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NDT Advance Access originally published online on November 2, 2006
Nephrology Dialysis Transplantation 2007 22(2):538-544; doi:10.1093/ndt/gfl605
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Subclinical hypothyroidism is linked to micro-inflammation and predicts death in continuous ambulatory peritoneal dialysis

Giuseppe Enia, Vincenzo Panuccio, Sebastiano Cutrupi, Patrizia Pizzini, Giovanni Tripepi, Francesca Mallamaci and Carmine Zoccali

CNR-IBIM, Institute of Biomedicine, Clinical Epidemiology and Physiopathology of Renal Diseases and Hypertension & Nephrology Unit of Reggio Calabria, Italy

Correspondence and offprint requests to: Giuseppe Enia, CNR-IBIM, Istituto di Biomedicina, Epidemiologia Clinica e Fisiopatologia, delle Malattie Renali e dell’Ipertensione Arteriosa, c/o Ki Point-Gransial Srl, Via Filippini, n. 85, 89125 Reggio Calabria, Italy. Email: eniag{at}libero.it



  Abstract

Background. Low T3 is a frequent alteration in patients with ESRD. This derangement has been recently linked to inflammation in haemodialysis patients. Whether this association holds true in peritoneal dialysis patients has not been studied.

Methods. We investigated the relationship between low-grade inflammation [IL-6, C-reactive protein (CRP) and serum albumin levels] and free tri-iodothyronine (fT3) in a cohort of 41 CAPD patients (mean age, 66 years; M, 26; F, 15) without heart failure and inter-current illnesses.

Results. CAPD patients had lower fT3 levels (2.7 ± 0.8 pg/ml) than healthy subjects (3.7 ± 1.0 pg/ml, P < 0.001) of similar age. Free T3 levels were directly related to those of serum albumin (r = 0.52, P = 0.001) and inversely to IL-6 (r = –0.30, P = 0.05) and CRP (r = –0.54, P < 0.001). Age (r = –0.61, P < 0.001), haemoglobin levels (r = 0.32, P = 0.05) and diastolic blood pressure (r = 0.50, P = 0.001) were also related to fT3. In multiple regression models adjusting for all variables related to fT3, CRP and albumin were retained as independent correlates of fT3.

During the follow-up (2.8 ± 1.7 years) 27 patients died. Plasma fT3 levels were lower in patients who died (2.5 ± 0.8 pg/ml) compared with survivors (3.3 ± 0.5 pg/ml P = 0.001). In Cox analyses, fT3 was a significant predictor of mortality independent of the main traditional as well as non-traditional risk factors.

Conclusions. The relationship between fT3, CRP and serum albumin suggests that inflammation–malnutrition might be involved in the low T3 syndrome in CAPD patients. Thyroid dysfunction might be implicated in the pathogenic pathway which links micro-inflammation to survival in PD patients.

Keywords: CAPD; inflammation; low T3 syndrome; thyroid


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