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Biomedical subjects

C Rugiu

Publications and source records attributed to C Rugiu.

At least 19 recordsLinked to original sources
PubMed1996

Selenium status and plasma glutathione peroxidase in patients with IgA nephropathy.

The abnormal proliferation of mesangial cells with IgA deposition in the glomeruli characterizes primitive mesangial glomerulonephritis (IgA nephropathy, IgAN); this disease reduces the normal renal parenchyma while renal function becomes progressively impaired. The possible role of selenium has never been considered in evaluating factors involved in the pathogenesis of IgAN. In this work we compared the Se status of 14 IgAN patients (8 with normal renal function, IgAN NRF; 6 with impaired renal function, IgAN IRF) to that of 14 normal individuals (CG NRF) before and after an oral supplementation with selenite (0.13 mol Se/kg b.w./day for 60 days). The following indices of Se status were measured: Se in plasma and urine samples by PIXE; glutathione peroxidase activity in the cytosol of platelets (PLTs-GSH-Px) and of erythrocytes (RBCs-GSH-Px). Both concentrations and activities of plasma glutathione peroxidase (pl-GPx), a selenoenzyme mainly synthesized in and secreted by the kidney, were measured in plasma samples and results compared among groups. IgAN patients showed lower pl-Se and lower activities of selenoenzymes than normal controls before Se supplementation (p < 0.001). These findings suggest that an impaired Se status coexisted with the proliferation of mesangial cells in patients. Selenite induced PLTs-GSH-Px activity in all individuals (p < 0.001), but no variation was observed in RBCs-GSH-Px activity or in the concentration of pl-GPx in the plasma. On the other hand, selenium induced pl-GPx activity in CG NRF (p < 0.001) and in IgAN NRF (p < 0.01), but poorly stimulated pl-GPx activity in IgAN IRF (p = n.s.). However, only 17% and 25% of the pl-GPx activity of normal controls was measured in the plasma of IgAN IRF and IgAN NRF patients, respectively (p < 0.001). In conclusion, selenite only partially restored a normal Se status in patients whose low pl-GPx activity probably reflects an impaired synthesis of this protein as a consequence of reduced normal functioning of the parenchyma in kidneys affected by IgA nephropathy.

Glomerulonephritis, IGA↗
PubMed1995

Renal reserve in patients with solitary kidneys.

The first part of this article focuses on the risk of functional deterioration in subjects with solitary kidneys; the long-term clinical outcome of various subgroups of patients is reviewed. Thereafter, the pathophysiology of the renal functional reserve in subjects with a 50% reduction in renal parenchyma and the results coming from studies eliciting the renal reserve in these subjects are summarized. Finally, the clinical significance of the renal functional reserve and its usefulness in clinical practice are critically discussed.

Glomerular Filtration Rate↗
PubMed1994

Nutrition and the kidney: how to manage patients with renal failure.

Nutrition is believed to play a key role in the management of chronic and acute renal failure. Considerable evidence suggests that unrestricted protein diets accelerate the progression of chronic renal failure. As a result, recommendations have evolved limiting the quantity and quality of nitrogen intake with the goal of slowing the progression to dialysis dependency. Acute renal failure offers different challenges in view of its common association with hypermetabolic states. With respect to nitrogen substrate administration, the use of mixed formulations of essential plus nonessential amino acids seems to be as effective as essential amino acids alone.

Dietary Proteins↗
PubMed1994

ACE inhibition reduces proteinuria in normotensive patients with IgA nephropathy: a multicentre, randomized, placebo-controlled study.

A multicentre, randomized, placebo-controlled study was performed in 39 adult patients with biopsy-proven IgA nephropathy with the aim of comparing the effects of the ACE inhibitor fosinopril and placebo on proteinuria. All patients had normal blood pressure and normal renal function. Proteinuria ranged from 1.0 to 2.5 g/24 h. After a 3-month run-in period, fosinopril and placebo were randomly administered in two 4-month sequences separated from cross-over treatment by a 1-month interval. The mean values of creatinine clearance did not change during either the placebo or the treatment sequences. The mean values of mean arterial pressure (MAP) were significantly lower during the fosinopril sequence (90.4 +/- 9.0 mmHg) than in basal conditions (92.8 +/- 9.1 mmHg) (P = 0.034). The mean basal values of proteinuria were 1.74 +/- 0.84 g/24 h. They were unchanged during the placebo sequence (1.79 +/- 1.20) and fell to 1.37 +/- 0.98 g/24 h after 4 months of fosinopril treatment. Using a multivariate statistical analysis, the treatment effect by time on proteinuria was significantly evident only in the fosinopril sequence (Wilks test, P = 0.033). Changes in protein excretion were not correlated with changes in MAP, baseline plasma renin activity, and urinary sodium excretion. This controlled study shows that fosinopril can significantly reduce proteinuria even in normotensive patients with IgA nephropathy. Obviously, the results of treatment with ACE inhibitors on long-term renal prognosis remain to be elucidated.

Adolescent↗
PubMed1991

Is there a "point of no return" in progressive renal disease?

