American journal of kidney diseases : the official journal of the National Kidney Foundation · 2005
IgA nephropathy with crescents in kidney transplant recipients.
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Kowalewska Jolanta, Yuan Shan, Sustento-Reodica Neodjema, Nicosia Roberto F, Smith Kelly D, Davis Connie L, Alpers Charles E
Аннотация
BACKGROUND: Crescentic glomerulonephritis is an uncommon finding in renal allografts. Recurrence or de novo mesangial deposition of immunoglobulin A (IgA) in renal allografts most often is clinically benign, but some case reports have shown that IgA nephropathy in renal allografts can present as crescentic glomerulonephritis and may lead to rapid deterioration of graft function and/or graft loss.
METHODS: We reviewed diagnoses of all allograft biopsies at University of Washington Medical Center (Seattle, WA) from 1989 to 2003 and found 33 cases of glomerulonephritis with crescents. Eight of these cases were the result of recurrent or de novo IgA nephropathy. Clinical and pathological features of these patients were reviewed.
RESULTS: Six of 8 cases with crescents were the result of recurrent IgA nephropathy, and 2 cases were presumptive de novo IgA nephropathy. Of the 8 patients with IgA nephropathy with crescents, 6 patients presented clinically with increasing serum creatinine levels; 4 patients, with proteinuria; and 4 patients, with hematuria. In 6 patients, there was 10% to 30% involvement of glomeruli, with crescents partially or completely filling urinary spaces. The other patients showed lesser (approximately 7% of sampled glomeruli) involvement. Four patients with IgA nephropathy with crescents developed renal failure and returned to hemodialysis therapy. Three patients had a benign clinical course, with stabilization of renal function. One patient was lost to follow-up.
CONCLUSION: We identified a cohort of patients with glomerulonephritis with crescents in renal allografts with IgA nephropathy as the cause. In half the affected patients, this led to early progressive renal insufficiency and return to hemodialysis therapy.
METHODS: We reviewed diagnoses of all allograft biopsies at University of Washington Medical Center (Seattle, WA) from 1989 to 2003 and found 33 cases of glomerulonephritis with crescents. Eight of these cases were the result of recurrent or de novo IgA nephropathy. Clinical and pathological features of these patients were reviewed.
RESULTS: Six of 8 cases with crescents were the result of recurrent IgA nephropathy, and 2 cases were presumptive de novo IgA nephropathy. Of the 8 patients with IgA nephropathy with crescents, 6 patients presented clinically with increasing serum creatinine levels; 4 patients, with proteinuria; and 4 patients, with hematuria. In 6 patients, there was 10% to 30% involvement of glomeruli, with crescents partially or completely filling urinary spaces. The other patients showed lesser (approximately 7% of sampled glomeruli) involvement. Four patients with IgA nephropathy with crescents developed renal failure and returned to hemodialysis therapy. Three patients had a benign clinical course, with stabilization of renal function. One patient was lost to follow-up.
CONCLUSION: We identified a cohort of patients with glomerulonephritis with crescents in renal allografts with IgA nephropathy as the cause. In half the affected patients, this led to early progressive renal insufficiency and return to hemodialysis therapy.