# Lipoprotein Combine Index Is Associated with Multi-Compartment Oxidative Stress in Clinically Stable Peritoneal Dialysis Patients: A Cross-Sectional Study

**Authors:** Natalia Stepanova, Lesya Korol

PMC · DOI: 10.3390/biomedicines14020456 · Biomedicines · 2026-02-18

## TL;DR

This study finds that higher lipid levels in peritoneal dialysis patients are linked to lower solute transport and increased oxidative stress.

## Contribution

The study introduces the Lipoprotein Combine Index as a novel indicator of oxidative stress in peritoneal dialysis patients.

## Key findings

- Higher LCI is independently associated with lower peritoneal solute transport.
- LCI correlates with increased oxidative stress markers in serum, urine, and dialysate.
- LCI is linked to impaired antioxidant defenses in erythrocytes and dialysate.

## Abstract

Background/Objectives: Background: Dyslipidaemia and oxidative stress (OS) are frequent in peritoneal dialysis (PD). The Lipoprotein Combine Index (LCI) integrates lipid parameters, but its relationship with peritoneal transport and OS is unclear. Methods: This cross-sectional study included 100 clinically stable adults on continuous ambulatory PD with preserved ultrafiltration and adequate dialysis. LCI was calculated as (total cholesterol × triglycerides × LDL-C)/HDL-C and analyzed by tertiles. Lipid peroxidation and antioxidant markers were measured in serum, erythrocytes, urine, and spent dialysate. Multivariable regression models examined associations between LCI, peritoneal solute transport, and dialysate OS markers. Results: Higher LCI was independently associated with lower peritoneal solute transport. LCI correlated inversely with the 4 h dialysate-to-plasma creatinine ratio (ρ = −0.32, p = 0.001) and remained significant after adjustment (adjusted R2 = 0.224, p < 0.001). Increasing LCI was associated with higher malondialdehyde levels in serum, urine, and dialysate (all p ≤ 0.008) and impaired antioxidant defenses, including lower total peroxidase activity in erythrocytes and dialysate (both p = 0.001), reduced serum sulfhydryl groups (p = 0.011), decreased oxidative resistance of erythrocytes, and increased peroxide-induced hemolysis (both p = 0.001). In adjusted models, logLCI was independently associated with higher dialysate malondialdehyde (p < 0.001) and lower dialysate peroxidase activity (p = 0.005). Conclusions: In clinically stable PD patients, higher lipid burden assessed by LCI is independently associated with lower peritoneal solute transport and a marked increase in systemic and local OS. Our findings suggest that dyslipidaemia may contribute to early metabolic and oxidative changes even before overt peritoneal membrane dysfunction develops.

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, AP2B1 (adaptor related protein complex 2 subunit beta 1) [NCBI Gene 163] {aka ADTB2, AP105B, AP2-BETA, CLAPB1}, AIP (AHR interacting HSP90 co-chaperone) [NCBI Gene 9049] {aka ARA9, FKBP16, FKBP37, PITA1, SMTPHN, XAP-2}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, CP (ceruloplasmin) [NCBI Gene 1356] {aka AB073614, CP-2}, ACE (angiotensin I converting enzyme) [NCBI Gene 1636] {aka ACE1, CD143, DCP, DCP1}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}
- **Diseases:** myocardial infarction (MESH:D009203), uremic (MESH:D006463), infection (MESH:D007239), PD (MESH:D010538), malnutrition (MESH:D044342), atherogenic (MESH:D050197), OS (MESH:D000079225), atherogenic lipid (MESH:D011017), hepatitis (MESH:D056486), membrane dysfunction (MESH:D015433), heart failure (MESH:D006333), anuria (MESH:D001002), Diabetes (MESH:D003920), malignancy (MESH:D009369), LCI (MESH:C563618), dyslipidemia (MESH:D050171), peritoneal disease (MESH:D010532), injury to (MESH:D014947), liver disease (MESH:D008107), uremia (MESH:D014511), inflammation (MESH:D007249), hyperglycemia (MESH:D006943), hemolysis (MESH:D006461), autoimmune (MESH:D001327)
- **Chemicals:** Trichloroacetic acid (MESH:D014238), 1,2-phenylenediamine dihydrochloride (MESH:C034193), starch (MESH:D013213), malondialdehyde (MESH:D008315), Tris(hydroxymethyl)aminomethane (MESH:D014325), Peroxide (MESH:D010545), sulfhydryl (MESH:D013438), urea (MESH:D014508), Cr (MESH:D002857), potassium iodide (MESH:D011193), D (MESH:D003903), 1,4-phenylenediamine dihydrochloride (-), hydrogen peroxide (MESH:D006861), glucose (MESH:D005947), icodextrin (MESH:D000077607), creatinine (MESH:D003404), Indigo Carmine (MESH:D007203), calcium (MESH:D002118), sulfuric acid (MESH:C033158), reactive oxygen species (MESH:D017382), potassium chloride (MESH:D011189), acetate (MESH:D000085), sodium acetate (MESH:D019346), Lipid (MESH:D008055), iodine (MESH:D007455), TG (MESH:D014280), aldosterone (MESH:D000450), ferric ammonium citrate (MESH:C013531), MDA (MESH:D015104), phosphate (MESH:D010710), P (MESH:D010758), 8-hydroxy-2'-deoxyguanosine (MESH:D000080242), cholesterol (MESH:D002784), acetic (MESH:D019342), sodium fluoride (MESH:D012969), thiobarbituric acid (MESH:C029684), water (MESH:D014867)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12938693/full.md

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Source: https://tomesphere.com/paper/PMC12938693