# Risk prediction model for progression of type 2 diabetic nephropathy with and without metabolic syndrome: a retrospective cohort study

**Authors:** Yuan Fang, Siyi Rao, Yongjie Zhuo, Jiaqun Lin, Xiaohong Zhang, Jianxin Wan

PMC · DOI: 10.3389/fendo.2025.1592180 · 2025-07-30

## TL;DR

This study developed a risk prediction model to help doctors assess the progression of type 2 diabetic kidney disease in patients with and without metabolic syndrome.

## Contribution

A novel risk prediction model for T2DN progression incorporating metabolic syndrome components was developed and validated.

## Key findings

- Patients with metabolic syndrome had a significantly higher risk of T2DN progression.
- The number of metabolic syndrome components was an independent risk factor for T2DN progression.
- The prediction model showed good discrimination and calibration over a 5-year period.

## Abstract

To construct a risk prediction model for type 2 diabetic nephropathy (T2DN) progression in patients with and without metabolic syndrome (MetS).

In this retrospective study, we enrolled 130 T2DN patients diagnosed by renal biopsy. The clinicopathological characteristics of participants were analyzed. Survival analysis was performed using the Kaplan-Meier method. Cox regression analysis and least absolute shrinkage and selection operator (LASSO) regression were conducted to identify risk factors for T2DN progression, and a risk prediction model was constructed for T2DN progression. ROC curves, C-index and calibration curves were used to evaluate the discrimination and calibration of the model. Sensitivity analysis was conducted by redefining MetS using the 2004 Chinese Diabetes Society (CDS) criteria.

The Kaplan-Meier survival curve shows that the cumulative incidence rate of T2DN progression in patients with MetS is significantly higher than in those without MetS (Log-rank test: χ2 = 11.76, P<0.001). The number of MetS components was an independent risk factor for T2DN progression (HR=2.567, P=0.039; HR=3.392, P<0.001; HR=4.225, P=0.001 for 3,4,5 components respectively). A T2DN progression prediction model by nomogram was constructed, the AUC of ROC curves was 0.794 (95% CI: 0.685-0.908) at 1 year, 0.826 (95% CI: 0.739-0.913) at 2 years, 0.794 (95% CI: 0.694-0.893) at 3 years, and 0.833 (95% CI: 0.735-0.931) at 4 years. the C-index remained above 0.70 for the entire 5-year period. The calibration curves showed a good fit with the reference curves.

MetS is significantly relevant with T2DN progression. Our prediction model helps clinicians to make individualized medical decisions for T2DN patients.

## Linked entities

- **Diseases:** metabolic syndrome (MONDO:0000816)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, TLR4 (toll like receptor 4) [NCBI Gene 7099] {aka ARMD10, CD284, TLR-4, TOLL}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, FGF23 (fibroblast growth factor 23) [NCBI Gene 8074] {aka ADHR, FGFN, HFTC2, HPDR2, HYPF, PHPTC}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}, PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468] {aka CIMT1, FPLD3, GLM1, NR1C3, PPARG1, PPARG2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, ICAM1 (intercellular adhesion molecule 1) [NCBI Gene 3383] {aka BB2, CD54, P3.58}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}
- **Diseases:** sclerosis (MESH:D012598), proteinuria (MESH:D011507), T2DM (MESH:D003924), ESRD (MESH:D007676), Hypertension (MESH:D006973), inflammation (MESH:D007249), hyperphosphatemia (MESH:D054559), Hyperglycemia (MESH:D006943), hypocalcemia (MESH:D006996), Cerebrovascular disease (MESH:D002561), declining kidney function (MESH:D007680), diabetes complications (MESH:D048909), IgA nephropathy (MESH:D005922), glomerulosclerosis (MESH:D005921), secondary hyperparathyroidism (MESH:D006962), stroke (MESH:D020521), CDS (MESH:C000719191), renal vascular lesions (MESH:D014652), abdominal obesity (MESH:D056128), heart failure (MESH:D006333), hyperlipidemia (MESH:D006949), IFTA (MESH:D005355), obesity (MESH:D009765), CKD (MESH:D051436), insulin deficiency (MESH:D007333), cerebral infarction (MESH:D002544), cerebral hemorrhage (MESH:D002543), CVD (MESH:D002318), T1DM (MESH:D003922), myocardial infarction (MESH:D009203), renal insufficiency (MESH:D051437), edema (MESH:D004487), MetS (MESH:D024821), anemia (MESH:D000740), Kidney Disease (MESH:D007674), valvular heart disease (MESH:D006349), DN (MESH:D003928), DM (MESH:D003920), metabolic disease (MESH:D008659), malignant tumor (MESH:D009369), atrophy (MESH:D001284), overweight (MESH:D050177), dyslipidemia (MESH:D050171)
- **Chemicals:** vitamin D (MESH:D014807), sodium (MESH:D012964), phosphorus (MESH:D010758), glucose (MESH:D005947), uric acid (MESH:D014527), TG (MESH:D014280), calcium (MESH:D002118), TC (-), phosphate (MESH:D010710), urea (MESH:D014508), lipid (MESH:D008055), Cholesterol (MESH:D002784), blood glucose (MESH:D001786), creatinine (MESH:D003404)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12343258/full.md

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Source: https://tomesphere.com/paper/PMC12343258