Urinary transforming growth factor beta-1 as a marker of renal dysfunction in sickle cell disease |
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Authors: | Davoud Mohtat Rosemary Thomas Zangfang Du Yaa Boakye Thomas Moulton Catherine Driscoll Robert Woroniecki |
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Institution: | (1) Department of Pediatric Nephrology, Albert Einstein College of Medicine, Children’s Hospital at Montefiore, 111 East 210th Street, Bronx, NY 10467, USA;(2) Department of Pediatric Hematology/Oncology, Bronx Lebanon Hospital, Bronx, NY, USA;(3) Department of Pediatric Hematology/Oncology, Albert Einstein College of Medicine, Children’s Hospital at Montefiore, Bronx, NY, USA; |
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Abstract: | Renal dysfunction affects 5–18% of patients with sickle cell disease (SCD). To date, no studies have described urinary levels
of transforming growth factor β-1 (TGF-β1), a marker of fibrosis, and neutrophil gelatinase-associated lipocalin (NGAL), a
marker of acute/chronic kidney disease, as biomarkers in identifying patients at risk of developing renal disease in SCD.
We hypothesized that SCD subjects will have increased urinary excretion of TGF-β1 and NGAL compared with healthy controls
(CTR). We examined 51 SCD subjects: 42 HbSS, 8 HbSC, and 1 HbSD. Sixteen out of 42 patients with HbSS were on hydroxyurea
(HU). Urinary excretion of TGF-β1 was 26.4 ± 1.5 pg/mgCr in SCD subjects vs 15.0 ± 2.4 pg/mgCr in CTR (p < 0.00001). SCD patients with hemoglobin < 9 g/dl had higher urinary TGF-β1 than patients with milder anemia (p = 0.002). Urinary TGF-β1 trended lower in HbSS patients treated with HU (23.61 ± 2.6 pg/mgCr), vs patients not on HU (27.69 ± 1.8 pg/mgCr;
p = 0.055). There was no correlation between urinary TGF-β1 and microalbuminuria or estimated glomerular function. There was
no difference in urinary NGAL in SCD patients vs CTR. We suggest that urinary TGF-β1 may serve as a marker of early renal
injury in SCD. |
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