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E Perticucci

Publications and source records attributed to E Perticucci.

6 recordsLinked to original sources
PubMed1991

Low-protein diet and glomerular size-selective function in membranous glomerulopathy.

We studied the effect of dietary protein restriction on glomerular function and proteinuria in nine patients with membranous nephropathy. Patients were randomly assigned to a 3-month period of a normal protein diet (NPD, 1.3 mg/kg/d) or of a low-protein diet (LPD, 0.6 mg/kg/d), in a cross-over design. Dietary protein restriction did not affect glomerular filtration rate (47.8 +/- 10.7 and 49.0 +/- 13.5 mL/min/1.73 m2, LPD and NPD, respectively) and renal plasma flow (456 +/- 119 and 499 +/- 161 mL/min/1.73 m2, LPD and NPD, respectively), nor did it significantly improve glomerular permselective function, as shown by urinary protein excretion (3.1 +/- 2.2 and 3.5 +/- 2.8 g/d, LPD and NPD, respectively) and fractional clearance of albumin, IgG, and neutral dextran molecules of graded molecular size (radii ranging from 2.8 to 6.0 nm). These results indicate that reduction of protein intake to 0.6 g/kg/d does not improve glomerular size selectivity in membranous nephropathy. Thus, in current clinical practice, a protein-restricted diet does not appear to be effective in reducing proteinuria in this category of patients.

Adult↗
PubMed1991

Angiotensin converting enzyme inhibition improves glomerular size-selectivity in IgA nephropathy.

Clearances of uncharged dextrans of broad size distribution were used to evaluate the effects of a 30 day course of enalapril on glomerular barrier function in 10 patients with IgA nephropathy and proteinuria (from 1.4 to 5.6 g/day). Dextran clearance experiments were repeated three times: before enalapril therapy, after 30 days of enalapril and again 30 days after enalapril withdrawal. GFR, but not RPF, was significantly reduced by enalapril (basal 38.3 +/- 11.9, enalapril 30.2 +/- 12.6 ml/min/1.73 m2) and returned to basal values after enalapril withdrawal. Urinary protein excretion and fractional clearance of albumin were both significantly reduced by enalapril (basal 2.3 +/- 1.1 g/day and 102 +/- 90 x 10(-5), enalapril 1.2 +/- 0.6 g/day and 51 +/- 23 x 10(-5), respectively) and returned to basal values after enalapril withdrawal. Transglomerular passage of large dextrans (radii 54 to 62 A), but not of lower size (26 to 42 A) were significantly lowered by enalapril. When enalapril was withdrawn the dextran-sieving profile returned comparable to the baseline levels. A theoretical analysis of dextran-sieving profiles indicated that enalapril lowered the radius of largest membrane pores. This effect was independent from glomerular hemodynamic changes. We conclude that angiotensin converting enzyme inhibitors (CEI) in humans with IgA nephropathy reduces urinary protein excretion by a primary action on the intrinsic glomerular membrane properties enhancing barrier size-selective function. The hypofiltration associated with enalapril therapy in these patients, which was eliminated by its withdrawal, has to be taken into account as a possible undesired effect of CEI in long-term treatment.

Adult↗
PubMed1989

Supranormal von Willebrand factor multimers in scleroderma.

Platelet adhesion-aggregation reactions play an early and pivotal role in the pathogenesis of systemic sclerosis in scleroderma, but the mechanisms are incompletely understood. We determined whether or not plasma from 11 consecutive patients with scleroderma contained a subset of larger than normal ("supranormal") multimers of von Willebrand factor (vWF) that are potent inducers of platelet aggregation and adhesion. Supranormal multimers were found in all patients on at least one of two different occasions 9 to 12 months apart, whatever the duration and severity of the disease, but in none of the normal controls. Administration of low-dose aspirin (40 mg) to five of the 11 patients for ten days to inhibit the platelet release reaction slightly reduced the amounts of supranormal multimers suggesting that they might originate in part from platelets. Supranormal multimers may contribute to the pathogenesis of systemic sclerosis by inducing platelet aggregation and enhancing adhesion to subendothelium under the conditions of elevated shear stress occurring in the partially occluded vessels of the arterial microcirculation of scleroderma.

Adult↗
PubMed1989

[Von Willebrand factor multimers in systemic scleroderma].

In scleroderma endothelial cell damage plays an early and pivotal role in the pathogenesis of sclerotic lesions. In our study we determined whether or not plasma from 11 consecutive patients with scleroderma contained a subset of larger than normal (supranormal) multimers of von Willebrand factor which are potent inducers of platelet aggregation and adhesion. Supranormal multimers were found in all patients, but in none of the normal controls. Supranormal multimers may contribute to the pathogenesis of systemic sclerosis by inducing platelet aggregation and enhancing adhesion to subendothelium.

Adult↗
PubMed1988

Acidemia alone does not stimulate rat renal Na+-H+ antiporter activity.

To examine whether systemic acidemia is the cause of the adaptive increase in renal brush-border membrane (BBM) Na+-H+ exchange activity seen in metabolic acidosis, we examined the time course of changes in Na+-H+ exchange activity in rats with chronic metabolic or respiratory acidosis. Metabolic acidosis was created by allowing rats free access to a 1.5% NH4Cl drinking solution. Respiratory acidosis was created by housing rats in a chamber designed to maintain ambient PCO2 levels at 10%. All rats were fed normal rat chow. Control and respiratory acidosis rats had free access to tap water. Rats from each group were studied 1, 3, 5, 7, and 14 days after onset of treatment. Na+-H+ exchange activity was examined in renal BBM vesicles using acridine orange. In both metabolic acidosis and respiratory acidosis, arterial blood [H+] increased markedly at day 1 and returned toward normal thereafter; at day 14, [H+] was elevated to a comparable degree in both groups. In metabolic acidosis, Na+-H+ exchange activity remained at control levels for 3 days but increased markedly thereafter. In contrast, in respiratory acidosis no adaptive increase in activity occurred at any time. Because no correlation was found between blood [H+] and renal BBM Na+-H+ exchange activity, we conclude that stimuli other than systemic acidemia are responsible for the adaptation seen in chronic metabolic acidosis.

Acidosis↗