Low variability of plant protein intake in the CKiD cohort does not demonstrate changes in estimated GFR nor electrolyte balance.
Pediatric nephrology (Berlin, Germany)
BACKGROUND: Vegetable or plant-based sources of protein may confer health benefits in children with progressive kidney disease. Our aims were to understand the effect of the proportion of vegetable protein intake on changes in estimated GFR and to understand the effect of the proportion of vegetable protein intake on serum levels of bicarbonate, phosphorus, and potassium.METHODS: Children with baseline eGFR between 30 and 90 mL/min/1.73 m2 were recruited from 59 centers across North America as part of the chronic kidney disease in children (CKiD) study. The percentage of dietary vegetable protein (VP%) was gathered from annual Food Frequency Questionnaires. We performed longitudinal linear mixed models to determine the effect of VP% on eGFR and longitudinal logistic mixed models to determine the effect of VP% on electrolyte balance (potassium, phosphorus, bicarbonate).RESULTS: Two thousand visits from 631 subjects. Across all dichotomized groups of children (sex, African American race, Hispanic ethnicity, glomerular etiology of CKD, hypertension, anemia, hyperkalemia, hyperphosphatemia, acidosis, BMI < 95th percentile), the median VP% was 32-35%. The longitudinal mixed model analysis did not show any effect of VP% on eGFR electrolyte (bicarbonate, phosphorus, and potassium) abnormalities (p > 0.1).CONCLUSIONS: A diverse cohort of children with CKD has a narrow and homogeneous intake of vegetable protein. Due to the low variability of plant-based protein in the cohort, there were no associations between the percentage of plant protein intake and changes in eGFR nor electrolyte balance. A higher resolution version of the Graphical abstract is available as Supplementary information.
View details for DOI 10.1007/s00467-021-05334-y
View details for PubMedID 34796391
LDL-apheresis-induced remission of focal segmental glomerulosclerosis recurrence in pediatric renal transplant recipients.
Pediatric nephrology (Berlin, Germany)
Focal segmental glomerulosclerosis (FSGS) in pediatric patients is typically difficult to treat and will progress to end-stage renal disease (ESRD) in about 10% of cases. Following kidney transplantation, FSGS can recur in up to 56% of renal allografts-with a near 100% recurrence in subsequent transplants.Four different pediatric centers across the USA and the UK employed a protocol using LDL-apheresis (LDL-A) and pulse solumedrol to treat recurrent FSGS after transplantation in seven patients. All the patients included in this series demonstrated immediate, or early, recurrence of FSGS, which clinically presented as nephrotic-range proteinuria within hours to days after implantation of the kidney.All patients experienced reductions in urinary protein to creatinine ratios resulting in partial or complete remission. All patients demonstrated improvements in their estimated GFRs at their most recent follow-up since LDL-A discontinuation.This case series describes the successful treatment, across four different pediatric centers, of seven pediatric patients with recurrent post-transplant FSGS using the Liposorber® LA-15 in combination with pulse solumedrol.
View details for DOI 10.1007/s00467-019-04296-6
View details for PubMedID 31250206
A case of Fanconi syndrome due to a deferasirox overdose and a trial of plasmapheresis
JOURNAL OF CLINICAL PHARMACY AND THERAPEUTICS
2017; 42 (5): 634-637
Deferasirox has nephrotoxic effects in the context of chronic therapy. This case report illustrates proximal tubular dysfunction (Fanconi syndrome) due to an acute deferasirox overdose.In response, we trialled plasmapheresis to eliminate the drug. Deferasirox levels were obtained in the context of three rounds of plasmapheresis. Given the half-life model of decay, we concluded that plasmapheresis may not have been successful. The patient ultimately recovered normal tubular function after 2 months.This report is the first to describe acute deferasirox-induced nephrotoxicity, and the application of plasmapheresis that, ultimately, did not change the typical time to recovery.
View details for DOI 10.1111/jcpt.12553
View details for Web of Science ID 000409017900020
View details for PubMedID 28556939
Use of a Robotic Sampler (PIPER) for Evaluation of Particulate Matter Exposure and Eczema in Preschoolers
INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH
2016; 13 (2): 242
While the association of eczema with asthma is well recognized, little research has focused on the potential role of inhalable exposures and eczema. While indoor air quality is important in the development of respiratory disease as children in the U.S. spend the majority of their time indoors, relatively little research has focused on correlated non-respiratory conditions. This study examined the relationship between particulate matter (PM) exposures in preschool age children and major correlates of asthma, such as wheeze and eczema. Air sampling was carried out using a robotic (PIPER) child-sampling surrogate. This study enrolled 128 participants, 57 male and 71 female children. Ages ranged from 3 to 58 months with the mean age of 29.3 months. A comparison of subjects with and without eczema showed a difference in the natural log (ln) of PM collected from the PIPER air sampling (p = 0.049). PIPER's sampling observed an association between the ln PM concentrations and eczema, but not an association with wheezing history in pre-school children. Our findings are consistent with the hypothesis of the role of the microenvironment in mediating atopic dermatitis, which is one of the predictors of persistent asthma. Our findings also support the use of PIPER in its ability to model and sample the microenvironment of young children.
View details for DOI 10.3390/ijerph13020242
View details for Web of Science ID 000371900500058
View details for PubMedID 26907317
View details for PubMedCentralID PMC4772262
Addressing Narcotics in the Pediatric Population.
MD advisor : a journal for New Jersey medical community
2015; 8 (4): 7-14
View details for PubMedID 27603278
Drebrin A Knockout Eliminates the Rapid Form of Homeostatic Synaptic Plasticity at Excitatory Synapses of Intact Adult Cerebral Cortex
JOURNAL OF COMPARATIVE NEUROLOGY
2009; 517 (1): 105-121
Homeostatic synaptic plasticity (HSP) is important for maintaining neurons' excitability within the dynamic range and for protecting neurons from unconstrained long-term potentiation that can cause breakdown of synapse specificity (Turrigiano  Cell 135:422-435). Knowledge of the molecular mechanism underlying this phenomenon remains incomplete, especially for the rapid form of HSP. To test whether HSP in adulthood depends on an F-actin binding protein, drebrin A, mice deleted of the adult isoform of drebrin (DAKO) but retaining the embryonic isoform (drebrin E) were generated. HSP was assayed by determining whether the NR2A subunit of N-methyl-D-aspartate receptors (NMDARs) can rise rapidly within spines following the application of an NMDAR antagonist, D-APV, onto the cortical surface. Electron microscopic immunocytochemistry revealed that, as expected, the D-APV treatment of wild-type (WT) mouse cortex increased the proportion of NR2A-immunolabeled spines within 30 minutes relative to basal levels in hemispheres treated with an inactive enantiomer, L-APV. This difference was significant at the postsynaptic membrane and postsynaptic density (i.e., synaptic junction) as well as at nonsynaptic sites within spines and was not accompanied by spine size changes. In contrast, the D-APV treatment of DAKO brains did not augment NR2A labeling within the spine cytoplasm or at the synaptic junction, even though basal levels of NR2A were not significantly different from those of WT cortices. These findings indicate that drebrin A is required for the rapid (<30 minutes) form of HSP at excitatory synapses of adult cortices, whereas drebrin E is sufficient for maintaining basal NR2A levels within spines.
View details for DOI 10.1002/cne.22137
View details for Web of Science ID 000269848300007
View details for PubMedID 19711416
View details for PubMedCentralID PMC2839874