resistant membrane fractions. Consistent with this observation, immunogold electron microscopy demonstrated that Neph1 localized exclusively to lateral margins of podocyte foot processes at the insertion of the slit diaphragm. Neph1 and Nephrin participate in a direct cis-interaction involving their cytoplasmic domains. In addition, interactions between the extracellular domain of Nephrin and itself and between the extracellular domain of Nephrin and that of Neph1 were detected. Neph1 did not interact via a homophilic interaction. These observations suggest that Nephrin and Neph1 form a hetero-oligomeric receptor complex in the plane of the membrane that might interact across the foot process intercellular junction through interactions between Nephrin with itself and Neph1.

Animals↗