Serum Nitric Oxide in Post-Streptococcal Acute Glomerulonephritis | ||
| GEGET | ||
| Article 9, Volume 2, Issue 2, December 2002, Pages 33-36 PDF (300.65 K) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/geget.2002.48370 | ||
| Authors | ||
| Ayman Hammad1; Ashraf Bakr1; Gihan Fathy1; Manal Fathy2; Rizk El Baz3 | ||
| 1Department of Pediatrics, Faculty of Medicine, Mansoura University, National Research Institute, Cairo. | ||
| 2Ophthalmology Research Center, Cairo. | ||
| 3Clinical Pathology Department, Mansoura University Children Hospital, Egypt. | ||
| Abstract | ||
| Background: The role of nitric oxide in renal immune injury has recently become the focus of intense investigations. In various forms of glomerulonephritis, there is increased production of NO in isolated glomeruli and enhanced expression and activation of the inducible isoform of nitric oxide synthetase (iNOS). Objectives: To study the changes that occur in post-Streptococcal acute glomerulonephritis. Methods: Serum nitric oxide (NO) levels were measured in 20 children with post-streptococcal acute glomerulonephritis (PSAGN) during their initial presentation. Diagnosis of PSAGN was based on the presence of hematuria, transient hypo complement aemia and positive laboratory evidence of recent Streptococcal infection. Patients were compared to 20 healthy children of matched age and sex. Results: Patients in the acute attack had significantly higher levels of NO when compared to controls (median = 38.45 Vs 30.45 umol/l respectively, p = 0.033). Serum NO levels were correlated significantly with serum complement 3 (C3) (r = -0.574, p = 0.008), and proteinuria (r = 0.698, p = 0.001). No significantly correlation was detected between serum NO levels and serum creatinine, hypertension (systolic and diastolic), degree of hematuria or oedema. Out of the studied 20 cases; 16 cases were reassessed 3 months after normalization of their complement level and a significant drop in NO was found (p = 0.039). Conclusions: We suggest that NO has a role in the pathogenesis of PSAGN mostly through mediation of immunologic injury to the glomeruli | ||
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