Nephropathies in the elderly. An epidemiological study.
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Biomedical subjects
Publications and source records attributed to A Baraldi.
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The expression of alpha 2; alpha 3; alpha 5; alpha 6-subunits of the beta 1 [very late activation (VLA)] integrin family was studied in kidney specimens using an immunofluorescent technique. 6 specimens from normal kidney were compared with 10 specimens from patients affected by various glomerulopathies [minimal change nephropathy (MCN), membranous nephropathy (MN) and systemic lupus erythematosus nephritis (SLEN)]. On normal glomeruli, alpha 3 was the dominant integrin, being mainly present on podocytes and showing a linear fluorescent pattern codistributed with laminin. In MCN and SLEN, alpha 3 presented a normal pattern. In MN, alpha 3 revealed a trabecular picture on thickened glomerular basement membranes. Moreover, in stage-III MN, a segmental loss of alpha 3-integrin was detected. In our opinion, VLA-3 may offer an interesting approach to the study of the relationships between podocytes and their substrate.
Most chronic renal failure patients suffer from generalized pruritus. An involvement of cutaneous nerve terminals in the pathogenesis of uremic pruritus has been suggested. Skin specimens from 24 uremic patients and 10 healthy subjects were processed with an indirect immunofluorescence method to investigate the presence and distribution of a number of neuronal markers and neuropeptides. No difference was found between the two groups in the distribution pattern of the positive nerve fibres. However, a reduction in the total number of skin nerve terminals in the uremic patients was detected. No correlation could be found between the immunohistochemical findings and the clinical features. Our results suggest that the skin innervation is altered in most chronic renal failure patients, possibly as a consequence of neuropathy.
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The technique of deep-freezing in liquid nitrogen of stripped saphenous veins permitted their long-term preservation, and the subsequent creation of a "bank" of venous allografts, used for arteriovenous internal shunts for hemodialysis. Histological, histochemical and immunological tests, and first clinical results have been favorable.
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Streptokinase (SK), a nonenzymatic protein produced by group C beta haemolytic streptococci, is a potent antigen. It is used worldwide as a thrombolytic agent in the treatment of acute myocardial infarction (AMI). Specific antiheart antibodies (AHA) have been found with a significantly high incidence in patients with AMI, and after streptococcal infection as a result of stimulation by constituents of the group A streptococci antigenically cross-reactive with sarcolemmal portion of the muscle fiber of the heart. Since there may be partial antigenic identity of group C streptococcal membranes with membranes isolated from group A streptococci, we have designed a prospective study to evaluate the incidence of serum AHA (and of other organ-specific and non-organ-specific antibodies) in 36 patients with AMI, 14 of whom treated with SK. AHA, of IgG class, were of the sarcolemmal-subsarcolemmal type, and did not fix complement. They were found in 4/36 patients already on admission; of the 32 patients negative, none developed AHA later, on days 7, 15 and 21 of hospitalization, also after treatment with SK (in 14 cases). There was no significant difference either within or between the two SK-treated and non-SK-treated groups also with regard to the incidence of organ-specific and non-organ-specific autoantibodies. These findings do suggest that the intravenous SK therapy does not facilitate the formation of AHA in AMI.
The purpose of this study was to compare the new multiple allergosorbent chemiluminescent assay (MAST CLA) system with the RAST and skin prick tests as an adjunct to the diagnosis of inhalant allergies. In this report, MAST CLA and RAST have given similar results, but no technique is as sensitive as skin tests for allergen-specific diagnosis of inhalant allergic disease.
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The in vitro effects of different lipoprotein fractions (VLDL, LDL and HDL) on human washed platelet aggregation, induced by collagen and thrombin, were evaluated in the presence and absence of PGI2. Although VLDL and LDL increased the platelet aggregation while HDL showed an opposite effect, none of the tested lipoprotein fractions affected the potency of PGI2 as inhibitor of platelet aggregation (IC50). In addition, studies were performed to evaluate the effects of lipoproteins on adenylate cyclase activity in human platelet membranes. The three lipoprotein classes inhibited both basal and PGI2-stimulated adenylate cyclase without affecting the EC50 for PGI2. This inhibitory activity was not specifically elicited by any protein or lipid since neither bovine serum albumin nor a lipid emulsion (Intralipid) displayed any inhibition. The effect on adenylate cyclase elicited by VLDL, LDL and HDL does not seem to be correlated with the activity on platelet aggregation. It is concluded that mediators other than cAMP might be involved in the control of platelet function by lipoproteins.
3 patients with myelofibrosis with myeloid metaplasia were splenectomized because of anaemia and disturbing splenomegaly. In the course of the 6 months following splenectomy, a polycythaemia developed. Erythrokinetic studies demonstrated that in all cases a reduction in plasma volume and an increase in red cell volume was obtained. Total erythropoiesis decreased along with normalization of ineffective erythropoiesis and peripheral haemolysis. The reappearance of an erythropoietic activity measured over the sacrum was a constant finding, while in 1 patient, a depression of activity over the liver was observed. The new distribution and organization of erythropoiesis in the splenectomized patients is hypothesized as being due to the removal of the influence of an enlarged spleen on erythropoietic organs.
Three patients with myelofibrosis with myeloid metaplasia are described. All three presented with grave anemia and red cell aplasia. Erythroid failure was the functional characteristic of erythropoiesis as resulted from erythrokinetic studies. Bone marrow was hypercellular or normocellular with hyperplasia of granuloblasts and megakaryocytes. Despite absent or mild splenomegaly at diagnosis, massive splenomegaly associated with a leukoerythroblastic blood film developed during the course of the disease. A relative young age (42-47 years), a subacute course of the disease and terminal blast crisis in two of them were the prominent clinical features of the patients. The differentiation from acute or malignant myelofibrosis is discussed. The patients appear to be a distinct subset within myelofibrosis with myeloid metaplasia.
A computer program for the analysis of 51Cr labelled red cell survival data was used in 84 patients and 8 normal subjects to estimate the parameters of 7 competing models derived from different hypotheses of the red cell destruction process. The purpose was to establish the optimal complexity of a red cell survival model to be used. Senescence or random destruction were the most common identified patterns of red cell death (79% of the cases). Models assuming different levels of death probability according to the age of cells, or 2 populations of cells with different death probabilities, were selected in 21% of the cases. These latter patients were characterized by the lowest values of MRCL. The conclusion of the work was that an automatic procedure for selecting the best model of red cell destruction is necessary when information concerning the mechanism of red cell death is required. For the more practical aim of obtaining an accurate measurement of the MRCL, the minimal set of competing models should account of at least 2 different populations of cells in addition to the random or senescence destruction models.
Relapse of the nephrotic syndrome in a patient who was in remission for 20 years is discussed. The initial renal biopsy performed 3 years after the onset of the nephrotic syndrome showed focal and segmental glomerulosclerosis (FSGS). The second renal biopsy performed 20 years later was compatible with a diagnosis of minimal change nephropathy (MCN).