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Corticosteroids significantly increase cystatin C levels in the plasma by promoting cystatin C production in rats.

ABSTRACT: Background: Several studies have shown that non-renal factors such as corticosteroids may increase plasma cystatin C levels without affecting kidney function. However, the mechanisms underlying this are unclear. We hypothesized that corticosteroids may increase cystatin C levels in the plasma by promoting its production in tissues. In the present study, we aimed to test our hypothesis in rats by investigating the effect of corticosteroids on cystatin C production in tissues and the glomerular filtration rate (GFR), as measured by the gold standard method (i.e., inulin clearance). Results: Dexamethasone treatment was associated with much higher concentrations of cystatin C in all organ tissue homogenates tested. Dexamethasone increased plasma cystatin C levels in rats, without any decrease in renal inulin clearance. The impact of dexamethasone on plasma and organ tissue cystatin C levels was abolished by RU486, indicating the effect was glucocorticoid receptor-mediated. Conclusions: Our study provides direct evidence that corticosteroids may increase cystatin C levels in the plasma by promoting its production, without any decrease in GFR.

SUBMITTER: Zhu XR

PROVIDER: S-EPMC6711078 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature

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Corticosteroids significantly increase cystatin C levels in the plasma by promoting cystatin C production in rats.

Zhu Xiao-Ran XR Ge Ning N Wang Yu Y Zhai Jian-Long JL Liu Chao C

Renal failure 20191101 1

<b>Background:</b> Several studies have shown that non-renal factors such as corticosteroids may increase plasma cystatin C levels without affecting kidney function. However, the mechanisms underlying this are unclear. We hypothesized that corticosteroids may increase cystatin C levels in the plasma by promoting its production in tissues. In the present study, we aimed to test our hypothesis in rats by investigating the effect of corticosteroids on cystatin C production in tissues and the glomer ...[more]

PMID: 31352865

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Project description:Objective:Beta 1-adrenergic receptor autoantibodies (?1ARAbs) have been identified as a pathogenic factor in atrial fibrillation (AF), but the underlying pathogenetic mechanism is not well understood. We assessed the hypothesis that elevated ?1ARAb levels increase AF susceptibility by promoting atrial fibrosis. Methods:A total of 70 patients with paroxysmal AF were continuously recruited. The serum levels of ?1ARAb and circulating fibrosis biomarkers were analyzed by ELISA. Linear regression was used to examine the correlations of ?1ARAb levels with left atrial diameter (LAD) and circulating fibrosis biomarker levels. Furthermore, we established a rabbit ?1ARAb overexpression model. We conducted electrophysiological studies and multielectrode array recordings to evaluate the atrial effective refractory period (AERP), AF inducibility and electrical conduction. AF was defined as irregular, rapid atrial beats > 500 bpm for > 1000 ms. Echocardiography, hematoxylin and eosin staining, Masson's trichrome staining, and picrosirius red staining were performed to evaluate changes in atrial structure and detect fibrosis. Western blotting and PCR were used to detect alterations in the protein and mRNA expression of TGF-?1, collagen I and collagen III. Results:Patients with a LAD ? 40 mm had higher ?1ARAb levels than patients with a smaller LAD (8.87 ± 3.16 vs. 6.75 ± 1.34 ng/mL, P = 0.005). ?1ARAb levels were positively correlated with LAD and circulating biomarker levels (all P < 0.05). Compared with the control group, the rabbits in the immune group showed the following: (1) enhanced heart rate, shortened AERP (70.00 ± 5.49 vs. 96.46 ± 3.27 ms, P < 0.001), increased AF inducibility (55% vs. 0%, P < 0.001), decreased conduction velocity and increased conduction heterogeneity; (2) enlarged LAD and elevated systolic dysfunction; (3) significant fibrosis in the left atrium identified by Masson's trichrome staining (15.17 ± 3.46 vs. 4.92 ± 1.72%, P < 0.001) and picrosirius red staining (16.76 ± 6.40 vs. 4.85 ± 0.40%, P < 0.001); and (4) increased expression levels of TGF-?1, collagen I and collagen III. Conclusion:Our clinical and experiential studies showed that ?1ARAbs participate in the development of AF and that the potential mechanism is related to the promotion of atrial fibrosis.

Dataset Information

Corticosteroids significantly increase cystatin C levels in the plasma by promoting cystatin C production in rats.

Publications

Corticosteroids significantly increase cystatin C levels in the plasma by promoting cystatin C production in rats.

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