The vicious circle of chronic kidney disease and hypertriglyceridemia: What is first, the hen or the egg?
Open accessAbstract
Chronic kidney disease (CKD) is documented to cause alterations in lipid metabolism, and this was considered a potent driver of increased cardiovascular risk. Among the diverse alteration of lipid traits in CKD, research endeavours have predominantly concentrated on low-density lipoproteins (LDL) in view of the potent pro-atherogenic role of these lipoprotein particles and the demonstration of protective cardiovascular effect of reducing LDL. However, few studies have focused on the metabolism of triglyceride-rich lipoproteins and even fewer on their role in causing kidney damage. Therefore, the comprehensive description of the impact of hypertriglyceridemia (HTG) in CKD pathophysiology remains largely undetermined. This reflects the difficulty of disentangling the independent role of triglycerides (TG) in the complex, bidirectional relationship between TG and kidney disease. Abnormal neutral lipid accumulation in the intrarenal vasculature and renal cells eventually due to HTG may also promote glomerular injury, throughout mechanisms including oxidative stress, mitochondrial dysfunction and proinflammatory responses. While epidemiological and experimental evidence suggests a potential role of TG in kidney damage, the causal mechanisms and their clinical relevance remain unclear, representing a significant area for future investigation. This review aims to highlight the intricate interplay between TG metabolism and kidney disease, shedding light on the mechanisms through which HTG may influence kidney functionality.
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In metabolic disorders such as insulin resistance, type 2 diabetes, chronic kidney disease, and nephrotic syndrome, an imbalance between production and clearance of TRLs favors their accumulation, promoting a lipid profile characterized by elevated TG, increased remnant particles, and changes in lipoprotein composition associated with atherogenic risk.
“However, in metabolic disorders such as insulin resistance, type 2 diabetes, chronic kidney disease, and nephrotic syndrome, an imbalance between production and clearance of TRLs favors their accumulation, promoting a lipid profile characterized by elevated TG, increased remnant particles, and changes in lipoprotein composition often associated with atherogenic risk [12, 13].”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [12]
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Experimental — accuracy not yet measuredFibrates may induce reversible increases in serum creatinine, especially in patients with pre-existing renal impairment, likely reflecting functional changes in renal hemodynamics rather than structural injury.
“Fibrates may also induce reversible increases in serum creatinine, especially in patients with pre-existing renal impairment, likely reflecting functional changes in renal hemodynamics rather than structural injury [12, 79].”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [12]
Section 3.3 reports that fibrates can raise serum creatinine, that the rise is generally not associated with permanent kidney damage, and that altered renal hemodynamics and filtration are the current hypothesized explanation. Table 2 describes the increase as reversible. Neither passage says the increase occurs especially in patients with pre-existing renal impairment. (LLM, conf=0.88)
Experimental — accuracy not yet measuredFibrate therapy is associated with reduced progression of albuminuria.
“Moreover, fibrate therapy has been associated with reduced progression of albuminuria, supporting its use in patients with hypertriglyceridemia and early-stage chronic kidney disease [12], although the impact on long-term renal outcomes remains uncertain.”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [12]
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- Authors
- Tramontano, D., D'Erasmo, L., Larouche, M., Brisson, D., Lauzière, A., Di Costanzo, A., Bini, S., Minicocci, I., Covino, S., Baratta, F., Pasquali, M., Cerbelli, B., Gaudet, D., & Arca, M.
- Affiliations
- Sapienza University of Rome (IT)
- Université de Montréal (CA)
- Policlinico Umberto I (IT)
- ORCID
- Venue
- Atherosclerosis
- Publisher
- Elsevier BV
- Published
- 2025-04
- Volume
- 403
- Pages
- 119146
- ISSN
- 0021-9150 (ISSN-L)
- OpenAlex
- W4407902462
- Cited by
- 23
- References
- 158
- Citations by year
- 2026: 14 · 2025: 9
- FWCI
- 3.35
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Atherosclerosis (publishedVersion, cc-by)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, other-oa)
- Funders
- Amgen
- Eli Lilly and Company
- Pfizer
- AstraZeneca
- Sanofi
- Regeneron Pharmaceuticals
- Ultragenyx Pharmaceutical
- Amarin Corporation
- Kowa Company
- Amryt Pharma
- Daiichi-Sankyo
- Novo Nordisk
- Swedish Orphan Biovitrum
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- chronic kidney disease, hypertriglyceridemia, triglyceride metabolism, triglyceride-rich lipoproteins, lipid metabolism, cardiovascular risk, LDL cholesterol, glomerular injury, oxidative stress, mitochondrial dysfunction, inflammation, kidney injury
- MeSH terms
- Animals, Humans, Kidney, Risk Factors, Triglycerides, Hypertriglyceridemia, Oxidative Stress, Lipid Metabolism, Renal Insufficiency, Chronic
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