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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Clin+Kidney+J
2013 ; 6
(5
): 478-83
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Exogenous thyrotropin improves renal function in euthyroid patients, while serum
creatinine levels are increased in hypothyroidism
#MMPMID26064512
Duranton F
; Lacoste A
; Faurous P
; Deshayes E
; Ribstein J
; Avignon A
; Mourad G
; Argilés À
Clin Kidney J
2013[Oct]; 6
(5
): 478-83
PMID26064512
show ga
BACKGROUND: There is evidence showing that the hypothyroid state results in
increased serum creatinine levels. However, whether this is only due to the
peripheral thyroid hormones or if thyroid-stimulating hormone (TSH) is also
involved is not known. METHODS: Serum creatinine levels and estimated glomerular
filtration rate (eGFR) were assessed in thyroidectomized patients with varying
thyroid hormones and TSH levels. Blood samples from Group 1 (21 patients) were
obtained 1 month after complete thyroidectomy, while under a hypothyroid state
(t1) and a sufficient time after thyroid hormones initiation (euthyroid state,
t2). Group 2 (20 euthyroid patients) were sampled after recombinant human
thyrotropin injections (rhTSH, t1) and later after rhTSH extinction (t2).
RESULTS: In Group 1, serum creatinine levels decreased after correction of
hypothyroidism (85.3 ± 4.3 versus 78.0 ± 3.9 µmol/L; P = 0.04). In Group 2, serum
creatinine levels increased after rhTSH withdrawal (70.6 ± 5.7 µmol/L versus 76.5
± 5.8 µmol/L; P = 0.007). Between t1 and t2, eGFR varied accordingly [Group 1,
71.7 ± 3.5 versus 81.2 ± 4.5 mL/min/1.73 m² (P = 0.02); Group 2, 97.7 ± 7.4
versus 87.5 ± 5.9 (P = 0.007)]. The changes in TSH and eGFR following
supplementation with thyroxine were significantly correlated (r = -0.6, P =
0.0041). CONCLUSIONS: Iatrogenic hypothyroidism significantly increases serum
creatinine and reversibly impairs eGFR, while treatment with rhTSH enhances renal
function in euthyroid patients, supporting the existence of an influence of TSH
level on renal function. The mechanisms by which peripheral thyroid hormones and
TSH influence GFR need to be identified in physiology-orientated studies.