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Modulation and Source of Procalcitonin in Reduced Renal Function and Renal Replacement Therapy
Author(s) -
HergetRosenthal S.,
Klein T.,
Marggraf G.,
Hirsch T.,
Jakob H.G.,
Philipp T.,
Kribben A.
Publication year - 2005
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.0300-9475.2005.01545.x
Subject(s) - procalcitonin , kidney disease , medicine , oliguria , peritoneal dialysis , gastroenterology , renal replacement therapy , peripheral blood mononuclear cell , dialysis , renal function , hemodialysis , nephrology , urology , sepsis , biology , biochemistry , in vitro
Serum procalcitonin (PCT), an accurate marker of severe infection, is moderately increased in chronic kidney disease (CKD), peritoneal dialysis (PD) and haemodialysis (HD). We studied the extent of PCT elevation and factors accounting for elevated PCT in CKD and dialysis, and whether peripheral blood mononuclear cells (PBMC) contribute to increased PCT. In 37 controls, 281 CKD, 31 PD, and 65 HD patients without infection, PCT was measured and correlated with CKD stage, PD, HD, C‐reactive protein (CRP), cardiovascular disease (CVD) and other clinical parameters. PCT release by PBMC from controls, advanced CKD, PD and HD patients (12 subjects each) was measured. PCT increased in parallel to the deterioration of CKD. Oliguria, advanced CKD, PD, HD, CVD and elevated CRP were independently associated with PCT elevation. PCT release from PBMC significantly increased in advanced CKD, PD and HD. PCT release from PBMC correlated closely with the corresponding serum PCT values ( r = 0.76, P < 0.001). In the absence of infection, PCT may increase due to reduced renal elimination and increased synthesis, as due to PBMC. Furthermore, serum PCT could serve as a marker of low‐grade inflammation and CVD, which substantially increase mortality in CKD and dialysis.