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Aim: To compare the possible pathogenetic and clinicodiagnostic value of antithyroid autoantibodies (autoAB) different in specificity, such as monospecific ones to thyroglobulin and thyroid peroxidase (anti-TG and anti-TPO autoAB) and bispecific ones to thyroglobulin and thyroid peroxidase simultaneously (anti-TGPO autoAB), in patients with autoimmune thyroid diseases., Materials and Methods: The sera from 240 patients with autoimmune thyroiditis (AIT) and from 124 with diffuse toxic goiter (DTG) were examined. The sera from 40 healthy donors served as a control. The sera were screened for anti-TG and anti-TPO autoAB, anti-TGPO autoAB, by employing enzyme immunoassay and/or radioimmunoassay. The results were statistically processed using the variation statistics-based programs., Results: The specific features of an autoantigenic component to thyroid tissues were found in the sera of patients with AIT and DTG. An association was established between the progression of disease and the phasic change of autoAB populations or their combinations., Conclusion: The procedure for evaluating seropositivity for antithyroid autoAB, which is referred to as non-invasive studies, can be considered as a criterion test in the diagnosis and prediction of the course of AIT and DTG.

The progression of chronic-relapsing infectious disease (CRID) depends on a combination of cumulative immune-mediated responses of the human body, which, in turn, are united by a number of the common mechanisms. The mechanisms are called as the post-infectious clinical-immunological syndrome (PICIS) to demonstrate the features and scale of imbalances of immune homeostasis. PICIS usually accompanies most of the known CRID to define the type of the disease, to predict the progression of and risks for the complications to be risen as well. PIFIS is generally provoked by either infectious pathogens of various nature or by the atypical immune responses from the infected patient, or by the onset of the disease itself, or by the inadequate antimicrobial therapy. Three forms of PICIS which depend on two key factors have been described. These included: (i) the spectrum of a microbial colonization landscape; (ii) the antimicrobial immunity itself to generate, for instance, either of three alternative PICIS, namely, (1) postinfectious secondary immunodeficiency syndrome (PISIS); (2) postinfectious autoimmune syndrome (PIAIS), and (3) PISIS combined with PIAIS, i.e. PISIDAS. The dominant monosyndrome-like form of associated immune imbalances in CRID patients is PISIS. PISIS occurs in more than a third of the clinical cases to stress the autoaggression (PIFAS), or combininative form of the immune-mediated imbalances, i.e. PISIDAS. In the process of the development of CRID, PISIS can give a way to either PIAIS or PISIDAS. Besides the immune-mediated imbalances, an essential role in the pathogenesis of CRID and PICIS is also attributed to the infectious factors capable of forming microbial associates in the pathogenesis of PICIS. Therefore, treatment of such patients should be directed not only at the elimination of the infectious pathogen(s), but also at the restoration of the physiological level of the immune homeostasis impaired by PICIS.

Aim: To compare the most significant architectonic parameters of peripheral blood cell subpopulations in patients with different variants of an autoimmune myocarditis (AIM) course and their clinical value in therapeutic practice., Material and Methods: Blood cell subpopulations were studied with flow cytometry in 99 blood samples from patients having different AIM variants and myocardiosclerosis as well as in 40 healthy donors., Results: Severe (malignant) AIM was characterized by growing indices of T-/B lymphocyte activation, expression of activation markers on the cells of both differentiation lines, disproportions in composition of subpopulations of the immunoregulatory cells, parallel rise in specific weight of dendritic cells, reduced intensity of apoptosis of autoreactive T-lymphocytes. In benign AIM marked immunopathology was not found. This group can be considered as a separate variant of AIM course necessitating an individual approach to planning pathogenetically sound therapeutic and rehabilitation measures., Conclusion: The study of activation markers expression on peripheral blood cells is superior to the study of endomyocardial biopsies providing a non-invasive method of immunodiagnosis.

Cyclophosphamide (CP) and methylprednisolone (MP) were tried on rats with experimental nephrotoxic serum nephritis and mice with experimental acute serum nephritis. Pathological processes were analyzed simultaneously in vivo and in vitro. CP reduced the antibody impairment and stimulated glomerular infiltration by mononuclear leukocytes whose mediator spectrum was oriented to repair. MP failed to stop the impairment and aggravated the infiltration. The resultant chaotic accumulation of the extracellular matrix raised the risk of sclerosis. CP showed the advantages in experiment demonstrable also in the clinical setting.

