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Lupus nephritis: a challenging cause of rapidly progressive crescentic glomerulonephritis
V Sumethkul1, P Chalermsanyakorn, S Changsirikulchai
1Department of Medicine, Faculty of Medicine, Ramathibodi Hospital, Mahidol University, Bangkok, Thailand. ravsm@mahidol.ac.th
Insights
Lupus nephritis frequently causes crescentic glomerulonephritis. Daily oral cytotoxic drugs offer a better alternative to intravenous cyclophosphamide (IVCY) for selected patients, improving outcomes.
Area of Science:
- Nephrology
- Rheumatology
- Immunology
Background:
- Lupus nephritis is a significant cause of rapidly progressive crescentic glomerulonephritis.
- Understanding treatment outcomes is crucial for managing this severe kidney disease.
Purpose of the Study:
- To evaluate the outcomes of lupus patients with rapidly progressive crescentic glomerulonephritis.
- To compare the efficacy of different maintenance immunosuppressive therapies.
Main Methods:
- Retrospective study of 32 lupus patients with biopsy-proven crescentic glomerulonephritis.
- Patients received induction therapy followed by maintenance with prednisolone alone, prednisolone plus intermittent IVCY, or prednisolone plus daily oral cytotoxic drugs.
- Clinical outcomes and survival rates were analyzed.
Main Results:
- Lupus nephritis comprised over 50% of crescentic glomerulonephritis cases.
- Patients treated with daily oral cytotoxic drugs showed a significantly better clinical outcome compared to those receiving intermittent IVCY (P=0.01).
- Three-year survival rates were 27.6% for intermittent IVCY and 83.3% for daily oral cytotoxic drugs.
Conclusions:
- Lupus nephritis is a common cause of crescentic glomerulonephritis.
- Intermittent IVCY is not essential for favorable outcomes.
- Daily oral cytotoxic drugs represent a viable and effective alternative maintenance therapy for selected patients.
Abstract:
The outcomes of 32 lupus patients with rapidly progressive crescentic glomerulonephritis were studied. Lupus nephritis accounted for 51.6% (32/62) of all patients with biopsy proven rapidly progressive crescentic glomerulonephritis during a six year observation period that includes 961 consecutive native kidney biopsies. Median entry serum creatinine was 221 micromol/l. All patients received induction therapy with pulse methylprednisolone (n =27) or intravenous cyclophosphamide (n = 5). Maintenance therapies included prednisolone alone (group 1), prednisolone plus intermittent pulse intravenous cyclophosphamide (IVCY) (group 2) and prednisolone plus daily oral cytotoxic drugs (group 3). Twelve patients eventually had uremia. Seven further patients died of infection during therapy. One patient still had renal insufficiency and twelve patients had favorable clinical outcome (serum creatinine < 200 micromol/l). Patients in group 3 were more likely to have favorable clinical outcome than group 2 (P = 0.01; Fisher's exact test). Survival analysis found that the three year survival of 'group 2' was 27.6% while that of 'group 3' was 83.3%. Our results suggest that lupus nephritis is not an infrequent cause of crescentic glomerulonephritis. Therapy with IVCY is not necessary associated with good outcome. Selected patients can be effectively treated with daily oral cytotoxic drugs as a reasonable alternative therapy.