Correlation between serum prolactin and the systemic immune-inflammation index in diabetic kidney disease: a cross-sectional study.

OBJECTIVE

Prolactin (PRL) is increasingly recognized as a pleiotropic hormone with potent immunoregulatory properties; however, its involvement in systemic inflammation among diabetic kidney disease (DKD) patients has not been defined. This study aimed to investigate the potential association between serum PRL levels and micro-inflammation in patients with DKD.

METHODS

In this cross-sectional investigation, 994 patients with type 2 diabetes mellitus (T2DM)-associated DKD were enrolled. Multivariable linear mixed-effects models were used to quantify the relationship between serum PRL and the systemic immune-inflammation index (SII) and other clinical parameters. Restricted cubic spline (RCS) analyses were fitted to test for non-linearity and stratified and sensitivity analyses were performed to assess robustness.

RESULTS

The median serum PRL level was 344.40 mIU/L (interquartile range: 258.80-463.10). After multivariable adjustment, serum PRL were positively associated with white blood cell count, neutrophil count, serum ferritin, serum phosphorus and intact parathyroid hormone (iPTH) levels, and inversely associated with serum albumin. For every 100 mIU/L increase in serum PRL, the SII increased by an average of 7.10 units (95% CI: 3.13 to 11.07; p = 5.12 × 10-4). Stratified and sensitivity analyses confirmed the robustness of this association. RCS analysis revealed a significant nonlinear relationship between serum PRL and SII (p for nonlinearity = 0.002), with an inflection point at 282.85 mIU/L. PRL levels above this inflection point showed a significant positive association with SII, whereas levels below it showed a negative association.

CONCLUSION

In patients with DKD, serum PRL exhibits an independent, nonlinear association with SII, characterized by a threshold around 282.85 mIU/L. This finding suggests that PRL may be linked to the dysregulated immune-inflammation axis in DKD, warranting further mechanistic and longitudinal investigation.