PubMed Health⌕ Search

Biomedical subjects

M Balletta

Publications and source records attributed to M Balletta.

At least 19 recordsLinked to original sources
PubMed1997

Pathophysiological role and diuretic efficacy of atrial natriuretic peptide in renal patients.

It has been suggested that renal disease is characterized by the presence of resistance to the natriuretic effects of atrial peptide (ANP). In this study, plasma ANP (pANP) and renal function were evaluated during stepwise infusion of low ANP doses (2, 4, 8, and 16 ng/kg per min) in glomerulonephritic patients with (CRF) or without (GN) moderate renal failure, and in normal subjects (NOR), kept at low-sodium diet (LSD; 35 mEq NaCl/day). To assess the physiological ANP levels, pANP was also measured in the three groups after normal-sodium diet (NSD; 235 mEq NaCl/day). ANP did not affect systemic and renal perfusion at any of the doses tested; a significant increment of GFR was observed only in NOR and GN. The 2-, 4-, and 8-ng/kg doses increased pANP to values overlapping the physiological concentrations measured at NSD; this was associated with a dose-dependent increment of urinary excretion of sodium (UNaV) that reached analogous levels in the three groups. ANP accounted for approximately 40% of the UNaV increment evoked by NSD in patients and in normal subjects. The 16-ng/kg dose led to supraphysiological levels that induced a similar marked enhancement of UNaV (from the basal value of 0.12 +/- 0.02 to 0.42 +/- 0.08 mEq/min in CRF, from 0.13 +/- 0.02 to 0.73 +/- 0.08 in GN, and from 0.09 +/- 0.02 to 0.49 +/- 0.11 in NOR). In CRF, the normal natriuretic response to the highest dose was caused by a larger increase of fractional UNaV that was strictly dependent on the greater pANP increment, as demonstrated by similar changes in the fractional excretion of cGMP, and, in part, on the greater aldosterone decrease. In all groups, ANP also induced a dose-dependent urinary loss of phosphate, potassium, and urea, resulting in a significant 15 to 25% decrease in the plasma levels. Thus, in GN and CRF patients, ANP plays a significant role in the renal handling of sodium; moreover, the achievement of low supraphysiological pANP levels leads to a conspicuous natriuresis associated with unique extranatriuretic effects.

Adult↗
PubMed1996

Effects of hypercholesterolemia of renal hemodynamics: study in patients with nephrotic syndrome.

Experimental and clinical studies have demonstrated a positive relationship between hyperlipidemia and rate of progression of renal disease, suggesting that lipids can induce or aggravate glomerular injury mainly by interacting with mesangial cells. Nevertheless, recently has been demonstrated that increased cholesterol levels can also induce endothelial cell dysfunction. Thus, since endothelium is known to play a major role in modulating the vascular tone, we have tested the possibility that hypercholesterolemia impairs the renal hemodynamics in patients with active nephrotic syndrome and elevated serum cholesterol levels. In this single-blind, nonrandom study, 12 patients were treated with pravastatin (group T, treated, n = 12) and 8 with placebo (group C, controls, n = 8). The controls were studied after the pravastatin group had been completed. Before starting the treatment the patients underwent basal determinations including routine laboratory investigations and PAH and inulin clearances. The same determinations were repeated after 48 h, and 6 and 12 weeks from the beginning of the treatment. The study at 48 h was performed to see if pravastatin had a direct, cholesterol-independent effect on renal function. The following basal results were reported (mean +/- SEM; group T vs. group C): serum cholesterol (mmol/l) 9.7 +/- 0.4 vs. 9.1 +/- 0.3 (NS); proteinuria (g/24 h): 6.2 +/- 0.2 vs. 7.0 +/- 0.7 (NS); PAH clearance (ml/min): 353 +/- 21 vs. 385 +/- 31 (NS); inulin clearance (ml/min): 62.5 +/- 7.7 vs. 67 +/- 9.3 (NS). After 48 h, no changes were observed in both groups. Subsequently, in group T, the following percentage changes of basal levels were observed: serum cholesterol -21.4 +/- 3.2% at 6 weeks (p < 0.05) and -34.9 +/- 3.2% at 12 weeks (p < 0.01); inulin clearance +3 +/- 3.7% at 6 weeks (NS) and +9.3 +/- 2.9% at 12 weeks (p < 0.05); PAH clearance +7 +/- 3.1% at 6 weeks (p < 0.05) and +21.2 +/- 5.5% at 12 weeks (p < 0.01). By contrast, no significant changes of these parameters occurred in group C at any time, so that the percent changes of baseline values of CPAH were significantly greater in group T (at 6 weeks: p < 0.05; at 12 weeks p < 0.005). These results indicate that the reduction of cholesterol is associated with a significant increase in renal plasma flow, thus, suggesting that hypercholesterolemia may actually impair the renal hemodynamics. We speculate that this effect may contribute to increase the risk of ischemic acute renal failure in nephrotic patients and, along with changes induced in the mesangium by other mechanisms, to contribute to the progression of renal disease.

