# Clinical rationale behind glucose-sparing strategies in peritoneal dialysis: a narrative review

**Authors:** Bengt Lindholm, Antoine Barbari, Jennifer Allen, Inès Dufour, Donald Fraser, Annette Heider, Rumeyza Kazancioglu, Monika Lichodziejewska-Niemierko, Anabela Malho-Guedes, Loris Neri, Alena Parikova, Juan Carlos Quevedo-Reina, Adonay Santana-Quintana, Udaya Udayaraj

PMC · DOI: 10.1186/s12882-025-04732-w · BMC Nephrology · 2026-01-13

## TL;DR

This review discusses why reducing glucose use in peritoneal dialysis is important to avoid health risks and how alternative solutions might help.

## Contribution

The paper provides a clinical rationale for using glucose-sparing strategies in peritoneal dialysis to mitigate metabolic and peritoneal damage.

## Key findings

- Glucose-based dialysis solutions can damage the peritoneal membrane and cause metabolic issues.
- Alternative osmotic agents like icodextrin and amino acids may reduce these harmful effects.
- Glucose-sparing strategies could improve clinical outcomes for dialysis patients.

## Abstract

The effectiveness of peritoneal dialysis (PD) relies on dialysate-induced solute and water transport across the peritoneal membrane, facilitated by concentration and type of osmotic agents. Standard PD solutions predominantly use glucose as an osmotic agent due to its well-known metabolism, effective ultrafiltration during shorter dwells, and low cost. However, glucose exposure may damage the structure and function of the peritoneal membrane and cause systemic metabolic complications, including insulin resistance and cardiovascular disease, underscoring the need for glucose-sparing strategies with alternative solutions, such as solutions with icodextrin and amino acids as osmotic agents, and glucose-based, less bioincompatible fluids with physiological pH and reduced glucose degradation products. This brief narrative review examines the unwanted effects of glucose-based solutions and the clinical rationales behind glucose-sparing strategies that may reduce these effects and potentially improve clinical outcomes.

## Linked entities

- **Chemicals:** glucose (PubChem CID 5793)

