[Rapidly progressive proliferative glomerulonephritis with monoclonal immunoglobulin G deposits despite the mild histological changes. Case report]. / Enyhe szövettani eltérések ellenére gyors progressziójú proliferativ glomerulonephritis monoklonális immunglobulin-G-depozitumokkal.

Proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits is characterized by granular deposits of monoclonal IgG; histologically it has typically a membranoproliferative or endocapillary pattern, and seen electronmicroscopically there are dense deposits without substructure. Here, we present the case of a 62-year-old Caucasian woman who was admitted with rapidly progressive kidney failure. The patient's status, the laboratory and imaging examinations did not support prerenal, postrenal and - among the intrinsic causes - vascular and tubulointerstitial origin. The proteinuria and dysmorphic microhematuria suggested rapidly progressive glomerulonephritis. Tests for anti-neutrophil cytoplasmic antibodies, anti-glomerular basement membrane, antinuclear antibodies and cryoglobulins were negative, the C3 and C4 levels were normal. The biopsy evaluation diagnosed proliferative glomerulonephritis with monoclonal IgG deposits because of mesangial granular deposits of IgG3-kappa, C3, and C1q, and ultrastructurally electron-dense deposits (incidence in our adult native kidney biopsy series: 0.18%). 31 glomeruli were assessed histologically. 29 glomeruli displayed mild mesangial hypercellularity, 2 glomeruli were globally sclerotic. Crescents were not observed. Mild arteriolar hyalinosis, interstitial fibrosis and tubular atrophy accompanied the glomerular alterations. In the postbiopsy evaluation, paraprotein or multiple myeloma was not detected. Despite the mild histological findings, the kidney failure progressed, and hemodialysis had to be started two weeks after the biopsy. Steroids, cyclophosphamide and rituximab did not affect her kidney function, and she remained on hemodialysis during the follow-up of 39 months. This report presents for the first time proliferative glomerulonephritis with monoclonal IgG deposits as the possible cause of rapidly progressive nephritic syndrome in the absence of pronounced glomerular proliferative, sclerotic or tubulointerstitial lesions. Orv Hetil. 2018; 159(38): 1567-1572.

[25 years experiences on diabetic ketoacidotic patients]. / Diabeteses ketoacidosis--25 év tapasztalatai.

INTRODUCTION: In the past 25 years the authors regularly assessed the clinical characteristics of patients with diabetic ketoacidosis who were admitted to their diabetes unit. AIM: The aim was to examine the possible changes in the incidence, causes, treatment and mortality of diabetic metabolic disorders. METHODS: Retrospective analysis of the data obtained by the assessment of case histories. RESULTS: Between 1981 and 2005, 288 patients were admitted with 364 ketoacidotic episodes. The mean age of the patients was 42 +/-16.9 -- 53.2 +/- 12.6 years. Approximately 60% of them had type 1 diabetes and the proportion of the male patients was almost the same. The mean duration of diabetes was 7.8 +/- 8.1 -- 10 +/- 7.1 years. The ratio of manifest comas was approximately 10%. Among the precipitating factors the dominance of infections decreased (from 77.3% to 50.4%). During the treatment the aim of the authors was to supply fluids and electrolytes properly and to administer insulin for a prolonged period of time and in a dose as small as possible. The dose of the insulin bolus significantly decreased in the last period (8.29 +/- 4.31 U; p < 0.05). In the observed period 43 patients died (14.93% of the patients), the mortality rate decreased to 7.2% during the last period. CONCLUSIONS: Despite the intensive education, care and treatment of diabetic patients, the number of hospitalizations due to diabetic ketoacidosis has not decreased. In order to prevent ketoacidotic episodes proper team work is needed in the management of diabetic patients.