The pathogenesis of progressive renal damage is most probably multifactorial. Whatever the mechanisms involved in renal disease progression, the existence of a "point of no return" has been hypothesized, that is, a stage of structural and functional damage beyond which progression of renal disease occurs independently of dietary measures and/or pharmacological treatment. In experimental animals, dietary protein and phosphate restriction is not fully successful in ameliorating the progression of functional deterioration if administered when renal injury is severe and long standing. Similarly, late treatment with various pharmacological agents (mainly antihypertensive drugs) is less effective than early administration of the same substances. A serum creatinine of 176 mumol/L seems a critical point discriminating the results of either dietary protein and phosphate restriction or antihypertensive treatment in patients with chronic renal disease. The protective effects of both dietary and nondietary intervention seem to be most effective when at least 50% of the residual renal mass is still functioning. The extent to which glomerular sclerosis, vascular hyalinosis, and interstitial fibrosis have already developed can probably blunt or avert the expected results of treatment. Some clinical tests may identify those patients who would benefit from measures such as the reduction in glomerular hemodynamic stress, the long-term inhibition of the renin-angiotensin system, and the aggressive treatment of systemic hypertension. The continuous search for a rational preventive treatment before the disease process has reached the "point of no return" will undoubtedly constitute a formidable task for the modern nephrologist.

Animals↗
PubMed1991

Effect of dietary proteins and lipids in patients with membranous nephropathy and nephrotic syndrome.

Twenty-four patients with idiopathic membranous nephropathy, long-lasting nephrotic syndrome and serum creatinine less than 2 mg/dl ate sequentially, in a randomized cross-over design, a normal protein diet containing 1.1 +/- 0.3 g/kg/day of proteins and a low protein diet containing 0.7 +/- 0.1 g/kg/day of protein, each diet for a period of 3 months. Both diets were low in fat (less than 30% of total calories) and cholesterol (less than 200 mg/day) content and rich in polyunsaturated fatty acids and in linoleic acid (10% of energy). Random assignment to one of the two 3 month diet periods was done after a RUN-IN period of at least one month on the hypolipidic normal protein diet. Glomerular filtration rate (inulin clearance), 24 hour urinary protein loss and serum albumin concentration did not significantly differ at the end of the two diet periods, indicating that long-term restriction of protein intake does not modify GFR or urinary protein loss in nephrotic patients. Serum total and LDL-cholesterol and daily proteinuria were significantly lower at the end of both diet periods than at the beginning and at the end of the RUN-IN period. We suggest that these changes were a consequence of the manipulation of dietary fat intake.

Adult↗
PubMed1991

Effect of dietary manipulation on the lipid abnormalities in patients with chronic renal failure.

Disorders of lipid metabolism could play an important role in mediating the progression of chronic renal disease toward uremia. The hypothesis of the nephrotoxicity of lipids has been considered in a large population of patients on long-term dietary protein restriction. In our experience, there is no evidence that lipid disorders may accelerate the progression of renal disease. Hypercholesterolemia and/or hypertriglyceridemia are probably only some of the many factors affecting the prognosis of renal disease. Dietary protein restriction seems to be effective in maintaining normal or only slightly elevated serum lipids in patients with early renal failure, even after years of dietary treatment, despite the natural progression of renal functional deterioration. Moreover, this dietary regimen has a favorable effect on lipid composition of erythrocyte membrane when compared with those of patients on a free diet.

Humans↗
PubMed1989

Different protein diets in renal failure: a self-controlled study.

The progression of renal failure on 2 different protein and phosphate diets was evaluated in 7 patients with chronic renal failure. We decided on three study periods for each patient: period A (low-protein diet: 0.6 g/kg of protein, 600 mg of phosphate) averaged 12 months; period B (normal protein diet: 0.9 g/kg of protein, 800 mg of phosphate) lasted 9 months; period C (low-protein diet as for period A) averaged 9 months. The slopes of 1/Scr were 0.003 (period A), -0.016 (period B) and 0.009 dl/mg/month (period C). The GFR (125I-iothalamate clearance) changed from 42.6 to 45.6 ml/min/1.73 m2 in period A, from 51.9 to 40.7 in period B and from 40.5 to 44.6 in period C. The results show changes in renal function when dietary protein and phosphate intakes exceeding 0.6 g/kg and 600 mg/day, respectively, are administered to patients with GFRs ranging from 24 to 66 ml/min.

Adult↗
PubMed1989

Effects of a protein load in patients with early chronic renal failure before and after angiotensin II blockade.

We studied the effects of mid-term enalapril administration on protein-load-induced renal responses in 10 patients with early chronic renal failure (serum creatinine 2.70 +/- 1.0 mg/dl). The oral protein load was performed twice, before and after a 10-day therapy with enalapril. Glomerular filtration rate (125I-iothalamate clearance) rose from 22.5 +/- 10.6 to 60.1 +/- 32.8 ml/min after the protein load before enalapril; it did not change after the protein load during enalapril therapy. Percent fractional excretion of sodium, urinary osmolality and free water clearance were significantly affected only by the protein load before enalapril. Enalapril blunts the protein-load-induced changes in glomerular filtration rate and in tubular function; these effects might be mediated by angiotensin II blockade.

Adult↗