Henoch-SchÖlein Purpura Nephritis in Children: A Severe IgA Mediated Glomerulonephritis

Background: Henoch-SchÖlein purpura nephritis (HSPN) and IgA nephropathy (IgAN) are common in children and characterized by IgA deposits in glomeruli. HSPN shows more severe glomerular lesions than IgAN; however, a systematic approach to compare pathological features of both diseases is lacking. The objective of this study was to compare histological parameters, using those from “Oxford Classification of IgA Nephropathy” as well as from active glomerular lesions to distinguish these two entities. Methods: Renal biopsies performed at the Children's Hospital of Michigan during 2004-2010 with the diagnosis of HSPN and IgAN were reviewed. The “Oxford Classification of IgA nephropathy” was applied to measure mesangial cellularity, endocapillary proliferation, segmental glomerulosclerosis, and tubular atrophy/interstitial fibrosis. Measurements for active glomerular lesions, (i.e. the highest number of mesangial cells, percentage of glomeruli with endocapillary proliferation, cellular crescents and segmental necrosis) were also performed. Clinical presentations, including hypertension, protein/creatinine ratio, hematuria, and estimated glomerular filtration rate were compared between HSPN and IgAN patients. Findings in HSPN and IgAN were compared using student t-test Results: A total of 23 HSPN and 26 IgAN patients were diagnosed during study period. HSPN patients were significantly younger than those with IgAN (7.8 ± 3.3 vs 12.4 ± 3.2, year-old, p<0.05). Patients with HSPN had more mesangial cells (11 ± 3.2 vs 8.3 ± 2.4), higher percentage of glomeruli with endocapillary proliferation (14.9 ± 2.2 vs 4.9 ± 8.2), cellular crescents (10.4 ± 1.2 vs 4.3 ± 2.8), and segmental necrosis (6.6 ± 1.3 vs 0.7 ± 1.1), all p<0.05). There was no significant difference between HSPN and IgAN in the Oxford Classification (p>0.05). There was a trend toward higher in protein/creatinine ratio in HSPN than IgAN that was not significant. Conclusion: HSPN and IgAN share histopathological features of mesangial/endocapillary proliferation, but HSPN has more extensive mesangial/endocapillary proliferation and a higher percentage of glomeruli with cellular crescents and segmental necrosis, indicating more severe glomerular damage.