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Bone metaplasia associated with chronic allograft nephropathy
ne p hro l o g y i ma g e
http://www.kidney-international.org © 2006 International Society of Nephrology Kidney International (2006) 70, 407. doi:10.1038/sj.ki.5001678
Bone metaplasia associated with chronic allograft nephropathy K Tousignant1, V Phan2, MJ Clermont2, K Metellus3, G Perreault4 and H Sartelet3 1Department of Nephrology, Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Québec, Canada; 2Department of Pediatric Nephrology,
Centre Hospitalier Universitaire Ste-Justine, Montréal, Québec, Canada; 3Department of Pathology, Centre Hospitalier Universitaire Ste-Justine, Montréal, Québec, Canada; and 4Department of Pediatric Radiology, Centre Hospitalier Universitaire Ste-Justine, Montréal, Québec, Canada Correspondence: K Tousignant, Department of Nephrology, Centre Hospitalier Universitaire de Sherbrooke, 3001, 12ième avenue Nord, Sherbrooke, Québec J1H 5N4, Canada. E-mail: [email protected]
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Figure 1 | Renal allograft biopsy. (a) Histological features of renal cortex with two glomeruli surrounded by a lymphocytic interstitial infiltrate associated with acute cellular rejection. The usual morphology of the cortex is disrupted by multiple zones of bone metaplasia, which consist of osseous matrix, osteocytes, and osteoblasts hematoxylin–phloxin–safran; original magnification, ×200.) (b) Cross section of an interlobular artery, showing an intimal fibrous narrowing compatible with chronic allograft nephropathy. (hematoxylin–phloxin–safran; original magnification, ×100.)
A 15-year-old white girl with end-stage kidney disease from renal dysplasia received a cadaveric renal allograft. There was excellent renal function on an immunosuppressive protocol that included corticosteroids, tacrolimus, and mycophenolate mofetil. In the setting of noncompliance a year and a half later, the patient developed severe acute rejection (Banff III), for which she was treated with intravenous methylprednisolone and antilymphocytic serum. A second bout of rejection 6 months later (Banff Ib) was treated with intravenous steroids. Her renal function did not improve, and she started hemodialysis. Because of the subsequent development of gross hematuria, an allograft nephrectomy was performed. Pathologic examination showed intense diffuse cortical fibrosis associated with severe tubular atrophy. The glomeruli displayed features of chronic
Kidney International (2006) 70
transplant glomerulopathy. There was interposition of multiple millimeter-length areas of bone metaplasia within the fibrotic cortical tissue. Osseous tissues were mature with osteoid matrix associated with osteocytes, osteoblasts, and infrequent multinucleated osteoclasts. The osteoid matrix was often mineralized (Figure 1a). Severe chronic transplant arteriopathy was found in all arteries (Figure 1b). Associated with these chronic changes, there also was severe tubulitis and endarteritis. Previous sonographic images of the allograft did not reveal calcification. As in animal models (J Gruhn, ER Fisher, Arch Pathol 1960; 69: 82–92), connective tissue cells of the normal kidney have osteoblastic potential in chronic ischemic conditions, such as our case of severe and diffuse transplant arteriopathy associated with chronic allograft nephropathy.
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http://www.kidney-international.org © 2006 International Society of Nephrology Kidney International (2006) 70, 407. doi:10.1038/sj.ki.5001678
Bone metaplasia associated with chronic allograft nephropathy K Tousignant1, V Phan2, MJ Clermont2, K Metellus3, G Perreault4 and H Sartelet3 1Department of Nephrology, Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Québec, Canada; 2Department of Pediatric Nephrology,
Centre Hospitalier Universitaire Ste-Justine, Montréal, Québec, Canada; 3Department of Pathology, Centre Hospitalier Universitaire Ste-Justine, Montréal, Québec, Canada; and 4Department of Pediatric Radiology, Centre Hospitalier Universitaire Ste-Justine, Montréal, Québec, Canada Correspondence: K Tousignant, Department of Nephrology, Centre Hospitalier Universitaire de Sherbrooke, 3001, 12ième avenue Nord, Sherbrooke, Québec J1H 5N4, Canada. E-mail: [email protected]
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B
Figure 1 | Renal allograft biopsy. (a) Histological features of renal cortex with two glomeruli surrounded by a lymphocytic interstitial infiltrate associated with acute cellular rejection. The usual morphology of the cortex is disrupted by multiple zones of bone metaplasia, which consist of osseous matrix, osteocytes, and osteoblasts hematoxylin–phloxin–safran; original magnification, ×200.) (b) Cross section of an interlobular artery, showing an intimal fibrous narrowing compatible with chronic allograft nephropathy. (hematoxylin–phloxin–safran; original magnification, ×100.)
A 15-year-old white girl with end-stage kidney disease from renal dysplasia received a cadaveric renal allograft. There was excellent renal function on an immunosuppressive protocol that included corticosteroids, tacrolimus, and mycophenolate mofetil. In the setting of noncompliance a year and a half later, the patient developed severe acute rejection (Banff III), for which she was treated with intravenous methylprednisolone and antilymphocytic serum. A second bout of rejection 6 months later (Banff Ib) was treated with intravenous steroids. Her renal function did not improve, and she started hemodialysis. Because of the subsequent development of gross hematuria, an allograft nephrectomy was performed. Pathologic examination showed intense diffuse cortical fibrosis associated with severe tubular atrophy. The glomeruli displayed features of chronic
Kidney International (2006) 70
transplant glomerulopathy. There was interposition of multiple millimeter-length areas of bone metaplasia within the fibrotic cortical tissue. Osseous tissues were mature with osteoid matrix associated with osteocytes, osteoblasts, and infrequent multinucleated osteoclasts. The osteoid matrix was often mineralized (Figure 1a). Severe chronic transplant arteriopathy was found in all arteries (Figure 1b). Associated with these chronic changes, there also was severe tubulitis and endarteritis. Previous sonographic images of the allograft did not reveal calcification. As in animal models (J Gruhn, ER Fisher, Arch Pathol 1960; 69: 82–92), connective tissue cells of the normal kidney have osteoblastic potential in chronic ischemic conditions, such as our case of severe and diffuse transplant arteriopathy associated with chronic allograft nephropathy.
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