Adult↗
PubMed1992

Bilateral renal artery occlusion in a patient with primary antiphospholipid antibody syndrome: thrombosis, vasculitis or both?

A 43-year-old man presented with oliguria and hypertension. Renal arteriography showed bilateral renal artery occlusion. Circulating antiphospholipid antibodies were found together with a change in natural anticoagulant plasma levels. Immunofluorescence of examined vessels showed immune complex vasculitis. We discuss the pathogenetic mechanism leading to the development of this rare occlusive event.

Adult↗
PubMed1991

Effects of a two-month treatment with low oral doses of cyclosporin on renal function.

To test the effects of short-term therapy with low doses (LD) of cyclosporin A (CsA) in subjects with normal renal function, seven patients receiving CsA to treat psoriasis were studied. Clearances in maximal H2O diuresis were performed to evaluate changes in GFR (CIn), RPF (CPAH) and tubular function before starting CsA (BAS), after 2 days (S1) and 1 month (S2) of oral therapy with 5 mg/kg per day CsA. The study was repeated at the withdrawal of CsA after tapering (S3) and 2 months after the withdrawal (S4). The studies were performed 12 h after the evening dose of CsA. RPF was significantly less than in BAS throughout the therapy and returned almost to basal values in S4. GFR was significantly less than in BAS both in S2 and in S3. In S4, in spite of an increase, GFR was still significantly less than in BAS. Both in S2 and in S3 proximal tubular fractional sodium reabsorption was significantly less than in BAS and, consequently, both sodium delivery to diluting segments and sodium reabsorption in diluting segments increased. Moreover, both in S2 and in S3 fractional sodium reabsorption in diluting segments and free-water generation were greater than in BAS. In S4 tubular function returned almost to basal values. Our data suggest that short-term therapy with low dose CsA impairs renal function; this impairment is not completely reversed after drug withdrawal.

Administration, Oral↗
PubMed1991

Acute effects of ciclosporin on renal hemodynamics and urinary protein excretion in patients with the nephrotic syndrome.

The possibility that the renal hemodynamic abnormalities associated with ciclosporin (CS) administration are enhanced in nephrotic patients (NP), leading to severe impairment of renal function and/or to modifications in proteinuria, has not hitherto been tested. Ten NP and 8 healthy subjects (NC) were examined before and after oral CS administration (10 mg/kg body weight in NP and 12 mg/kg body weight in NC: a lower dosage was adopted in NP because of edema overestimating the actual body weight) under water diuresis by standard renal clearance methods. Basal blood volume was lower in NP. Blood CS levels were not significantly different in the two groups. Basal glomerular filtration rate (GFR) was similar in NP and NC, while renal plasma flow (RPF) was lower in NP. After CS, both GFR and RPF significantly decreased in the two groups, but the percent decrease in inulin clearance was greater in NP. Filtration fraction increased only in NC. Basal renal vascular resistances were greater in NP, and significantly increased after CS in both groups. Basal fractional sodium excretion (FENa) was lower in NP: after CS FENa decreased only in NC. Neither plasma renin activity, nor plasma aldosterone changed after CS. When urinary protein excretion (UP) was corrected by GFR, no change was observed after CS; by contrast, selectivity of proteinuria (as assessed by the CIgG/CTransferrin ratio) markedly increased. Our data indicate that CS induces a greater fall in the GFR in hypovolemic NP than in healthy subjects, probably because in the former GFR becomes extremely plasma flow dependent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Therapy of systemic candidiasis].

