A Study of Crescentic Glomerulonephritis - Etiology, Clinical profile, prognostic factors and outcome.

Subrahmanian, SP S (2010) A Study of Crescentic Glomerulonephritis - Etiology, Clinical profile, prognostic factors and outcome. Masters thesis, Madras Medical College, Chennai.


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BACKGROUND Crescentic glomerulonephritis is the histologic manifestation of any severe glomerular injury resulting from immune/ inflammatory mechanisms. It is characterized by the proliferation of resident glomerular and infiltrating inflammatory cells in the Bowmans space. Rapidly Progressive Glomerulonephritis (RPGN) is the clinical counterpart of Crescentic glomerulonephritis and is characterized by a rapid decline in renal function over days to weeks. The urine sediment is typically active in RPGN, showing dysmorphic erythrocyturia and erythrocytic cylindruria. RPGN is a medical emergency because of the potential for relentless and rapid progression to end stage renal failure, if not treated. The crescents evolve through various stages and ultimately transform into fibrous elements resulting in permanent glomerular scarring. Therefore therapeutic interventions in Crescentic glomerulonephritis should precede such irreversible alterations in glomerular structure. Early identification and treatment of RPGN gain importance in this respect. Crescentic glomerulonephritis is the culmination of severe glomerular injury and the etiology of Crescentic glomerulonephritis is heterogeneous. The clinical presentation and immuno pathologic characteristics of Crescentic glomerulonephritis are influenced by the etiology. Identification of the etiology is essential for instituting appropriate treatment. The annual incidence of Crescentic glomerulonephritis is 0.7 to 1.0 per 1,00,000 population. Crescentic glomerulonephritis accounts for 9. 5% of glomerular diseases(4) and 5.1% of all biopsies done. Geographic variations exist with respect to the incidence and etiology of Crescentic glomerulonephritis. The present study has attempted to identify Crescentic glomerulonephritis and study the etiology, clinico epidemiological features and outcome of the disease in our region. AIM OF THE STUDY : This study aims to identify patients with Crescentic glomerulonephritis and study the etiology, clinical profile, prognostic factors and outcome of Crescentic glomerulonephritis. CONCLUSION : 1) Crescentic glomerulonephritis was found to be equally distributed among both sexes in adults. 2) In most patients, crescentic glomerulonephritis occurred as a denovo manifestation, while a few others had pre existing glomerulonephritis like lupus nephritis and Henoch Schonlein nephritis. 3) Fever, diarrhea, respiratory and skin infection preceded crescentic glomerulonephritis in majority (53%) of patients. 4) Major symptoms at presentation included oliguria, anuria and haematuria. About 35% of the patients had a non oliguric presentation. 5) Extra renal manifestations were pronounced in immune complex nephritis and anti GBM nephritis, while most of the patients (66%) with pauci immune nephritis had a renal limited disease. 6) Hypertension was seen in all but one patient and about 42% of the patients had severe hypertension (BP ≥ 161/101 mm Hg). 7) Immune complex nephritis was the predominant immunopathologic category of crescentic glomerulonephritis accounting for about 69% of all cases, followed by pauci immune nephritis (23% of cases) and Anti GBM nephritis (8% of cases). 8) A half of immune complex glomerulonephritis was due to Lupus nephritis. PIGN accounted for 22%, IgA nephropathy and Henoch Schonlein purpura for 22% and membranous nephropathy accounted for 6% of immune complex nephritis. 9) Urine protein excretion was highest in Anti GBM nephritis and lowest in Pauci immune nephritis. Mean urine protein excretion was in the nephrotic range in both Anti GBM nephritis and Immune complex nephritis. 10) Most patients with pauci immune nephritis were ANCA negative. Only P – ANCA was detectable in the study population. One patient was “double positive” and had both circulating Anti GBM antibody and P – ANCA. 11) On an average 77.46% of the glomeruli revealed crescents. All ages of crescents were seen. Glomerular tuft necrosis was seen in 11.5% of the patients. 12) About 88% of patients required dialysis. Mean serum creatinine at presentation was 642μmol/L. 13) IV and oral steroids, Cyclophosphamide and plasmapheresis were employed as treatment modalities. 14) Mean latency between symptom onset and specific treatment was 17.45 days. 15) At three months about 7.6% died, 27% remained dialysis dependent (ESRD), 46% had partial or complete recovery of renal function and remained dialysis free and 19.5% were lost to follow up. 16) Outcome was worst in Anti GBM nephritis with 50% mortality and 50% ESRD. 17) Pauci immune nephritis had the best outcome with none dying or remaining dialysis dependent. 18) Outcome was mixed in immune complex nephritis with 33% mortality, 44% recovering renal function and about 5% developing ESRD. 19) Poor prognostic factors identified in the present study include diastolic BP ≥ 105 mm Hg, a crescent score ≥ 92.77% and involvement of atleast 69.5% of the sampled glomeruli by fibrous or fibro cellular crescents.

Item Type: Thesis (Masters)
Uncontrolled Keywords: Crescentic Glomerulonephritis ; Etiology ; Clinical profile ; prognostic factors ; outcome.
Subjects: MEDICAL > Nephrology
Depositing User: Kambaraman B
Date Deposited: 11 Jul 2017 04:17
Last Modified: 11 Jul 2017 04:17
URI: http://repository-tnmgrmu.ac.in/id/eprint/1370

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