The role of circulating cytokines and thyroid hormones in the development of the nephrotic variant of glomerulonephritis

Abstract

The purpose of the research — studying the features of the production of pro- and anti-inflammatory cytokines, as well as indicators of thyroid status in patients with nephrotic variant of glomerulonephritis (GN). Research methods. The examination involved 78 patients with primary GN, including 30 patients with nephrotic syndrome (NS) and 48 GN patients who had no NS symptoms. Laboratory researches included the determination of the concentration of the main cytokines circulating in the blood — IL-1b, IL-2, IL-4, IL-10, IFN-g and the receptor antagonist of IL-1b — Rа-IL-1b by the method of solid-phase enzyme linked immunosorbent assay enzyme immunoassay (ELISA) in the system of the bideterminant definition of antigen with the use of peroxidase as indicator enzyme using standard sets (“Cytokine”, St.-Petersburg) according to the technique attached to a set. The investigation of the basic indicators of thyroid status — free thyroxine (FT4), free triiodothyronine (FT3), thyroid-stimulating hormone (TSH), anti-thyroid peroxydase antibodies (TPOAb) is carried out by the ELISA using standard sets and NGO techniques «Diagnostic systems» (N-Novgorod). The researches were conducted twice — before the hospitalization (1–2 days) and after the end of a stationary stage of treatment (12–14 days). Results. In 90% of patients with nephrotic option of GN there have been identified laboratory signs of hypothyroidism of different degrees of severity accompanied by increasing of production levels of proinflammatory cytokine IL-1b and IL-4, related to the activity of a humoral link of adaptive immunity. The reduction of glomerular, erythropoietic, concentration kidney functions, as well as proteinuria in patients with nephrotic option GN are associated with the decrease of T4 levels in the blood and increased levels of the cytokines circulating in the blood — IL-1b and IL-4. Conclusion. The obtained data demonstrate that the high level of production of IL-1b and IL-4 in GN patients causes hypothyroidism resulting in the formation of NS.