Biomedical subjects

Sevinc Emre

Publications and source records attributed to Sevinc Emre.

3 recordsLinked to original sources

PubMed2006

Crescentic glomerulonephritis in a child with infective endocarditis.

Renal manifestations associated with infective endocarditis (IE) may present with different clinical patterns, and the most common renal histopathological finding is diffuse proliferative and exudative type of glomerulonephritis, leading to hematuria and/or proteinuria. Renal failure due to crescentic glomerulonephritis (CGN) in children with IE is a very rare condition. We report here a 6-year-old boy, who had a history of cardiac surgery for pulmonary atresia and ventricular septal defect, presenting with the clinical findings of IE and hematuria associated with renal failure due to CGN. He was treated with a combination of intravenous (IV) methylprednisolone pulses and appropriate antibiotics, but also received one dose of IV cyclophosphamide. Complete serological, biochemical, and clinical improvement was achieved after 2 months of follow-up. Antibiotic therapy is the essential part of the treatment of IE-associated glomerulonephritis; however, this case also highlights the importance of aggressive immunosuppressive therapy to suppress the immunological process related with infection in this life-threatening condition leading to renal failure.

Anti-Bacterial Agents↗

PubMed2004

Biochemical bone markers in nephrotic children.

In this study we evaluated the effects of high-dose corticosteroid (CS) therapy and the character of the nephrotic syndrome (NS) itself on bones in patients with normal glomerular filtration rate. We measured serum osteocalcin (OC), alkaline phosphatase (ALP), intact parathyroid hormone (iPTH), 25-hydroxyvitamin D, calcium (Ca), phosphorus (P), and magnesium (Mg) levels, and urinary Ca and protein excretion in nephrotic children during the active phase before (group Ia) and after CS treatment (group Ib). The results were compared with age-matched control subjects. A significant increase in urinary Ca excretion was observed after CS treatment. Serum ALP, OC, and iPTH levels were within normal limits at the time of study entry. However, both serum OC and ALP levels showed a significant decrease after the completion of CS treatment (OC from 13.6+/-9.2 ng/ml to 6.7+/-5.2 ng/ml and ALP from 151.8+/-60.2 U/l to 116+/-43.8 U/l). 25-Hydroxyvitamin D levels increased to 17.2+/-8.9 microg/l from 9.9+/-6.9 microg/l after CS treatment. The effects of recurrent use of CSs were assessed by dividing nephrotic patients into two subgroups: infrequent relapsers (IFR) and frequent relapsers (FR). The cumulative dose of CS was 28,125 mg/m(2) for IFR and 105,000 mg/m(2) for FR. The changes in OC, ALP, and 25-hydroxyvitamin D levels after CS treatment were significantly different between IFR and FR. We conclude that high-dose CS treatment causes a decrease in bone formation, as shown by the changes in OC and ALP levels. 25-Hydroxyvitamin D levels remained lower than control subjects after CS therapy. The higher the cumulative dose of CS used the more marked the changes in biochemical bone markers. The contribution of FR to baseline 25-hydroxyvitamin D levels needs further study.

Biomarkers↗

PubMedDate not supplied

Is paraoxonase 192 gene polymorphism a risk factor for membranoproliferative glomerulonephritis in children?

We investigated the effects of paraoxonase (PON1) 192 polymorphism on serum PON1 activity and the impact of phenotypic expression on the risk and prognosis of Turkish children with membranoproliferative glomerulonephritis (MPGN). Eighteen children with biopsy-proven Type I MPGN (10 boys, 8 girls) and age-matched 53 healthy controls were included in the study. PCR (polymerase chain reaction), RFLP (restriction fragment length polymorphism) and agarose gel electrophoresis techniques were used to determine the PON1 192 genotype. PON1 activity was measured by spectrophotometric assay of p-nitrophenol production following addition of paraoxon. We found that PON1 192 genotype distribution (AA, AB, BB) in MPGN patients were 61.1%, 22.3%, 16.6% and 15.1%, 35.8%, 49.1% in controls, respectively. The frequency of AA genotypes was significantly higher in the MPGN group (0.611) compared with the healthy controls (0.151) (p < 0.001). Although the serum PON1 activity was lower in MPGN patients (103.3 +/- 55.2 U/l) than the healthy controls (130.9 +/- 71.2 U/mol), the difference was not statistically significant (p = 0.0563). In the genotypes of patients and controls classified according to PON1 A/B polymorphism; serum PON1 activities were significantly increased (p < 0.001, ANOVA) in the order of PON1 AA, AB and BB in both MPGN patients (82.4, 91.7 and 173.6 U/l) and healthy controls (85.9, 119.9 and 193.1 U/l), respectively. There was a significant relationship between the poor prognosis and having AA genotype and low PON1 activity. Of the 8 patients with poor prognosis, 7 had genotype AA and the remaining one was AB heterozygote. Our results suggest that homozygosity for the A allele might have an important role on the risk for developing MPGN and may also be associated with the poor prognosis of disease. In conclusion, we suggest that the PON1 activities are affected by PON1 genetic variability in Turkish patients with MPGN.

Adolescent↗