Chronic allograft nephropathy

ESRD secondary to PCKD and failed previous transplant. One prior renal transplant that occurred in 1995 (received kidney from husband), which failed secondary to chronic allograft nephropathy in 2004 (presumably from multiple rejection episodes within the first few years after transplant). For the previous transplant, the patient was maintained on cyclosporine, mycophenolate, and prednisone. 

Afzali B, Taylor AL, Goldsmith DJ. What we CAN do about chronic allograft nephropathy role of immunosuppressive modulations. Kidney Int 2005 68 2429-2443. 

Ruster M, Sperschneider H, Funfstuck R, Stein G, Grone HJ. Differential expression of beta-chemokines MCP-1 and RANTES and their receptors CCR1, CCR2, CCR5 in acute rejection and chronic allograft nephropathy of human renal allografts. Clin Nephrol 2004 61 30-39. 

The reports from initial clinical trials suggest that the level of immunosuppression achieved by belatacept is equivalent to cyclosporine in renal transplant patients with less chronic allograft nephropathy, stable kidney function and improved cardiovascular and metabolic profiles. 

Nankivell BJ, Borrows RJ, Fung CL, O Connell PJ, Allen RD, Chapman JR. The natural history of chronic allograft nephropathy. N Engl J Med. 2003 349 2326-2333. 

While CSA remarkably improved short-term graft and patient survival as compared to azathioprine-based immunosuppression, the same outcome has not been consistently demonstrated on long-term survival. One of the factors possibly related to this paradox is the role of chronic CSA nephrotoxicity in chronic allograft nephropathy. Marcen et al compared 128 CSA-treated and 185 azathioprine-treated cadaveric first renal transplant recipients followed for at least 10 years. In the first three years, post-transplant actuarial... 

There are few data on clinical strategies to avoid or minimize TAC-induced chronic nephrotoxicity. Patients with biopsy proved chronic allograft nephropathy or TAC chronic nephrotoxicity showed renal function improvement after switch from TAC to sirolimus or reduction of TAC dosage and introduc-... 

Bakker RC, Hollander AA, Mallat MJ, Bruijn JA, Paul LC, de Fijter JW. Conversion from cyclosporine to azathioprine at three months reducesthe incidence of chronic allograft nephropathy. Kidney int 2003 64 1027-1034. 

Marcen R, Pascual J,Teruel JL, Villafruela JJ, Rivera ME, Mampaso E, Burgos EJ, Ortuno J. Outcome of cadaveric renal transplant patients treated for 10 years with cyclosporine is chronic allograft nephropathy the major cause of late graft loss Transplanta-... 

Weir MR, Ward MT, Blahut SA, Klassen DK,CangroCB, Bartlett ST, Fink JC. Long-term impact of discontinued or reduced calcineurin inhibitor in patients with chronic allograft nephropathy. Kidney Int 2001 59 1567-1573. 

Campistol JM, Inigo P, JimenezW, Lario S, Clesca PH, Oppenheimer F, Rivera F. Losartan decreases plasma levels ofTGF-betal in transplant patients with chronic allograft nephropathy. Kidney Int 1999 56 714-719. 

Weir MR, Anderson L, Fink JC, Gabregiorgish K, Schweitzer EJ, Hoehn-Saric E, et al. A novel approach to the treatment of chronic allograft nephropathy. Transplantation 1997 64 1706-10. 

Campistol JM, Inigo P, Larios S, Bescos M, Oppenheimer F. Role of transforming growth factor-pi in the progression of chronic allograft nephropathy. Nephrol Dial Transplant 2001 16(Suppl 1) 114-116. 

Romagnani et al. (1999) assessed the expression of iNOS mRNA and protein in the kidneys of patents with graft failure due to chronic rejection. In chronic allograft nephropathy, iNOS protein was localised not only in inflammatory cells, but also in vascular, glomerular, and, more rarely, tubular structures. 

The principal cause of graft loss after the first year is chronic allograft nephropathy (CAN), followed by patient death, late acute rejections, nephropathy recurrence and polyomavirus infection (Hariharan 2001). However, prolongation of graft survival also means extended exposure of the patient to side-effects associated with immunosuppressive therapies, mainly infections and cancers, and other late-onset cardiovascular, bone and/or metabolic complications. The first year after transplantation is special, as it is characterized by the highest rates of acute rejection and opportunistic infections, such as cytomegalovirus. In this review, we successively address the presurgical evaluation of the patient, the operation itself and its possible complications, then the early (first year) and late (after the first year) medical complications. 

Halloran P, Melk A, Barth C (1999) Rethinking chronic allograft nephropathy the concept of accelerated senescence. J Am Soc Nephrol 10 167-181 Hariharan S (2001) Long-term kidney transplant survival. Am J Kidney Dis 38 S44-S50... 

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