Chronic kidney disease (CKD) represents a growing global health burden, affecting approximately 10–13% of the adult population worldwide. In India, the prevalence of CKD is steadily rising, largely due to increasing rates of diabetes mellitus, hypertension, aging

populations, and lifestyle-related risk factors. CKD is characterized by a progressive and irreversible decline in renal function, ultimately leading to end-stage renal disease (ESRD) and the need for renal replacement therapy.

Beyond its renal manifestations, CKD is increasingly recognized as a systemic disorder associated with metabolic, cardiovascular, and immunological disturbances. Cardiovascular disease remains the leading cause of mortality in CKD patients, accounting for more than half of deaths even before progression to ESRD. Traditional cardiovascular risk factors alone do not fully explain this excess risk, suggesting the involvement of non-traditional mechanisms such as chronic inflammation.

Persistent low-grade inflammation has emerged as a central pathophysiological feature of CKD. Elevated circulating levels of inflammatory cytokines are detectable even in early stages of disease and tend to increase as renal function deteriorates. Several mechanisms contribute to this inflammatory state, including reduced renal clearance of cytokines, increased production by activated immune cells, oxidative stress, uremic toxin accumulation, intestinal dysbiosis, and recurrent infections.

Inflammatory mediators such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) play pivotal roles in CKD progression. CRP is an acute-phase reactant synthesized in the liver under the influence of IL-6 and serves as a marker of systemic inflammation. Elevated CRP levels have been independently associated with faster CKD progression and increased cardiovascular events.

IL-6 is a multifunctional cytokine involved in immune regulation, endothelial dysfunction, and hepatic acute-phase response. Higher IL-6 levels are associated with protein-energy wasting, atherosclerosis, and increased mortality in CKD patients. TNF-α is a potent pro-inflammatory cytokine that promotes apoptosis, endothelial injury, and fibrotic pathways within the kidney, contributing to nephron loss.

Despite growing evidence linking inflammation to CKD progression, there remains a paucity of data from Indian tertiary care settings, where patients often present at advanced stages of disease. Understanding the relationship between inflammatory mediators and CKD severity in this population may provide valuable prognostic insights and help identify targets for therapeutic intervention.

The present study was therefore undertaken to evaluate inflammatory marker levels across different stages of CKD and to assess their correlation with renal function in patients attending a tertiary care teaching hospital.

Study Design and Setting

A hospital-based cross-sectional observational study was conducted in the outpatient and inpatient departments of a tertiary care teaching hospital.

Study Population

A total of 150 adult patients diagnosed with CKD were enrolled in the study after obtaining informed written consent.

Inclusion Criteria

• Age ≥18 years
• Diagnosed cases of CKD (Stages 1–5)
• Willingness to participate in the study

Exclusion Criteria

• Acute kidney injury
• Active infections or inflammatory diseases
• Malignancy
• Chronic liver disease
• Autoimmune disorders

Clinical and Laboratory Evaluation

Detailed clinical history and physical examination were performed for all participants. Blood samples were collected under aseptic conditions for laboratory analysis.

The following parameters were assessed:

• Serum creatinine
• Estimated glomerular filtration rate (eGFR)
• C-reactive protein (CRP)
• Interleukin-6 (IL-6)
• Tumor necrosis factor-alpha (TNF-α)

CKD staging was performed according to KDIGO guidelines based on eGFR values.

Statistical Analysis

Data were expressed as mean ± standard deviation or frequency and percentage as appropriate. Comparison of inflammatory markers across CKD stages was performed using one-way analysis of variance (ANOVA). Pearson correlation coefficient was used to assess the relationship between inflammatory markers and eGFR. A p-value <0.05 was considered statistically significant.

The study included 150 CKD patients with a mean age of 52.8 ± 13.6 years. Males constituted 61.3% of the study population. Diabetes mellitus and hypertension were present in 56.0% and 68.7% of patients, respectively.

Most patients belonged to moderate to advanced stages of CKD, with 30.7% in Stage 3, 25.3% in Stage 4, and 20.0% in Stage 5.

Renal function parameters showed a progressive increase in serum creatinine and a corresponding decline in eGFR with advancing CKD stage (p < 0.001).

Inflammatory marker levels increased significantly across CKD stages. Mean CRP levels rose from 3.1 ± 1.2 mg/L in Stage 1 to 18.4 ± 4.9 mg/L in Stage 5. Similarly, IL-6 levels increased from 6.4 ± 2.1 pg/mL in Stage 1 to 32.6 ± 8.1 pg/mL in Stage 5, while TNF-α levels increased from 7.8 ± 2.4 pg/mL to 36.2 ± 9.4 pg/mL. These differences were statistically significant (p < 0.001).

Correlation analysis demonstrated strong inverse relationships between eGFR and inflammatory markers. CRP, IL-6, and TNF-α showed correlation coefficients of −0.72, −0.78, and −0.75, respectively (p < 0.001).

Patients with advanced CKD (Stages 3–5) exhibited significantly higher inflammatory burden compared to those with early CKD (Stages 1–2).

Table 1. Sociodemographic and Clinical Characteristics of the Study Population (n = 150)

Table 2. Distribution of Patients According to Chronic Kidney Disease Stages

Table 3. Renal Function Parameters Across CKD Stages

Table 4. Inflammatory Marker Levels Across Chronic Kidney Disease Stages

Table 5. Correlation Between Inflammatory Markers and Renal Function (eGFR)

Table 6. Comparison of Inflammatory Markers in Early and Advanced CKD

The present study demonstrates a strong association between systemic inflammation and CKD severity. Inflammatory mediators increased progressively with advancing disease stage and showed significant inverse correlations with renal function.

These findings support the concept of CKD as a chronic inflammatory condition. Reduced renal clearance of cytokines, uremic toxin accumulation, oxidative stress, and immune activation contribute to persistent inflammation, which in turn accelerates nephron loss and fibrosis.

IL-6 showed the strongest correlation with eGFR decline, highlighting its role as a sensitive marker of disease severity. Elevated TNF-α levels reflect sustained immune activation and may contribute directly to renal cell apoptosis and interstitial fibrosis.

The high prevalence of diabetes and hypertension in the study population likely contributed to the inflammatory burden, as both conditions are known to promote endothelial dysfunction and cytokine production.

Our findings are consistent with previous international studies demonstrating elevated inflammatory markers in advanced CKD. However, the predominance of late-stage disease in this cohort underscores the need for earlier detection and intervention in Indian settings.

Measurement of inflammatory biomarkers may aid in risk stratification, prognostication, and identification of patients who may benefit from anti-inflammatory or renoprotective strategies.

Systemic inflammation increases progressively with advancing chronic kidney disease and is strongly associated with declining renal function. Elevated CRP, IL-6, and TNF-α levels reflect disease severity and may serve as useful biomarkers for identifying high-risk patients. Early recognition of inflammatory burden could facilitate timely therapeutic interventions aimed at slowing CKD progression and reducing associated cardiovascular risk.

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