# Correlation Between Thyroid Hormone Profiles and Kidney Disease: Improving Global Outcomes (KDIGO) Risk Categories in Diabetic Kidney Disease Patients

**Authors:** Kashif Abdullah, Anjum Shahzad, Seemab Javaid, Muhammad Albaz Khan Chandia, Muhammad Jamil, Adnan Ahmad Zafar, Alia Mirghani Ahmed Mirghani, Muhammad Irfan Jamil, Adeel Ahmed

PMC · DOI: 10.7759/cureus.81781 · 2025-04-06

## TL;DR

This study shows that thyroid hormone levels are linked to the severity of diabetic kidney disease, with worsening kidney function associated with lower thyroid hormones and higher TSH.

## Contribution

The study identifies specific thyroid hormone correlations with KDIGO risk categories and renal markers in diabetic kidney disease patients.

## Key findings

- Thyroid dysfunction prevalence increases with higher KDIGO risk levels in DKD patients.
- FT3 levels decrease significantly as DKD severity increases, correlating with improved eGFR and reduced ACR.
- TSH levels rise with higher KDIGO risk and are negatively associated with eGFR.

## Abstract

Background and aim

Thyroid dysfunction is commonly observed in individuals with diabetic kidney disease (DKD) and may influence disease progression. This study aimed to investigate the relationship between thyroid hormone profiles and Kidney Disease: Improving Global Outcomes (KDIGO) risk stratification in patients with DKD.

Methods

A cross-sectional analysis was conducted on 350 patients diagnosed with DKD, recruited from the nephrology outpatient department at Lahore General Hospital between December 2023 and June 2024. Participants were selected through consecutive sampling and categorized according to KDIGO risk levels. Thyroid hormones, including free triiodothyronine (FT3), free thyroxine (FT4), and thyroid-stimulating hormone (TSH), were assessed alongside renal and metabolic markers such as estimated glomerular filtration rate (eGFR), albumin-to-creatinine ratio (ACR), serum creatinine, glycated hemoglobin (HbA1c), and duration of diabetes.

Results

Among the 350 DKD patients, 195 (55.7%) were euthyroid, 71 (20.3%) had overt hypothyroidism, 64 (18.3%) had subclinical hypothyroidism, and 20 (5.7%) had hyperthyroidism. The prevalence of thyroid dysfunction increased with KDIGO risk, showing significant variation across groups (p = 0.005). FT3 levels declined significantly from 4.15 ± 0.52 pmol/L in the low-risk group to 3.66 ± 0.73 pmol/L in the very high-risk group (F = 13.08, p < 0.001). FT4 levels also showed a significant decrease (p = 0.003), while TSH levels increased progressively (p = 0.001). FT3 was positively correlated with eGFR (r = 0.277, p < 0.001) and negatively correlated with ACR (r = -0.185, p = 0.001) and serum creatinine (r = -0.277, p < 0.001). FT4 showed a weaker positive correlation with eGFR (r = 0.150) and inverse correlations with ACR and creatinine (p < 0.05). TSH was negatively associated with eGFR (r = -0.191, p < 0.001) and positively associated with creatinine (r = 0.191, p < 0.001).

Conclusions

This study highlights a strong association between thyroid dysfunction and the severity of DKD. As KDIGO risk increased, FT3 and FT4 levels declined while TSH levels rose. These thyroid hormone alterations were significantly correlated with key renal markers, suggesting their potential utility in monitoring renal function in DKD patients.

## Linked entities

- **Diseases:** diabetic kidney disease (MONDO:0005016), hypothyroidism (MONDO:0005420), hyperthyroidism (MONDO:0004425), kidney disease (MONDO:0001343)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** disease (MESH:D004194), Thyroid dysfunction (MESH:D013959), Kidney Disease (MESH:D007674), hypothyroidism (MESH:D007037), hyperthyroidism (MESH:D006980), DKD (MESH:D003928), diabetes (MESH:D003920)
- **Chemicals:** thyroxine (MESH:D013974), creatinine (MESH:D003404), FT3 (-), triiodothyronine (MESH:D014284)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12053021/full.md

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Source: https://tomesphere.com/paper/PMC12053021