Search PubMed⌕ Search

Biomedical subjects

M Carraro

Publications and source records attributed to M Carraro.

At least 37 records · Page 2Linked to original sources
PubMed1993

Involvement of the renin angiotensin system in the pathogenesis of postexercise proteinuria.

Proteinuria after strenuous exercise is common in healthy subjects. The pathophysiologic mechanism of postexercise proteinuria (PEP) is not clear, although the phenomenon has long been known and many explanatory theories have been proposed. It is widely recognized that angiotensin II may increase filtration of protein through the glomerular membrane, and that its concentration in plasma increases during exercise. The aim of this study was to evaluate possible involvement of angiotensin II in the pathogenesis of PEP. Of 25 young volunteers who performed maximal aerobic exercise, eight showed PEP. The exercise was repeated after an interval of at least one week, now 90 minutes after administration of captopril (25 mg). Captopril did not affect the achieved work load of the maximal blood pressure and heart rate during the exercise, but PEP was not found. As it was possible to prevent PEP by administering an angiotensin-converting enzyme inhibitor, the study supports the theory that the renin angiotensin system is involved in the pathogenesis of PEP.

Adult↗
PubMed1992

Power spectral analysis of heart-rate variations improves assessment of diabetic cardiac autonomic neuropathy.

Power spectral analysis (PSA) of heart-rate variations has recently proved a useful tool in evaluating cardiovascular autonomic activity. It offers the possibility of examining both the functioning of parasympathetic and sympathetic pathways through breakdown into two frequency bands, and of their effects on heart-rate cyclic variability. We applied an autoregressive model for PSA to study overall autonomic tone in 20 male age-matched control subjects and 53 insulin-dependent (type I) diabetic subjects, subdivided into three groups of 20, 15, and 18, each group presenting different degrees of autonomic involvement. We found that: 1) power spectrum density (PSD) values at high-frequency bands (parasympathetic dependent) were similar in diabetic subjects without cardiac autonomic neuropathy (CAN) and in control subjects, but differed significantly from diabetic subjects with mild CAN and severe CAN, both standing and lying; 2) PSD values at low frequency (mainly sympathetic dependent) were similar, or slightly different, in diabetic subjects without CAN and in control subjects, but differed significantly from diabetic subjects with mild and severe CAN, both standing and lying; 3) as an expression of parasympathetic versus sympathetic coherence, correlations, both standing and lying, existed between PSD values at low- and high-frequency bands in control and diabetic subjects without CAN, but not in diabetic subjects with CAN; and 4) different degrees of correlation characterized the PSD values of high and low frequencies versus traditional cardiovascular test values in the diabetic subjects. The best correlation was between PSD low-frequency values and the lying-to-standing maneuver.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Contrast agent nephrotoxicity: comparison of ionic and nonionic contrast agents.

The effects on glomerular and proximal tubular function of an ionic contrast agent (sodium meglumine diatrizoate) and a nonionic agent (iopamidol) were compared in 34 patients with normal renal function. The patients received large doses (2.5 ml/kg body weight) of contrast material for IV digital subtraction angiography. Urine samples, collected before, immediately after, and on the first and third days after digital subtraction angiography, were analyzed for albumin, alanil-aminopeptidase, alpha-glucosidase, and beta-2-microglobulin. The changes noted were mild and of short duration with both contrast agents, despite the high dose given. These results suggest that, at least as far as renal toxicity is measured by these tests is concerned, ionic monomers can be safely used instead of more expensive nonionic media in procedures, such as digital subtraction angiography, that require high doses of contrast material.

Adult↗
PubMedDate not supplied

Proteinuria in focal segmental glomerulosclerosis: role of circulating factors and therapeutic approach.