To specify the role of mononuclear (MN) leukocytes in the development of mesangial cell proliferation, which is one of the main manifestations of glomerulonephritis, cell cultures of renal glomeruli of rats with nephrotoxic serum (NTS) nephritis were examined for the intensity of mesangial cell proliferation, the MN-leukocyte count, and for IL-1 production. The amount of mesangial cells and the intensity of their proliferation in the cultures of glomerular cells from rats with NTS nephritis were much higher than in intact rat cultures. At the same time the glomerular cultures from rats with NTS nephritis demonstrated an increase in the MN leukocyte count together with enhancement of IL-1 production. The treatment with prednisolone averted accumulation of MN leukocytes by the glomerular cultures and noticeably reduced mesangial cell proliferation. The supernatant liquid of cultures of peripheral blood MN leukocytes from patients with active nephritis suppressed human fibroblast proliferation, exerting no such action on mesangial cell culture. During the treatment with prednisolone, the supernatant liquid produced a reverse effect on fibroblast and mesangial cell cultures, which was associated with the clinical improvement of the health status. It is assumed that mesangial cell proliferation seen in nephritis may be related to infiltration of the glomeruli by MN leukocytes and to elevated production by them of IL-1 and that the therapeutic action of prednisolone may be determined by suppression of these processes.

Ten patients with insulin-dependent diabetes mellitus not associated with any signs of diabetic nephropathy were examined for the reserves of filtration renal function and early morphological alterations in organ tissues. The reserves of filtration were detected under the conditions of acute oral administration of protein (1.5 g/kg) as difference between the initial and stimulated levels of glomerular filtration (GF). Two groups of patients were distinguished: group I included patients with preserved filtration reserves (increment of GF amounted to 35%), group II included patients with no filtration reserves (reduction of GF was 20%). Both the groups differed significantly only in the initial level of GF (120 and 209 ml/min, respectively) and in the degree of morphological changes in the glomeruli: group I manifested minimum structural changes, group II showed the commencing diabetic glomerulosclerosis characterized by pronounced injury to the manubrium of the glomeruli. Therefore, the lack of filtration reserves in diabetes mellitus patients suggests the presence of the commencing diabetic glomerulonephritis even with the lack of the clinical signs of renal injury, which does not require the resorting to organ biopsy. The primary injury to the manubrium of the glomeruli is likely to be related to a high gradient of intraglomerular hydrostatic pressure, resulting in hyperfiltration.

The authors described the results of an immunohistochemical, electron microscopic and morphometric study of the kidney bioptates of 45 patients with latent glomerulonephritis with hyperuricemia, 8 patients with primary gout and 12 patients with latent glomerulonephritis without hyperuricemia. Two possible variants of the involvement of the renal glomerula were revealed against a background of purine metabolism: typical immunocomplex glomerulonephritis and the so called "reactive" mesangial changes. The expression of interstitial changes (by the results of histometric investigation) was maximum in gout, slightly less in latent nephritis with hyperuricemia and minimum in nephritis without hyperuricemia. The authors emphasized the possibility of immunocomplex nephritis as one of the variants of renal lesion in gout and hyperuricemia and the necessity of specifying therapeutic modalities to be used in this condition including general nephrological approaches to the treatment of latent nephropathies.

To identify early markers of the preclinical stage of diabetic nephropathy, a study was made of the activity of the specific canalicular enzymes in urine: N-acetyl-beta-D-glucosaminidase (NAG), beta-glucuronidase (beta-G1), gamma-glutamyl transferase (GGT), alkaline phosphatase (AP) and lactate dehydrogenase (LDH) in patients with diabetes mellitus without (26) and with (15) proteinuria. Patients without the clinical signs of diabetic nephropathy manifested a significant rise of excretion of lysosomal enzymes of the proximal canaliculi (NAG and beta-G1). Concomitant elevation of the excretion of several enzymes (NAG, beta-Gl, GGT and AP) was observed in 50% of cases. Patients with diabetic nephropathy demonstrated an increase of the excretion of all enzymes under study. Puncture biopsy of the kidneys was made in 4 patients without proteinuria with insignificant duration of diabetes mellitus and concomitant elevation of the excretion of a number of enzymes. Light microscopy revealed minimal changes in the glomeruli, whereas electron microscopy changes both in the glomeruli and in the canaliculi. The morphological changes in renal tissue confirm the diagnostic importance of high concomitant excretion of canalicular enzymes (NAG, beta-Gl, AP) as a marker of the preclinical stage of diabetic nephropathy.

Peculiarities of a clinical course and prognosis of glomerulonephritis in Schönlein-Henoch disease (SH-nephritis) were studied in 42 adult patients. The 5- and 10-year survival rates were 87% and 72%, respectively. Of unfavorable prognostic value were proteinuria over 1 g/l, nephrotic syndrome, particularly combined with hypertension, marked stable microhematuria, and the detection of diffuse fibroplastic, extracapillary, and mesangiocapillary nephritis on biopsy. SH-nephritis was characterized by a more severe course in male patients, in persons aged over 30, and in the involvement of the kidneys one year and more after the appearance of the first clinical signs of skin vasculitis. The level of blood serum IgA and the gravity of skin vasculitis had no prognostic importance.