Evidence mapPaperPMID 40569673Full record

ReviewJournal of the American Society of Nephrology : JASN2025

Management of Kidney Disease with Sickle Cell Disease.

Momen Abbasi, Anand Srivastava, Santosh L Saraf

Abstract readReview
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Momen AbbasiDivision of Nephrology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois.ORCID 0000-0002-0555-1798
Anand SrivastavaDivision of Nephrology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois.ORCID 0000-0002-8109-1420
Santosh L SarafDivision of Hematology and Oncology, Department of Medicine, University of Illinois Chicago, Chicago, Illinois.ORCID 0000-0002-8584-4194

Funding

Utility of Biomarkers of Rejection and Kidney Injury in Tailoring Liver Transplant ImmunosuppressionU01AI163081 · NORTHWESTERN UNIVERSITY · 2025 to 2025
$3.5M
Functional MRI to Identify High-risk CKD PhenotypesR01DK139321 · UNIVERSITY OF ILLINOIS AT CHICAGO · 2025 to 2025
$794k
Non-invasive Imaging Biomarkers to Identify a High-risk Chronic Kidney Disease PhenotypeK23DK120811 · NIDDK · NORTHWESTERN UNIVERSITY · PI Anand Srivastava · 2022 to 2022
$191k
Kidney Precision Medicine Project Opportunity Pool U2CDK114886NHLBI Division of Intramural Research HL153161NHLBI Division of Intramural Research HL177273NIDDK NIH HHS DK120811NIDDK NIH HHS DK139321NIDDK NIH HHS K23 DK120811NIDDK NIH HHS R01 DK139321NIH HHS U01AI163081
6 · The paper itself

Abstract

Sickle cell disease is the most common inherited blood cell disorder in the United States. Vaso-occlusion and hemolysis are hallmark features of sickle cell disease that may lead to kidney damage through endothelial dysfunction and oxidative and inflammatory stress. Manifestations of sickle cell disease-related kidney disease include hyperfiltration that occurs early in the disease course followed by albuminuria and a progressive decline in eGFR. Patients with sickle cell disease have a faster rate of eGFR decline and the development of CKD is associated with higher morbidity and early mortality. The assessment of kidney function is challenged by the transition from the hyperfiltration phase to reduced eGFR and by tubular creatinine secretion, which may lead to overestimation of the true GFR. Cystatin C-based and race-free estimating GFR equations reduce the overestimation but require further validation. Complications of kidney dysfunction include hyperkalemia and metabolic acidosis that occur at higher eGFR thresholds compared with the general population. Coinheritance of genetic variants, such as APOL1 G1 and G2 kidney risk variants, may help identify patients with sickle cell disease at higher risk for CKD and guide treatment and screening strategies. Therapeutic approaches targeting the sickle cell disease pathophysiology, such as hydroxyurea, chronic red blood cell transfusions, and hematopoietic stem cell transplantation, have demonstrated some kidney protective effects, but larger studies with longer follow-up are needed. Novel agents, including endothelin receptor antagonists, pyruvate kinase activators, and APOL1 inhibitors, are currently under investigation. Kidney-protective therapies such as renin-angiotensin-aldosterone system inhibitors and sodium-glucose cotransporter 2 inhibitors offer promise but require prospective validation in sickle cell disease cohorts. Kidney transplantation is associated with better survival and should not be withheld based solely on sickle cell disease diagnosis. Early identification, individualized management, and ongoing research are essential to improve kidney outcomes and reduce mortality in this high-risk population.

Indexed as

Anemia, Sickle CellRenal Insufficiency, ChronicGlomerular Filtration RateHumansHydroxyureaHydroxyureaanemiaglomerular diseaseshyperfiltrationkidney transplantation

Identifiers

PMID40569673
PMCPMC12499626

What Socratic holds

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Registered trials

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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 Socratic graph.