The clinical course of primary Focal Segmental Glomerulosclerosis (FSGS) is frequently complicated by nephrotic range proteinuria and progression to renal failure. The high recurrence rate of the disease in transplanted kidney suggests the hypothesis that such patients have a circulating factor that alters glomerular capillary permeability. In recent years some authors found that serum from patients with FSGS increases glomerular permeability to albumin and partially identified the permeability factor (PF) as a protein of 30-50 Kd m.w. The removal of this protein by means of Plasma Exchange (PE) or plasma Immunoadsorption by Protein A (IA) decreased proteinuria. In this report we provide preliminary data about the prevalence of PF and the therapeutic effect of its removal by IA, in 3 pts with recurrence in the transplanted kidney, and 4 with FSGS of the native kidneys. They were resistant to corticosteroids (CS) and immunosuppressive (IS) therapy. 10 IA sessions were performed in 4 weeks: if a remission was achieved IA was gradually tapered. The level of PF in the serum was measured by an in vitro assay to determine the glomerular permeability to albumin. The FSGS was histologically proven in all cases and the degree of evolution was evaluated. PF levels, serum creatinine, daily proteinuria and serum albumin were monitored. The 3 patients with recurrent FSGS had a normalization of the PF levels; 2 had a clinical remission. In FSGS of native kidneys PF was elevated in 3/4 cases; 1 had a clinical remission; 2 with extensive sclerohyalinosis and 1 without PF levels did not improve. Our results confirm that most patients with FSGS have high PF serum levels and suggest that its removal can be beneficial.

Adolescent↗
PubMedDate not supplied

Nifedipine reduces postexercise proteinuria in young volunteers.

Previous studies have demonstrated that it is possible to prevent postexercise proteinuria with angiotensin-converting enzyme inhibitors. To determine whether calcium antagonists have the same effect, 40 young healthy volunteers underwent maximal aerobic exercise with and without nifedipine 10 mg per os 1 h before the first or second trial. Urinary excretion of albumin (UAE), transferrin (UTE) and alpha 1-microglobulin (UME) were examined before and after each trial. UAE, UTE and UME were significantly increased after exercise. Nifedipine significantly decreased UAE (p = 0.001) and UTE (p = 0.02) after exercise, and slightly decreased the maximal work load and the basal excretion of albumin. UME was unchanged. Therefore, the results of this study demonstrate that nifedipine administration before exercise significantly reduces postexercise proteinuria.

Adult↗
PubMedDate not supplied

Apheresis in primary focal segmental glomerulosclerosis of native and transplanted kidneys: a therapeutic protocol.

BACKGROUND: Patients with focal segmental glomerulosclerosis (FSGS) develop nephrotic syndrome and terminal renal failure in most cases. FSGS reappears in 15-50% of transplanted kidneys and frequently causes the graft loss. Sera from patients with FSGS of native or transplanted kidneys contain some proteinuric or permeability factors (PF) which can be removed by means of plasma exchange (PE) or protein A Immunoadsorption (IA). METHODS: We suggest a therapeutic protocol, for patients with biopsy proven FSGS of native or transplanted kidneys, resistant to steroid and immunosuppressive therapy, based on the association of PE or IA to conventional drug therapy. Daily proteinuria, renal function, serum albumin and circulating level of proteinuric factors (permeability test) will be monitored at regular time intervals during the apheresis cycle, which will be intensive at the beginning (8-10 sessions in 4 weeks) and very gradually discontinued. Results. We will consider satisfactory remission the reduction of proteinuria below 1 g/day, improvement of renal function, normalization of serum albumin level (> 3.5 g/dl). Partial remission will be considered: proteinuria below 3 g/day, stable renal function, serum albumin level between 3 and 3.5 g/dl. Permeability test, if positive at baseline examination, should be negative after apheresis. CONCLUSIONS: The primary endpoint of our protocol is: lasting remission (satisfactory or partial) after the apheresis suspension. Secondary endpoints are: maintained remission with continuing apheresis sessions, correlation between permeability activity and disease activity, identification of responders and non responders patients on the basis of positive permeability test.

Adolescent↗
PubMedDate not supplied

Humoral permeability factors in the nephrotic syndrome: a compendium and prospectus.

