Vol 78, No 6 (2003)

Aim. To study expression of topoisomerases (TI) I and Ha (DNA-bound enzymes involved in transcription and replication) in renal tissue as markers of activity and prognosis of glomerulonephritis (GN) decisive for choice of immunodepressive therapy. Material and methods. TI expression was studied immunohistochemically in renal biopsies from 177 patients with different morphological variants of GN and in the samples of unaffected kidney tissue removed in 12 patients for local tumors. Results. There are definite differences between proliferative and поп-proliferative GN variants - elevation of TI levels and monocytic infiltration in proliferative GN. Focal-segmental glomerulosclerosis is characterized by a high TI Ila level in mesangial cells and monocytic infiltration of the glomeruli which are typical for inflammation. A statistical relationship between TI levels in mesangial cells and glomerular epithelium suggests a pathogenetic relation between these links of the pathological process. Molecular markers of activation and proliferation of cells and direct inductors of the inflammatory process (cells of monocytic infiltrate) closely correlated with the activity index - an integral indicator of inflammatory activity, as well as with the integral indicator of sclerotic processes in renal tissuesclerosis index. Monocytic infiltration in the interstitium correlated both with morphological manifestations of activity, progression of nephritis and their clinical equivalents. In high TI expression GN resistance to immunodepressive therapy rose. To overcome the resistance, immunodepressive therapy must be more active - large doses and duration of treatment. In patients with lupus nephritis and merenal GN prognosis was worse in the presence of high TI expression in mesangial cells and epithelium of the renal canaliculi. Conclusion. The authors are the first to demonstrate TI expression in renal tissue of GN patients, correlation of its level with activity of renal process as well as its role in prediction of response to treatsangiocapillary ment and the rate of renal failure progression. It is suggested that high TI expression entails a progressive course of GN.

Aim. To elicit clinical features of nephropathy associated with antiphospholipid syndrome (APSN) in patients with primary antiphospholipid syndrome (PAPS). Material and methods. The analysis of clinical characteristics and course of APSN has covered 24 patients with PAPS (16 females and 8 males, mean age 34.3 years). Renal damage was represented by arterial hypertension (AH), urinary syndrome, functional decline. All the patients were tested for anticardiolipin antibodies and/or lupus anticoagulant. Renal biopsy was made in 7patients. Results. PAPS patients developed renal affection in the onset of APS or within the first 5 years of its course. In the majority of patients APSN combined with abnormalities of CNS, heart and skin. Arterial/arteriolar thromboses prevailed. APSN manifested with: AH (n = 23, severe AH in 11), abnormal renal fdtration (n = 17, creatinine rise in 8), urinary syndrome with proteinuria (n = 23, in 14 with hematuria). The following clinical variants of APSN were proposed: urinary syndrome with AH (n = 16; 67%), acute nephritic syndrome (n = 7; 29%), nephrotic syndrome (n = 1). Morphological studies of biopsies from APSN patients have revealed sclerotic changes, thrombotic microangiopathy, nonspecific alterations in the glomeruli. Conclusion. APSN is a variant of microvascular renal affection caused by thrombotic processes in intraorgan microcirculation, ft is an early clinical marker of APS. Clinically, APSN manifests with vascular renal affection, the earliest symptom being inhibition of glomerular filtration. Clinical combinations of the symptoms allow to distinguish variant of APSN suggesting the existence of acute and chronic APSN. Combination of APSN with affection of the CNS, heart and skin points to a special PAPS subtype characterized by generalized ischemic damage to the organs as a result of intraorganic arterial and/or arteriolar thromboses.

Aim. To study quality of life of patients with progressive renal pathology at the stage of conservative treatment. Material and methods. Quality of life and psychological features were examined in 40 patients with renal diseases (40% males, mean age 48.6 ±1.3 years). 77.5% examinees suffered from glomerulonephritis, the rest had diabetic nephropathy. Results. Personality, behavioral features of the patients were characterized as well as relationships between psychological and somatic factors in development of the disease. Factors influencing quality of life of the above patients are described. Conclusion. Correction of the variables influencing, primarily, the psychological component of the quality of life and, by this component, satisfaction of the patients with their state as a whole may have a good effect on their rehabilitation.

Aim. To examine blood flow in renal and intrarenal arteries and its changes in the acute pharmacological test with captopril in patients with chronic glomerulonephritis (CGN). Material and methods. Renal circulation was studied in 50 patients with CGN using ultrasound dopplerography (USDG) of renal vessels on the unit GE Logiq 400 CL PRO Series. The velocity and indices of peripheral blood resistance in the major renal artery (RA) and in intrarenal arteries were estimated. In 26 patients the blood flow was studied again after intake of 50 mg captopril. Results. Poor renal blood flow was registered in cortical parenchyma in 36% CGN patients (with chronic renal failure in 75%). Multifactorial regression analysis has demonstrated that only blood creatinine was independently related with slowing down of the blood flow at the level of RA and intrarenal arteries. Morphological index of activity correlated with resistance indices while a high sclerosis index correlated with blood flow slowing. Older patients had higher resistance indices. Captopril significantly accelerated Mod flow and insignificantly changed indices of peripheral resistance including those in CRF patients. Conclusion. Poor blood flow in the cortical layer of renal parenchyma in CGN, according to USDG, occurs rather frequently and was associated with CRF and older age of the patients. Blocking of reninangiotensin system at the level of angiotensin II formation improves renal blood flow in most of the patients.

Aim. To study causes and sequelae of intradialysis hypotension (IH) in patients with terminal renal failure (TRF). Material and methods. Forty one patients with TRF on chronic hemodialysis (CH) were divided into two groups. The study group consisted of 24 patients with episodes of IH. Seventeen patients of the control group had no IH. All the patients were examined with assessment of protein-energy deficiency residual renal function, left-ventricular hypertrophy, diastolic function of the heart. Hemodialysis effectiveness was estimated by Kt/V index. Survival of the patients was calculated according to Kaplan-Meier method. Results. In the study group IH episodes occurred in spite of low ultrafiltration velocity (8-10 ml/min). Those patients of the study group who had IH associated with polyneuropathy and left-ventricular hypertrophy had IH episodes more often and sharper falls of arterial pressure. Long-term IH decreased survival significantly. Conclusion. Repeated episodes of IH deteriorate effectiveness of hemodialysis because of acute coronary syndrome, acute disorder of cerebral circulation, complications of deficient dialysis syndrome (pericarditis, hyperkaliemia, pulmonary edema, congestive heart failure).