Candida septicaemia is an increasingly common problem. Candida Albicans may be found in yeast form in the intestinal tract, vagina, skin and mucous membranes of apparently healthy individuals. The organism is ubiquitous, and systemic disease occurs almost exclusively in individuals whose resistance to infections is impaired. Diagnosis of invasive candidiasis is often delayed because of the high rate of false negative results on blood cultures, the lengthy period of time required for the identification of positive cultures and the aspecificity of positive findings on blood cultures. The most effective treatment is a combination of amphotericin B and 5-flucytosine. Treatment must be prolonged for 7 days after the first negative culture. Amphotericin B must be administered in doses of 0.5-1 mg/kg/day. Meningitis requires the intrathecal injection of amphotericin B in doses of 0.1 mg/kg/day. Amphotericin B does not induce resistance, and it is highly nephrotoxic, so that blood urea, electrolytes, serum creatinine and platelets must be monitored. 5-flucytosine is not very toxic it does induce resistance after prolonged use. The dose is 100-200 mg/kg/day given orally at 6-hour intervals.

Amphotericin B↗
PubMed1989

Effectiveness of steroid therapy in different stages of membranous nephropathy.

The published studies on histological staging and response to steroid therapy of membranous glomerulonephritis are not consistent. We analysed data from 25 adult patients with stage I (group 1, n = 7) and stage II (group 2, n = 18) disease. The interval between clinical onset and admission was similar in the two groups. At admission all patients had normal creatinine clearance; proteinuria averaged 5.4 +/- 4.0 in group 1 and 9.0 +/- 4.0 in group 2 (g/day per 100 ml GFR). All patients received 6 months steroid therapy (months 1-2, 1 mg/kg b.w. per day; month 3-5: 0.65 mg/kg b.w. e.o.d.; month 6, tapering). After this cycle of steroid therapy, proteinuria declined by 84% in group 1 (five patients being in partial remission, i.e. 0.4-2 g/day, and two patients in complete remission, i.e. less than or equal to 0.3 g/day) and by 47% in group 2 (two patients being in complete remission and six in partial remission). Only 1 patient in group 1 relapsed with nephrotic proteinuria after 36 months, and renal function was still normal in all patients at the most recent follow-up (59 +/- 32 months). In contrast, 14 patients in group 2 had nephrotic syndrome and seven renal insufficiency at the most recent follow-up. We conclude that short-term steroid therapy is effective only in patients with early membranous changes.

Adolescent↗
PubMed1986

Serum profiles of the regulatory complement proteins during the progression of renal damage in human glomerulonephritis.

Persistent activation of the complement system after escape from control by the regulatory proteins results in an excessive release of split products with inflammatory properties. Serum levels of the regulatory proteins of the complement system (Cl-INH, H, I and AT III) were assayed by the radial immunodiffusion technique in 521 serum samples from 124 patients with idiopathic chronic glomerulonephritis divided into two groups: 81 cases with normal renal function (NRF), and 43 cases with deteriorated renal function (DRF). Significant high mean levels of Cl-INH, H, I and AT III were found in patients with NRF, when they were compared with DRF patient groups. Positive correlations between the regulatory proteins and the corresponding complement components were found in patients with NRF, whereas they were reduced considerably in patients with DRF. Serial measurement of the control proteins showed a decay of the levels of Cl-INH, H and I in patients with progressive impairment of renal function. The presence of high levels of regulatory proteins suggest that a control mechanism may occur in patients with NRF; measurement of these proteins could, therefore, be of prognostic value, as the presence of high levels are indicative of a block of the complement system.

Antithrombin III↗
PubMed1985

Mechanism of impaired urinary concentration in chronic primary glomerulonephritis.

To define the role of medullary damage and the influence of solute load and blood pressure (BP) in impairing urinary concentration, patients with chronic glomerulonephritis were investigated by histological and functional studies. In 59 biopsy specimens, the degree of medullary fibrosis was correlated inversely with urinary specific gravity and was significantly greater in hypertensive than in normotensive subjects. The following clearance studies were carried out in patients with a GFR of 15 to 40 ml/min in maximal antidiuresis: (1) Eight patients were studied while receiving a high sodium and protein diet and then after 1 week of low sodium, low protein diet; (2) ten patients were loaded with hypertonic saline (3%) to increase urine volume up to 25 to 30% of GFR; (3) the concentrating ability was compared in 15 normotensives and 15 hypertensives with comparable GFR; (4) the concentrating ability was studied in nine hypertensive patients before and after drug-induced normalization of BP. In (1) no change occurred in maximal urine osmolality (UOsm) even if fractional sodium excretion and filtered load of urea were reduced. In (2), values of UOsm fell below those of plasma osmolality. In (3), UOsm and negative free-water generation were lower in hypertensive than in normotensive subjects. In (4), normalization of BP was not associated with any change in UOsm. These results indicate that osmotic diuresis does not play a critical role in reducing urinary concentration. This defect is better accounted for by an intrinsic medullary damage, enhanced in hypertensive patients, which may impair the permeability of collecting ducts to water.