The concept that increased glomerular albumin permeability in steroid-resistant nephrotic syndrome is induced by circulating humoral factors is not new. Zimmermann (1) was among the first to demonstrate that serum from a renal transplant patient with recurrent focal segmental glomerulosclerosis (FSGS) could provoke increased albumin excretion when infused in the aorta of intact rats. Unfortunately, the experiment was not easily reproducible, and the possibility that human serum could induce serum sickness in rats was a serious limitation of the original experiment. We now know that inhibitors of permeability activity are present in both normal human and rat serum (see below), which explains the difficulty in replicating the disease in intact animals. In 1974 Shalhoub (2) theorized that a disordered clone of T lymphocytes, present in both minimal change disease and FSGS, secreted a circulating lymphokine "toxic" to the glomerular barrier. In support of this hypothesis, Koyama et al (3) formed hybridomas from T cells from four patients with minimal change disease and three control subjects. The hybridomas of the patients produced a substance that induced proteinuria when injected intravenously into normal rats. However, the study utilized stimulated and not quiescent T cells, and therefore the relevance to the pathogenesis of FSGS is unknown. Hoyer and colleagues first described recurrence of idiopathic nephrotic syndrome after renal transplantation in 1972 (4). Numerous subsequent reports have established the rate of recurrence as being about 30%. Timely plasmapheresis associated with aggressive immunosuppression resolves the proteinuria and disease progression in a large proportion of cases (5). FSGS not only recurs after renal transplantation, but the diseased kidney can also recover when kept protected from the pathological milieu. Rea et al (6) demonstrated that kidneys from a donor with FSGS transplanted into two uremic recipients were free from proteinuria, and that renal function was normal after one year. Ethical and legal considerations aside, recurrence of FSGS after transplantation is strong evidence supporting the role of a humoral factor in the pathogenesis of the disease.

Animals↗
PubMedDate not supplied

[The pathogenetical mechanisms of glomerular proteinuria.].

Although the pathologic mechanisms responsible for glomerular proteinuria have not been completely clarified, yet, it has become evident that structural and functional abnormalities of podocytes play an early and important role. These data come from recent studies analyzing podocyte behaviour in cell culture, in-depth clinical researches, the application of survey techniques on isolated glomeruli, proteomic studies on particular aspects of circulating factors. For most glomerulopathies, whether primary or secondary, podocytes are often the first target for many pathogenetic mechanisms, which, unexpectedly, have the common characteristic of inducing tropism in podocytes. Hopefully, advances in glomerular podocyte research will better define clinical diseases, which we now classify according to a static description of the histological damage, thus perhaps mistaking causes and effects.

Diabetic Nephropathies↗
PubMedDate not supplied

[Bolus thrombolysis in pulmonary embolism. Review of experimental and clinical data].

Although heparin is the primary drug used to treat pulmonary embolism, its limits include poor prevention of recurrence, and slow and delayed normalization of hemodynamic parameters. Over the past decades, thrombolysis has proved to be the most rapid and effective therapy to normalize hemodynamic parameters and angiographic and scintigraphic indexes of obstruction. Studies conducted up to the present have not, however, demonstrated a significant advantage over heparin with respect to mortality. Moreover, thrombolytic drugs carry a greater risk of hemorrhage than heparin. Various experimental studies have demonstrated that the short-term administration of recombinant tissue plasminogen activator (rt-PA) is more effective and decreases risk of hemorrhage. To our knowledge, only a few uncontrolled clinical studies on bolus thrombolysis with urokinase have been done. Studies comparing a 0.6 mg/Kg bolus of intravenous rt-PA versus the infusion of 100 mg over 2 hours have given conflicting results. Of these, some have demonstrated that bolus administration is safer and more effective while others have provided nearly overlapping results regarding safety and the reduction of pulmonary resistances. One study reports higher mortality in a group receiving 0.6 mg/Kg bolus rt-PA. Until these questions are clarified, administration of thrombolytics in the following doses is advised: streptokinase bolus 250,000 U over 30 min + 100,000 U/hour for 24 hours; urokinase bolus 4400 U/Kg for 10 min + 4400 U/Kg/hour for 12-24 hours; rt-PA 100 mg for 2 hours.

Animals↗