Objective of the study layed in assessment of the pathophysiological relation between cell-mediated immunity (tumor necrosis factor-alpha (TNF-α) inflammatory cytokine) activation and renal dysfunction in the patients with early rheumatoid arthritis. We analyzed the data from 35 early rheumatoid arthritis (RA) patients of average age of 50,71±2,25 years (ranged 18-76 years, 80% of women) with 9,21±0,43 months mean duration of the disease by the time of the study initiation. Urine and blood tests were performed to verify the main indicators of kidney function and inflammation cytokines significant interaction. All signs of renal dysfunction at the baseline in the patients with early RA were associated with glomerular filtration rate decrease and excretion of urine protein increase. Dynamics of albuminuria, according to the analysis of variance for one-factor scheme, were significantly determined by the state of disease activity, reflecting the severity of joint damage. High urine β-2-microglobulin level was significantly associated with the expression rate of main inflammatory cytokines as per binary regression analysis. The obtained dependence showed the dynamics of expression of tubular disorders in early RA with a progressive deterioration which did associate with the levels of TNF-α expression, and variety of the urine miсroglobulin rates in the interval 200-350 μg/L. Reliable correlation (r=0.51, p<0.05) between beta-2-microglobulinuria and TNF-α levels was clearly shown, revealing the relationship described by the formula MGU=- 81+937×log10 (TNF-α) as per regression analysis. The severity of tubular damage in early RA is associated with TNF-α expression, especially in the patients with TNF-α above 250 pg/mL, when microalbuminuria rates were significantly higher (p=0.00043). We identified robust data that in the early RA patients with high TNF-α, the number of reported cases of microalbuminuria was significantly higher than in those with low levels.