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Objective: to investigate the impact of the selectivity and half-life of nonsteroidal anti-inflammatory drugs (NSAIDs) on the development of subclinical kidney injury (SKI). A standard physical examination was made.Patients and methods. The study included 80 patients with a verified rheumatoid arthritis (RA) diagnosis. The patients filled in a specially designed questionnaire to explore a history of drug use. As markers of SKI, the investigators determined the concentrations of albumin, α1-microglobulin (α1-MG), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) in urine. A control group consisted of 20 apparently healthy individuals matched for age and gender.Results. 80 patients suffering from RA received drug therapy. Of them, 82.5% and 87.5% took NSAIDs and disease-modifying antirheumatic drugs, respectively. The levels of SKI markers were compared in three groups of the examinees: 1) NSAID-treated patients; 2) NSAID-untreated patients; 3) a control group. There were statistically significant differences between all the groups (p< 0.05). Comparison of the levels of SKI markers revealed no statistically significant difference in the groups receiving selective cyclooxygenase-2 (COX-2) inhibitors (n=18.6%), in those taking nonselective ones (n=68.6%), and the control group. Comparison of the levels of SKI markers demonstrated significantly higher α1-MG levels in the long-acting NSAID groups (n=8.6%) than in the short-acting NSAID group (n=80%). ALT, ALP, and microalbuminuria showed a similar trend that failed to reach statistical significance.Conclusion: NSAIDs remain a group of medications with a certain nephrotoxic effect. At the same time, the design of selective COX-2 inhibitors has failed to solve the problem of nephrotoxicity. NSAIDs with long half-lives are characterized by greater nephrotoxicity. The available data provide preconditions for the more differentiated use of NSAIDs, particularly in patients with RA.

Objective. To assess participation of tubulointerstitial and glomerular components in renal damage progression in pts with systemic lupus erythematosus (SLE) using immuno-morphological data. Material and methods. 45 SLE pts with lupus nephritis, 34 pts with chronic glomerulonephritis (CGN), 19 pts with drug induced chronic tubulointerstitial nephritis (DCTN) and 30 control persons were included. Concentration of anti-DNA antibodies, C-reactive protein (CRP), transforming growth factor β (TGFβ), tumor necrosis factor α (TNFα), monocytic chemotactic protein 1 (MCP1) was evaluated by immunoenzyme assay. Morphological examination of renal biopsies with semiqantitative assessment of measures reflecting process activity, sclerosis and renal blood vessels changes was performed. Results. Elevated concentration of TNFα and CRP was revealed in pts with SLE, CGN and DCTN. Pts with DCTN had highest, pts with CGN – lowest and SLE pts – intermediate values of these measures. There was a clear tendency of TNFα elevation with increase of SLE activity. Pts with lupus nephritis and DCTN had high values of MCP1. TGFβ level was significantly decreased in SLE. Glomerular component of lupus nephritis was characterized mainly by moderate proliferation and sclerosis while tubulointerstitial component signs were prominent. Conclusion. Further examination of tubulointerstitial changes, MCP1 and TGFβ appear to be worthwhile.