Abstract
Crescentic glomerulonephritis (CrGN) is characterized by the presence of crescents in more than 50% of glomeruli. This study aims to identify the etiology and clinicopathological features and outcomes of CrGN. In this observational study, 80 biopsy-proven CrGN were included. Patients’ demographic profile, clinical parameters, treatments, and outcomes were collected and analyzed. The mean age in our study population was 40.86 ± 16.5 years. Type II CrGN was the most common type of CrGN. Female predominance was observed in type I and type II CrGN. The highest percentage of glomeruli with crescents was seen in type I (87 ± 15.2%, P = 0.04), followed by type III and type II. At the last follow-up, mean estimated glomerular filtration rate was 25.8 ± 11.41 mL/min/1.73 m2 and was significantly lower in type I CrGN (11.6 ± 4.8 mL/min/1.73 m2 P = 0.001). The overall 5-year renal survival rate was 55% and was highest in type II (69.4%), followed by type III and type I (27.3%) CrGN (P = 0.0299). In our study, oliguria at the time of presentation, percentage of crescents, glomerular sclerosis, and moderate/severe IFTA were associated with poor renal outcomes. In conclusion, CrGN was seen in 5.7% of kidney biopsies in our study. Type II CrGN was the most common type of CrGN followed by type III CrGN. Renal survival was poor in type I CrGN patients compared to type II and type III CrGN. Also, oliguria, crescents, glomerular sclerosis, and moderate/severe IFTA were associated with poor renal outcomes.
Highlights
Patients in type III Crescentic glomerulonephritis (CrGN) were older than patients in type I and type II CrGN
Oliguria at the time of presentation, a higher percentage of crescents, glomerular sclerosis, and moderate/severe Interstitial fibrosis and tubular atrophy (IFTA) were associated with poor renal outcomes
Renal survival was poor in type I CrGN patients, compared to type II and type III CrGN
Summary
Crescentic glomerulonephritis (CrGN) is a histopathological entity characterized by the presence of crescents, usually in more than 50% of the glomeruli sampled [1]. Disruption of glomerular basement membrane (GBM) due to the antibody or immune-complex-mediated injury leads. Clinicopathological study of crescentic glomerulonephritis to the accumulation of circulating leukocytes, inflammatory mediators, and coagulation factors in the Bowman’s space. Fibrin exudation and proliferation of parietal epithelial cells, macrophages, and interstitial fibroblasts result in the obliteration of Bowman’s space and crescent formation [3]. The extent of crescent formation correlates with the severity of glomerular damage [4]. Crescents with predominant cellular components represent acute glomerular injury which can resolve with treatment, whereas fibrous crescents, interstitial fibrosis, or tubular atrophy may not have favorable renal outcomes [5]
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