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Chronic allograft nephropathy.

Fletcher JT, Nankivell BJ, Alexander SI - Pediatr. Nephrol. (2008)

Bottom Line: CAN is the result of immunological and nonimmunological injury, including acute rejection episodes, hypoperfusion, ischaemia reperfusion, calcineurin toxicity, infection and recurrent disease.Protocol biopsy monitoring is not current practice in paediatric transplantation for CAN monitoring but may have a place if new treatment options become available.Newer immunosuppression regimens, closer monitoring of the renal allograft and management of subclinical rejection may lead to reduced immune injury leading to CAN in the paediatric population but must be weighed against the risk of increased immunosuppression and calcineurin inhibitor nephrotoxicity.

View Article: PubMed Central - PubMed

Affiliation: Department of Paediatrics, The University of Sydney, Nepean Clinical School, Nepean Hospital, Sydney, NSW, Australia.

ABSTRACT
Chronic allograft nephropathy (CAN) is the leading cause of renal allograft loss in paediatric renal transplant recipients. CAN is the result of immunological and nonimmunological injury, including acute rejection episodes, hypoperfusion, ischaemia reperfusion, calcineurin toxicity, infection and recurrent disease. The development of CAN is often insidious and may be preceded by subclinical rejection in a well-functioning allograft. Classification of CAN is histological using the Banff classification of renal allograft pathology with classic findings of interstitial fibrosis, tubular atrophy, glomerulosclerosis, fibrointimal hyperplasia and arteriolar hyalinosis. Although improvement in immunosuppression has led to greater 1-year graft survival rates, chronic graft loss remains relatively unchanged and opportunistic infectious complications remain a problem. Protocol biopsy monitoring is not current practice in paediatric transplantation for CAN monitoring but may have a place if new treatment options become available. Newer immunosuppression regimens, closer monitoring of the renal allograft and management of subclinical rejection may lead to reduced immune injury leading to CAN in the paediatric population but must be weighed against the risk of increased immunosuppression and calcineurin inhibitor nephrotoxicity.

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Schematic illustration of biopsy of a renal allograft showing histopathological features characteristic of chronic allograft nephropathy (CAN). Italics indicate potential precipitating factors for CAN associated with the areas they specifically target. Reprinted with permission from [51]
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Fig1: Schematic illustration of biopsy of a renal allograft showing histopathological features characteristic of chronic allograft nephropathy (CAN). Italics indicate potential precipitating factors for CAN associated with the areas they specifically target. Reprinted with permission from [51]

Mentions: The histological features that define CAN in the kidney transplant allograft include interstitial fibrosis and tubular atrophy, as mentioned above, as well as features of glomerulosclerosis and fibrointimal hyperplasia (Fig. 1). CAN is graded as mild, moderate or severe based on the severity of chronic interstitial fibrosis and tubular atrophy and the area of cortex affected in the biopsy specimen. Interstitial fibrosis, denoted as ci, is scored by the area fibrosed and ranges from mild (ci1 6–25%) to severe (ci3 >50%). Tubular atrophy refers to the loss of tubular height and increased luminal size of the tubules and is denoted as ct (ct0–ct3). Tubular atrophy and interstitial fibrosis are often nonspecific by themselves. Chronic transplant glomerulopathy refers to the thickening of the glomeruli and is quantified by the percentage of glomeruli developing “double contours” of peripheral capillary loops and is denoted as cg (cg0–cg3) (Fig. 2a). Arteriolar hyalinosis, as suggested by the term, denotes thickening of arterioles within the kidney based on the amount of periodic-acid-Schiff-positive hyalinosis and is denoted as ah (ah0–ah3), often implying calcineurin inhibitor (CNI) nephropathy. More in-depth quantification of all of these criteria is readily available [1].Fig. 1


Chronic allograft nephropathy.

Fletcher JT, Nankivell BJ, Alexander SI - Pediatr. Nephrol. (2008)

Schematic illustration of biopsy of a renal allograft showing histopathological features characteristic of chronic allograft nephropathy (CAN). Italics indicate potential precipitating factors for CAN associated with the areas they specifically target. Reprinted with permission from [51]
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2697362&req=5

Fig1: Schematic illustration of biopsy of a renal allograft showing histopathological features characteristic of chronic allograft nephropathy (CAN). Italics indicate potential precipitating factors for CAN associated with the areas they specifically target. Reprinted with permission from [51]
Mentions: The histological features that define CAN in the kidney transplant allograft include interstitial fibrosis and tubular atrophy, as mentioned above, as well as features of glomerulosclerosis and fibrointimal hyperplasia (Fig. 1). CAN is graded as mild, moderate or severe based on the severity of chronic interstitial fibrosis and tubular atrophy and the area of cortex affected in the biopsy specimen. Interstitial fibrosis, denoted as ci, is scored by the area fibrosed and ranges from mild (ci1 6–25%) to severe (ci3 >50%). Tubular atrophy refers to the loss of tubular height and increased luminal size of the tubules and is denoted as ct (ct0–ct3). Tubular atrophy and interstitial fibrosis are often nonspecific by themselves. Chronic transplant glomerulopathy refers to the thickening of the glomeruli and is quantified by the percentage of glomeruli developing “double contours” of peripheral capillary loops and is denoted as cg (cg0–cg3) (Fig. 2a). Arteriolar hyalinosis, as suggested by the term, denotes thickening of arterioles within the kidney based on the amount of periodic-acid-Schiff-positive hyalinosis and is denoted as ah (ah0–ah3), often implying calcineurin inhibitor (CNI) nephropathy. More in-depth quantification of all of these criteria is readily available [1].Fig. 1

Bottom Line: CAN is the result of immunological and nonimmunological injury, including acute rejection episodes, hypoperfusion, ischaemia reperfusion, calcineurin toxicity, infection and recurrent disease.Protocol biopsy monitoring is not current practice in paediatric transplantation for CAN monitoring but may have a place if new treatment options become available.Newer immunosuppression regimens, closer monitoring of the renal allograft and management of subclinical rejection may lead to reduced immune injury leading to CAN in the paediatric population but must be weighed against the risk of increased immunosuppression and calcineurin inhibitor nephrotoxicity.

View Article: PubMed Central - PubMed

Affiliation: Department of Paediatrics, The University of Sydney, Nepean Clinical School, Nepean Hospital, Sydney, NSW, Australia.

ABSTRACT
Chronic allograft nephropathy (CAN) is the leading cause of renal allograft loss in paediatric renal transplant recipients. CAN is the result of immunological and nonimmunological injury, including acute rejection episodes, hypoperfusion, ischaemia reperfusion, calcineurin toxicity, infection and recurrent disease. The development of CAN is often insidious and may be preceded by subclinical rejection in a well-functioning allograft. Classification of CAN is histological using the Banff classification of renal allograft pathology with classic findings of interstitial fibrosis, tubular atrophy, glomerulosclerosis, fibrointimal hyperplasia and arteriolar hyalinosis. Although improvement in immunosuppression has led to greater 1-year graft survival rates, chronic graft loss remains relatively unchanged and opportunistic infectious complications remain a problem. Protocol biopsy monitoring is not current practice in paediatric transplantation for CAN monitoring but may have a place if new treatment options become available. Newer immunosuppression regimens, closer monitoring of the renal allograft and management of subclinical rejection may lead to reduced immune injury leading to CAN in the paediatric population but must be weighed against the risk of increased immunosuppression and calcineurin inhibitor nephrotoxicity.

Show MeSH
Related in: MedlinePlus