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Recurrence of Henoch–Schönlein purpura nephritis superimposed on severe pre‐eclampsia in a kidney transplant patient
Author(s) -
Tanno Yudo,
Yamamoto Hiroyasu,
Yamamoto Izumi,
Yaginuma Tatsuhiro,
Mitome Jun,
Kawamura Yoshimi,
Miyazaki Yoichi,
Yokoyama Keitaro,
Utsunomiya Yasunori,
Yamaguchi Yutaka,
Hosoya Tatsuo
Publication year - 2007
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/j.1399-0012.2007.00716.x
Subject(s) - medicine , transplantation , renal function , proteinuria , kidney transplantation , creatinine , eclampsia , pregnancy , urology , renal biopsy , kidney disease , gastroenterology , kidney , surgery , biology , genetics
Henoch–Schönlein purpura nephritis (HSPN) frequently recurs in patients following kidney transplantation, and pregnancy has been reported to be an exacerbating factor. However, little is known about the recurrence of HSPN during pregnancy in patients with superimposed pre‐eclampsia having excellent graft function who had experienced kidney transplantation. Here, we report a case of recurrent HSPN complicating severe pre‐eclampsia six yr after transplantation. A 31‐yr‐old woman who had received a living‐related kidney transplant at age 25 became pregnant. The cause of her end‐stage renal disease was biopsy‐proven HSPN. She had an excellent clinical course after transplantation, with good allograft function (serum creatinine <0.9 mg/dL, no proteinuria or hematuria, no episode of rejection), and normal blood pressure. We discontinued the angiotensin II receptor blocker that had been prescribed to prevent glomerular hyperfiltration. After week 17 of pregnancy, proteinuria and blood pressure increased markedly, and then her kidney function deteriorated progressively with intermittent mild microhematuria. At week 28 of pregnancy, umbilical blood flow and fetal growth were impaired, prompting preterm cesarean delivery. Subsequently, her blood pressure and serum creatinine normalized immediately, although the urinary protein excretion decreased insufficiently from 6.0 to 1.0 g/d at six months postpartum. In general, hematuria has a predictive value for the recurrence of HSPN. Clinically, we considered this case to be superimposed pre‐eclampsia, not recurrent HSPN. However, a biopsy conducted seven months postpartum suggested recurrent HSPN on her renal allograft. In addition, focal segmental membranous nephropathy with C1q deposition was observed. It was difficult to determine when the HSPN and membranous lesions occurred. This case suggests that a pathological evaluation is important in HSPN patients after transplantation to reduce adverse risks during and after pregnancy.