HLA-B27 is a potential risk factor for posttransplantation diabetes mellitus in autosomal dominant polycystic kidney disease patients.

The aim of this work was to investigate HLA phenotype predisposition to posttransplantation diabetes mellitus (PTDM) in kidney transplant recipients stratified according to kidney failure etiology. Ninety-eight transplant recipient pairs with kidney grafts from the same cadaveric donor were qualified for the study. In each pair, 1 kidney was grafted to an individual with autosomal dominant polycystic kidney disease (ADPKD group) and 1 to recipient with a different cause of kidney failure (non-ADPKD group). All class II HLA antigens were determined with the PCR-SSP molecular method. To identify class I HLA molecules we used both molecular and serologic methods. Diabetes was diagnosed according to the American Diabetes Association criteria. The posttransplantation observation period was 12 months. In the ADPKD group, HLA-B27 was more common in PTDM than non-PTDM patients; 31.6% versus 11.4% (P = .069). The difference achieved significance when comparing insulin-treated with non-insulin-treated patients (44.4% vs 12.4%; P = .029). In the non-ADPKD group, HLA-A28 and HLA-B13 were observed more frequently in patients with PTDM than in recipients without diabetes (22.2% vs 2.5% [P = .0099] and 22.2% vs 3.8% [P = .020]). All of these associations were significant upon multivariate analysis. HLA-B27 allele is a factor predisposing ADPKD patients to insulin-dependent PTDM. Antigens predisposing to PTDM among kidney graft recipients without ADPKD include HLA-A28 and B13.

Chronic hypokalaemia--how to establish a diagnosis?

We present three cases of patients with symptomatic, chronic, diagnosis-resistant hypokalaemia. Differential diagnosis of renal potassium loss between Gitelman's syndrome, Bartter's syndrome and loop diuretic abuse was made. Key elements in differential diagnosis of chronic hypokalaemia are blood pressure assessment, acid base equilibrium, serum calcium concentration, 24-hour urine potassium and calcium excretion.

[Pseudo-Gitelman's syndrome as consequence of loop diuretics abuse]. / Rzekomy zespól Gitelmana u pacjentki naduzywajacej diuretyków petlowych.

We describe a case of 40-year old patient with chronic, resistant to treatment hypokalaemia. Differential diagnosis of renal potassium loss among Gitelman's syndrome, Bartter's syndrome and loop diuretic abuse was made.

[Malonyldialdehyde, uric acid and white cell count as markers of oxidative stress in acute myocardial infarction and acute coronary insufficiency]. / Dwualdehyd malonowy, kwas moczowy i leukocytoza jako wykladniki stresu oksydacyjnego w swiezym zawale serca i ostrej niewydolnosci wiencowej.

UNLABELLED: Free radicals, produced in large amounts during myocardial ischemia and reperfusion, take part in the degradation of cellular and subcellular membrane structures. The source of oxygen radicals in the ischemic myocardium are neutrophils recruited into the necrotic region, as well as metabolic transformation of hypoxantine and xantine to uric acid. Subsequent reactions generate lipid peroxides and cytotoxic and-products of oxidation, among which is malondialdehyde (MDA). The aim of this study was to measure of MDA, uric acid and white cell count as markers of oxidative stress in patients with acute coronary insufficiency and acute myocardial infarction. We studied 75 participants (20 females and 55 males) aged 38-75, including 13 patients with acute myocardial insufficiency (group I: 6 females and 7 males, aged 40-66 years, mean 59.4 +/- 6.52), 40 patients with acute myocardial infarction (group II: 8 females and 32 males aged 38-72 years, mean 57.3 +/- 9.57) and 22 healthy volunteers (control group: 6 females and 16 males aged 39-75 years, mean 53.1 +/- 9.62). CONCLUSIONS: 1. Elevated levels of MDA in patients with acute myocardial infarction may reflect secondary disorders of cellular metabolism and late appearance of degradation products of lipid peroxides; 2. Uric acid may serve as an additional marker of free radical reactions in patients with acute myocardial infarction and acute coronary insufficiency.

[Disseminated tuberculosis--diagnostic difficulties in a patient with chronic heart failure]. / Gruzlica prosówkowa rozsiana--trudnosci diagnostyczne u chorego z przewlekla niewydolnoscia serca.

We presented case 64 year old patient with disseminated tuberculosis. The main symptom was fever and his death was due to respiratory and circulatory failure. In spite of extensive diagnostic research the aetiology of sepsis was not identified and the treatment was ineffective. In patients with severe disseminated tuberculosis the traditional diagnostic methods are often not effective.

[Elevated cortisol level in blood of patients with unstable coronary disease and acute myocardial infarction--new approach]. / Wzrost stezenia kortyzolu we krwi u pacjentów z niestabilna choroba wiencowa i swiezym zawalem serca--nowe spojrzenie.

The aim of this study was to assess changes in serum cortisol concentration, enzymatic markers of myocardial ischemia and necrosis, leucocytosis and glucose in patients with unstable coronary disease and acute myocardial infarction. The study was performed in 75 patients (20 females and 55 males aged 38-75 years; mean age 59.4 +/- 6.52), including 13 patients with unstable coronary disease (6 females and 7 males aged 40-66 years; mean age 59.4 +/- 6.52; group I), 40 patients with acute myocardial infarction (8 females and 32 males aged 38-72 years; mean age 57.3 +/- 9.57; group II) and 22 healthy volunteers (6 females and 16 males aged 39-75 years; mean age 53.1 +/- 9.62; control group). Acute ischemia as well as myocardial infarction are potent stress factors that destabilisate the functional equilibrium of the body. Considering the mechanism of action of cortisol and its physiological role, it seems that current views on elevated plasma cortisol levels as a response to stress and pain in infarction and acute ischemia should be supplemented. Anti-inflammatory properties of cortisol deserve more attention, while elevated levels might be of prognostic value in the above-mentioned diseases.

Effects of kinins, kallikrein and its inhibitor on certain indices of cell-mediated immunity and humoral immunity in rabbits.

The experiments were carried out on 54 rabbits in 9 groups of 6 animals each: group I -- controls, groups II, III, IV -- bradykinin i.v., groups V, VI, VII -- Depot-Kallikrein i.m. every other day for 3 weeks, groups VIII and IX -- Traskolan (trasylol) i.v. four times at intervals of 1 or 12 hours. The determined indices of cell-mediated and humoral immunity included: phagocytic activity of the reticuloendothelial system and peripheral blood leucocytes and their leukergic adhesiveness, haemagglutinin and haemolysin levels, serum complement titre, and the number of cells forming rosettes (RFC) or plaques (PFC) in the blood and spleen. These indices were determined 15 minutes, 3 and 24 hours after bradykinin administration, after 1, 2 and 3 weeks of kallikrein administration, and 1 or 12 hours after the last dose of Traskolan. Most determined indices showed always some fall. Only the phagocytic activity of the reticuloendothelial system was moderately increased in all groups, and in the bradykinin group leucocyte phagocytosis was increased slightly while their leukergic reaction was increased very strongly.