ArticleBlood advances2019
Hyperfiltration predicts long-term renal outcomes in humanized sickle cell mice.
Article in Blood advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07175051 (Targeting the Pathophysiology of Sickle Cell-Related Kidney Disease Using the SGLT2 Inhibitors, Empagliflozin), which is not on this map. Cited by 31 papers.
What it found
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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.
The trial behind it
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.
Targeting the Pathophysiology of Sickle Cell-Related Kidney Disease Using the SGLT2 Inhibitors, Empagliflozin
Who cites it
31 citing papers in PubMed, 37 citations in OpenAlex.
- Impact of renal iron overload on sickle cell nephropathy in a humanized mouse model.American journal of physiology. Renal physiology · 2026Article
- Augmenting hemopexin-mediated heme scavenging mitigates sepsis-induced acute kidney injury in humanized sickle cell mice.Blood vessels, thrombosis & hemostasis · 2026Article
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- Fibroblast histone deacetylase-1 promotes kidney interstitial fibrosis following ischemia-reperfusion injury.American journal of physiology. Renal physiology · 2026Article
- Endothelium-derived endothelin-1 mediates sickle cell nephropathy.Function (Oxford, England) · 2026Article
- Diurnal function and expression of aquaporins in the mouse kidney.American journal of physiology. Renal physiology · 2025Article
- Wheat-Based Protein Slows Disease Progression in Pkd1 Knockout Mice.Function (Oxford, England) · 2025Article
- Addressing the pathophysiology of venous thrombosis and chronic kidney disease in sickle cell trait using a mouse model.Blood advances · 2025Article
- Endothelin-1 signaling in the kidney: recent advances and remaining gaps.American journal of physiology. Renal physiology · 2025Review
- 17(R)-Resolvin D1 protects against sickle cell-related inflammatory cardiomyopathy in humanized mice.Blood · 2025Article
- Hydroxyurea Mitigates Heme-Induced Inflammation and Kidney Injury in Humanized Sickle Cell Mice.International journal of molecular sciences · 2025Article
- Base editing HbS to HbG-Makassar improves hemoglobin function supporting its use in sickle cell disease.Nature communications · 2025Article
- Prevalence and associated factors of glomerular hyperfiltration among adult stable sickle cells in Kinshasa, DR Congo.Renal failure · 2024Article
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- Pulmonary and renal long COVID at two-year revisit.iScience · 2024Article
- Mouse models of sickle cell disease: Imperfect and yet very informative.Blood cells, molecules & diseases · 2024Review
- Proteomic analyses of urinary exosomes identify novel potential biomarkers for early diagnosis of sickle cell nephropathy, a sex-based study.Frontiers in physiology · 2024Article
- Natural history and variability in albuminuria in pediatric and murine sickle cell anemia.Blood advances · 2023Article
- Glomerular hyperfiltration: part 2-clinical significance in children.Pediatric nephrology (Berlin, Germany) · 2023Review
- Sex differences in progression of kidney disease in sickle cell disease.Haematologica · 2023Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
We previously reported that humanized sickle cell (HbSS) mice develop spontaneous nephropathy, a major cause of morbidity and mortality in sickle cell disease (SCD). Because sex-dependent protective mechanisms in SCD have been reported, we examined the course of nephropathy in male and female HbSS mice to determine contributors and/or predictors of disease severity. In male HbSS mice, glomerular filtration rate was characterized by a rapid onset of hyperfiltration and subsequent progressive decline of renal function over 20 weeks. Early tubular injury presented with increased excretion of kidney injury marker 1 (KIM-1), progressive loss of tubular brush border, and interstitial fibrosis that preceded the onset of glomerular damage, suggesting a tubuloglomerular mechanism of kidney injury in these mice. Additionally, we observed a strong association between the magnitude of hyperfiltration and the degree of long-term kidney injury in male HbSS mice. Unlike males, female HbSS mice did not demonstrate a significant loss of renal function or severe kidney damage during the time course of the study. These results suggest that magnitude of hyperfiltration predicts the onset of chronic kidney damage in male HbSS mice, whereas protective mechanisms in female HbSS mice delay the onset of SCD nephropathy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.