ArticlePediatric nephrology (Berlin, Germany)2011
Urinary transforming growth factor beta-1 as a marker of renal dysfunction in sickle cell disease.
Article in Pediatric nephrology (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 2 syntheses or guidelines pooled it, 17 citations in OpenAlex.
- Clinical and Genetic Predictors of Sickle Cell Nephropathy: A Global Systematic Review.Omics : a journal of integrative biology · 2025Pooled it
- Cardiomyopathy With Restrictive Physiology in Sickle Cell Disease.JACC. Cardiovascular imaging · 2016Pooled it
- Biomarkers for early detection of sickle nephropathy.American journal of hematology · 2011Trial
- Proteomic analyses of urinary exosomes identify novel potential biomarkers for early diagnosis of sickle cell nephropathy, a sex-based study.Frontiers in physiology · 2024Article
- End points for sickle cell disease clinical trials: renal and cardiopulmonary, cure, and low-resource settings.Blood advances · 2019Article
- Albuminuria correlates with hemolysis and NAG and KIM-1 in patients with sickle cell anemia.Pediatric nephrology (Berlin, Germany) · 2014Article
- The prevalence of hypertension and abnormal kidney function in children with sickle cell disease -a cross sectional review.BMC nephrology · 2013Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
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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