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41 Serum C‐Reactive Protein in Kidney Transplant Patients – A Useful Marker of Immune Activation
Author(s) -
BubićFilipi L,
Barišić I,
Hršak Puljić I,
BašićJukić N,
Puretić Z,
Kes P
Publication year - 2005
Publication title -
therapeutic apheresis and dialysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.415
H-Index - 53
eISSN - 1744-9987
pISSN - 1744-9979
DOI - 10.1111/j.1526-0968.2005.222_41_41.x
Subject(s) - medicine , methylprednisolone , prednisolone , azathioprine , gastroenterology , acute tubular necrosis , c reactive protein , asymptomatic , transplantation , nephrotoxicity , kidney transplantation , immunosuppression , renal function , corticosteroid , kidney , urology , surgery , inflammation , disease
The clinical manifestations of different complications after kidney transplantation are often vague and simple laboratory tests for early diagnosis would be valuable. This study investigated whether serial measurements of serum C‐reactive protein could help differentiate episodes of transplant dysfunction due to rejection, infection, acute tubular necrosis, or cyclosporine A nephrotoxicity in renal allograft recipients. We retrospectively analyzed our data on the daily measurements of serum C‐reactive protein (sCRP) in 117 renal allograft recipients (a total of 543 measurements were performed and 391 episodes of elevated sCRP were recorded) in the diagnosis of acute rejections and other complications in the immediate post‐transplant period. Nineteen patients were treated with cyclosporine A, azathioprine, and prednisolone and 98 patients with cyclosporine A, mycophenolate mophetil, and prednisolone. In patients with stable graft function the sCRP concentrations were in the normal range. Serum C‐reactive protein concentration was initially significantly increased in 23 episodes of rejection responsive to methylprednisolone (median of 54 mg/L) but fell very rapidly in response to treatment (median 15 mg/L). In episodes of rejection unresponsive to methylprednisolone, median initial sCRP levels were significantly higher, with a median of the 69 mg/L at the end of the treatment. Twenty‐nine patients with graft dysfunction caused by CsA nephrotoxicity showed no incraese in sCRP concentration. A similar pattern was seen in patients with acute tubular necrosis. Bacterial infections other than asymptomatic bacteriuria were accompained by the significant increase in sCRP (median of 77 mg/L). The most significant elevations were associated with bacterial infections. Serum C‐reactive protein seemed to be a more sensitive marker than fever or white blood cell count in diagnosis of all complications. Serial sCRP measurements provide economical and reproducible evidence of immune activation, help discriminate renal dysfunction due to CsA nephrotoxicity or rejection, and may be helpful in modification of immunosuppressive therapy.