ArticleMolecular neurobiology2016
Factors Responsible for Plasma β-Amyloid Accumulation in Chronic Kidney Disease.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis 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
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Medical Histories of Control Subjects Influence the Biomarker Potential of Plasma Aβ in Alzheimer's Disease: a Meta-analysis.Journal of molecular neuroscience : MN · 2020Pooled it
- Blood amyloid levels and risk of dementia in the Ginkgo Evaluation of Memory Study (GEMS): A longitudinal analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2019Trial
- New insight into Alzheimer's disease: small molecule-Aβ in the brain transport and peripheral organ clearance.Frontiers in aging · 2026Review
- Kidney function is associated with plasma ATN biomarkers among Hispanics/Latinos: SOL-INCA and HCHS/SOL results.Alzheimer's research & therapy · 2025Article
- Circulating amyloid beta 1-40 peptide as an associate of renal function decline.European journal of clinical investigation · 2025Article
- Cognitive impairment in chronic kidney disease: role of brain imaging, functional imaging, electroencephalography, cerebrospinal fluid biomarkers and sensors.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- The Peripheral Amyloid-β Nexus: Connecting Alzheimer's Disease with Atherosclerosis through Shared Pathophysiological Mechanisms.Neuromolecular medicine · 2025Review
- Temporal Dynamics and Biological Variability of Alzheimer Biomarkers.JAMA neurology · 2025Article
- Peripheral immune and metabolic regulation of Aβ and Tau by exercise in Alzheimer's disease.Frontiers in immunology · 2025Review
- PrecivityAD2™ Blood Test: Analytical Validation of an LC-MS/MS Assay for Quantifying Plasma Phospho-tau217 and Non-Phospho-tau217 Peptide Concentrations That Are Used with Plasma Amyloid-β42/40 in a Multianalyte Assay with Algorithmic Analysis for Detecting Brain Amyloid Pathology.Diagnostics (Basel, Switzerland) · 2024Article
- Influence of Physiological Variables and Comorbidities on Plasma Aβ40, Aβ42, and p-tau181 Levels in Cognitively Unimpaired Individuals.International journal of molecular sciences · 2024Article
- Association of Kidney Function With Dementia and Structural Brain Differences: A Large Population-Based Cohort Study.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- Associations of Blood and Cerebrospinal Fluid Aβ and tau Levels with Renal Function.Molecular neurobiology · 2023Article
- Advances in Amyloid-β Clearance in the Brain and Periphery: Implications for Neurodegenerative Diseases.Experimental neurobiology · 2023Review
- Medical comorbidities and ethnicity impact plasma Alzheimer's disease biomarkers: Important considerations for clinical trials and practice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- The Association of Kidney Function with Plasma Amyloid-β Levels and Brain Amyloid Deposition.Journal of Alzheimer's disease : JAD · 2023Article
- Based on molecular structures: Amyloid-β generation, clearance, toxicity and therapeutic strategies.Frontiers in molecular neuroscience · 2022Review
- Physiological clearance of amyloid-beta by the kidney and its therapeutic potential for Alzheimer's disease.Molecular psychiatry · 2021Article
- Diabetes, Albuminuria and the Kidney-Brain Axis.Journal of clinical medicine · 2021Review
- The Role of Plasma Neurofilament Light Protein for Assessing Cognitive Impairment in Patients With End-Stage Renal Disease.Frontiers in aging neuroscience · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disturbed brain-to-blood elimination of β-amyloid (Aβ) promotes cerebral Aβ accumulation in Alzheimer's disease. Considering that the kidneys are involved in Aβ elimination from the blood, we evaluated how chronic kidney disease (CKD) affects plasma Aβ. In 106 CKD patients stages 3-5 (including 19 patients on hemodialysis and 15 kidney recipients), 53 control subjects with comparable vascular risk profile and 10 kidney donors, plasma Aβ was determined using electrochemiluminescence immunoassay and gel electrophoresis followed by Western blotting. Plasma Aβ increased with CKD stage (control = 182.98 ± 76.73 pg/ml; CKD3A = 248.34 ± 103.77 pg/ml; CKD3B = 259.25 ± 97.74 pg/ml; CKD4 = 489.16 ± 154.16 pg/ml; CKD5 = 721.19 ± 291.69 pg/ml) and was not influenced by hemodialysis (CKD5D = 697.97 ± 265.91 pg/ml). Renal transplantation reduced plasma Aβ (332.57 ± 162.82 pg/ml), whereas kidney donation increased it (251.51 ± 34.34 pg/ml). Gel electrophoresis confirmed stage-dependent elevation namely of Aβ1-40, the most abundant Aβ peptide. In a multivariable regression including age, sex, estimated glomerular filtration rate (eGFR), potassium, hemoglobin, urine urea, and urine total protein, the factors eGFR (β = -0.42, p < 0.001), hemoglobin (β = -0.17, p = 0.020), and urine protein (β = 0.26, p = 0.008) were associated with plasma Aβ. In a regression including age, sex, eGFR, potassium, hemoglobin and the vascular risk factors systolic blood pressure, smoking, LDL, HDL, HbA1c, body mass index, brain-derived natriuretic peptide and fibrinogen, the factors eGFR (β = -0.53, p < 0.001), body mass index (β = -0.17, p = 0.022), and fibrinogen (β = 0.18, p = 0.024) were associated with plasma Aβ. Our results demonstrate a stage-dependent plasma Aβ increase that is augmented by loss of glomerulotubular integrity, low body weight, and inflammation, demonstrating a multifaceted role of renal dysfunction in Aβ retention.
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Registered trials
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.