## Full-text entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, SERPINE1 (serpin family E member 1) [NCBI Gene 5054] {aka PAI, PAI-1, PAI1, PLANH1}, GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, PTGES (prostaglandin E synthase) [NCBI Gene 9536] {aka MGST-IV, MGST1-L1, MGST1L1, MPGES, PGES, PIG12}, TF (transferrin) [NCBI Gene 7018] {aka HEL-S-71p, PRO1557, PRO2086, TFQTL1}, RHOA (ras homolog family member A) [NCBI Gene 387] {aka ARH12, ARHA, EDFAOB, RHO12, RHOH12}, PDP1 (pyruvate dehydrogenase phosphatase catalytic subunit 1) [NCBI Gene 54704] {aka PDH, PDP, PDPC, PDPC 1, PPM2A, PPM2C}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, AGER (advanced glycosylation end-product specific receptor) [NCBI Gene 177] {aka RAGE, SCARJ1, sRAGE}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, HIF1A (hypoxia inducible factor 1 subunit alpha) [NCBI Gene 3091] {aka HIF-1-alpha, HIF-1A, HIF-1alpha, HIF1, HIF1-ALPHA, MOP1}, CDH1 (cadherin 1) [NCBI Gene 999] {aka Arc-1, BCDS1, CD324, CDHE, ECAD, LCAM}, OCLN (occludin) [NCBI Gene 100506658] {aka BLCPMG, PPP1R115, PTORCH1}, SLC2A1 (solute carrier family 2 member 1) [NCBI Gene 6513] {aka CSE, DYT17, DYT18, DYT9, EIG12, GLUT}, SLC2A3 (solute carrier family 2 member 3) [NCBI Gene 6515] {aka GLUT3}, ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58] {aka ACTA, ASMA, CFTD, CFTD1, CFTDM, CMYO2A}, CPT1A (carnitine palmitoyltransferase 1A) [NCBI Gene 1374] {aka CPT I, CPT1, CPT1-L, CPTI-L, L-CPT1}, RENBP (renin binding protein) [NCBI Gene 5973] {aka RBP, RNBP}, SNAI1 (snail family transcriptional repressor 1) [NCBI Gene 6615] {aka SLUGH2, SNA, SNAH, SNAIL, SNAIL1, dJ710H13.1}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, CCN2 (cellular communication network factor 2) [NCBI Gene 1490] {aka CTGF, HCS24, IBP-8, IGFBP8, KMD, NOV2}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, ARG1 (arginase 1) [NCBI Gene 383], GCG (glucagon) [NCBI Gene 2641] {aka GLP-1, GLP1, GLP2, GRPP}, MLYCD (malonyl-CoA decarboxylase) [NCBI Gene 23417] {aka MCD}, APOB (apolipoprotein B) [NCBI Gene 338] {aka FCHL2, FLDB, LDLCQ4, apoB-100, apoB-48}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, IL1A (interleukin 1 alpha) [NCBI Gene 3552] {aka IL-1 alpha, IL-1A, IL1, IL1-ALPHA, IL1F1}, PPP1R12A (protein phosphatase 1 regulatory subunit 12A) [NCBI Gene 4659] {aka GUBS, M130, MBS, MYPT1}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, CD24 (CD24 molecule) [NCBI Gene 100133941] {aka CD24A}, PDK1 (pyruvate dehydrogenase kinase 1) [NCBI Gene 5163], SMAD3 (SMAD family member 3) [NCBI Gene 4088] {aka HSPC193, HsT17436, JV15-2, LDS1C, LDS3, MADH3}, CYBA (cytochrome b-245 alpha chain) [NCBI Gene 1535] {aka CGD4, p22-PHOX}, HK2 (hexokinase 2) [NCBI Gene 3099] {aka HKII, HXK2}
- **Diseases:** cytotoxicity (MESH:D064420), type 2 diabetes (MESH:D003924), fatigue (MESH:D005221), PD (MESH:D010538), metabolic acidosis (MESH:D000138), fibrosis (MESH:D005355), mesothelial injury (MESH:D018301), Hyperglycemia (MESH:D006943), kidney failure (MESH:D051437), obesity (MESH:D009765), skin rashes (MESH:D005076), hyperinsulinemia (MESH:D006946), mitochondrial dysfunction (MESH:D028361), hyperlipidemia (MESH:D006949), uremia (MESH:D014511), hyperglycemic (MESH:D006944), dyslipidemia (MESH:D050171), peritoneal fibrosis (MESH:D056627), Chronic inflammation (MESH:D007249), OS (MESH:D000079225), vasculopathy (MESH:D000090122), ESKD (MESH:D007676), loss of residual kidney function (MESH:D018365), hypertrophy (MESH:D006984), APD (MESH:C585640), chronic kidney disease (MESH:D051436), endothelial (MESH:D005642), endothelial dysfunction (MESH:D014652), left ventricular mass reduction (MESH:D018487), heart failure (MESH:D006333), CVD (MESH:D002318), malnourished (MESH:D044342), hypoxia (MESH:D000860), glucose intolerance (MESH:D018149), PM damage (MESH:D010532), insulin resistance (MESH:D007333), diabetes (MESH:D003920), atherogenesis (MESH:D050197)
- **Chemicals:** L-carnitine (MESH:D002331), Malonyl-CoA (MESH:D008316), 2-deoxyglucose (MESH:D003847), lactate (MESH:D019344), Bicarbonate (MESH:D001639), iron (MESH:D007501), canagliflozin (MESH:D000068896), sodium (MESH:D012964), Nutrineal (MESH:C482915), nitric oxide (MESH:D009569), AA-PD (-), AGEs (MESH:D017127), salt (MESH:D012492), sugar alcohol (MESH:D013402), lithium chloride (MESH:D018021), Amino-acid (MESH:D000596), Ala-Gln (MESH:C054122), Anhydrous glucose (MESH:D005947), Pyruvate (MESH:D019289), empagliflozin (MESH:C570240), nitrogen (MESH:D009584), dipeptide (MESH:D004151), DCA (MESH:D003999), phloretin (MESH:D010693), Lipid (MESH:D008055), fatty acid (MESH:D005227), erythritol (MESH:D004896), calcium (MESH:D002118), hydrogen peroxide (MESH:D006861), water (MESH:D014867), NADPH (MESH:D009249), hydroxyl radicals (MESH:D017665), MDA (MESH:D008315), TG (MESH:D014280), hydrogen (MESH:D006859), blood glucose (MESH:D001786), cholesterol (MESH:D002784), dapagliflozin (MESH:C529054), tricarboxylic acid (MESH:D014233), NAD+ (MESH:D009243), ROS (MESH:D017382), corn starch (MESH:D013213), Icodextrin (MESH:D000077607), N-acetylcysteine (MESH:D000111), carbohydrate (MESH:D002241), Xylitol (MESH:D014993), GDPs (MESH:D006153), carbon (MESH:D002244)
- **Species:** Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## References

9 references — full list in the complete paper: https://tomesphere.com/paper/PMC12849473/full.md

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Source: https://tomesphere.com/paper/PMC12849473