Adolescent↗
PubMed1984

Role of plasma vasopressin in the impairment of water excretion in nephrotic syndrome.

To verify whether or not an increased secretion of ADH may cause the water retention commonly observed in nephrotic syndrome, 16 nephrotic patients and 13 normal control subjects were studied in basal conditions and following a water load or an iso-osmotic blood volume expansion by 20% albumin infusion. In the basal condition there were no differences in plasma ADH, urine output, urinary osmolality (UOsm), and plasma renin activity between nephrotic patients and control subjects; POsm, PNa+, UNaV, and blood volume (BV) instead, were significantly lower in nephrotic patients than in control subjects. Following the water load control subjects reached a minimal UOsm of 82 +/- 12 mOsm/kg at 60 min and excreted completely the ingested water in 150 min; nephrotic patients reached a minimal UOsm of 160 +/- 111 mOsm/kg at 120 min, and the water was eliminated completely in 240 min. Plasma ADH decreased significantly in the first hour following water load only in control subjects. A significant direct correlation was observed between plasma ADH and POsm in control subjects (ADH = -85 + 0.30 POsm, P less than 0.001) but not in nephrotic patients. Plasma ADH was inversely correlated with BV in nephrotic patients (ADH = 15.47 -0.17 BV, P less than 0.001) but not in normal control subjects. In nephrotic patients with reduced BV the expansion of BV with 20% albumin was effective in reducing the plasma levels of ADH and promoting a water diuresis. Our results demonstrate a sustained volume mediated secretion of ADH in the nephrotic syndrome, which is responsible for the impairment in water excretion.

Adolescent↗
PubMed1984

Mechanism of impaired urinary concentrating ability in normokalemic primary aldosteronism.

Renal clearance studies were performed during anti-diuresis (before and after hypertonic saline infusion) and during water diuresis in three hypertensive patients with normokalemic primary aldosteronism (NPA) and in matched patients with normoreninemic essential hypertension (EH). The NPA patients showed an impaired ability to concentrate urine. By progressively increasing Cosm with saline loading, TcH2O plateaued both in NPA and in EH patients; in the former, however, the plateau occurred earlier and was lower than in the latter. In water diuresis, absolute values of CH2O were higher in NPA due to increased distal delivery secondary to impairment in proximal tubular reabsorption. Fractional CH2O (i.e. the ratio between CH2O and distal sodium delivery), however, was lower in NPA than in EH patients. Both in antidiuresis (after saline loading) and in water diuresis the NPA patients exhibited an enhanced fractional excretion of sodium. In one of NPA patients, clearance studies were repeated after adrenalectomy. In this patient, normalization of BP and reduction of body weight were associated with a rise in Uosm and a reduction in Cosm in antidiuresis; Uosm and Cosm were restored to pre-surgical values by expanding extracellular fluid volume (ECV) with saline loading. In summary our results suggest that ECV expansion is the mechanism by which urine concentration is impaired in patients with NPA.

Adult↗
PubMed1983

Long-term follow-up of minoxidil therapy in refractory hypertension. A prospective trial in patients with various degrees of renal insufficiency.

Thirty patients with various degrees of renal insufficiency (4 on dialysis treatment) and severe hypertension refractory to conventional agents were treated with minoxidil and followed for up to 182 weeks. BP averaging 203 +/- 8.8/125 +/- 4.1 mm Hg supine and 194 +/- 7.8/125 +/- 3.9 upright before treatment, fell to 155 +/- 6.2/92 +/- 3.4 and 146 +/- 6.3/92 +/- 3.2 respectively within 1 week with 5 to 30 mg daily of minoxidil and remained stabilized around these normal values for three years or more. However, increasing doses of the drug became necessary after 52 weeks of therapy. Serum creatinine increased slightly during long-term treatment in most patients suggesting that the fall in renal function with time should be attributed to the natural progression of normotensive chronic renal failure. Adequate dialysis (in the 4 dialyzed patients) and high-ceiling diuretics prevented fluid imbalance during minoxidil therapy, while beta-blocking agents allowed complete control of reflex tachycardia.

Adolescent↗