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M Sabbatini

Publications and source records attributed to M Sabbatini.

At least 73 records · Page 4Linked to original sources
PubMed1990

Absence of acute nephrotoxicity with low doses of cyclosporin: experimental study in the rat.

No study has, to our knowledge, evaluated the acute effects of low immunosuppressive doses of cyclosporin (CsA) on renal function. To establish whether a relationship exists between the dosage of CsA and the onset of nephrotoxicity, 28 rats were studied by renal clearances before (control) and after i.v. administration of different doses of CsA: 3 mg/kg b.w. (group 1); 7 mg/kg b.w. (group 2); 11 mg/kg b.w. (group 3); 15 mg/kg b.w. (group 4). No change in renal function was observed between control and the post-CsA period in groups 1 and 2. GFR (inulin clearance) was decreased vs the control period in group 3 and group 4 (-22% and -37%, respectively, P less than 0.001); the difference between these two groups was statistically significant (P less than 0.01). Effective renal plasma flow (PAH clearance) was similarly decreased in groups 3 and 4 vs their control periods (-21% and -28%, respectively, P less than 0.001) due to the increase of total renal vascular resistance (+41% and +42%, respectively, P less than 0.001). Filtration fraction was significantly decreased by CsA in group 4 (P less than 0.01 vs the control period). PAH renal extraction, urinary volume, and sodium and potassium excretion were similar in all groups before and after CsA. PRA and ADH were significantly increased only in group 4 (P less than 0.01) vs the baseline values. A high and significant relationship was detected between CsA dosage and the decrease of GFR (r = 0.81, P less than 0.001) and RPF (r = 0.612, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1989

Acute cyclosporine renal dysfunction reversed by dopamine infusion in healthy subjects.

Up to now, no studies have been performed in normal humans to investigate the role of renal hemodynamic abnormalities in relation to acute-cyclosporin A (CsA) renal dysfunction and to verify whether the specific renal vasodilator, dopamine, can counteract these abnormalities. Eight normal subjects were examined both (A) after oral CsA (12 mg/kg body wt) and (B) after oral CsA + dopamine infusion (2 mg/kg body wt/min), under water diuresis. Both in protocols A and in B, four basal renal clearances were performed before CsA and every twenty minutes for four hours after CsA administration. In protocol A, after CsA, inulin (GFR) and PAH clearance (RPF) fell by up to 27% and to 41%, respectively, so that filtration fraction (FF) increased (P less than 0.01). A slight (not significant) hypertension occurred while renal resistances were markedly raised (P less than 0.001). Fractional urine and Na+ excretion as well as CH2O decreased, while UOsm increased (P less than 0.01). In protocol B, dopamine was infused from 120 to 180 minutes after CsA (that is, when the maximal adverse effects of CsA on renal hemodynamics had been observed in A). Dopamine infusion could reverse completely the effects of CsA on RPF, GFR, fractional urine output and CH2O; only UOsm remained higher than normal in conclusion with an increased fractional excretion of sodium (P less than 0.01). No changes were observed in plasma renin activity, aldosterone and in urinary epinephrine and norepinephrine excretion both in protocols.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Reversibility of acute cyclosporin nephrotoxicity by dopamine. Micropuncture study in the rat.

The ability of dopamine to neutralise the effects acutely induced by cyclosporin (CsA) on glomerular dynamics was evaluated in four groups of female Munich-Wistar rats, prepared for micropuncture: group I (n = 9), normal rats receiving saline as placebo; group II (n = 10), rats treated with CsA (20 mg/kg b.w. in 1 h); group III (n = 8) rats treated with CsA, as in group II, and then with vasodilating doses of dopamine (1.2-2.0 micrograms/100 g b.w./min in continuous intravenous infusion); group IV (n = 7), rats administered Cremophore EL, the vehicle of CsA, in corresponding doses. Single nephron GFR (SNGFR), glomerular plasma flow (GPF), afferent and efferent arteriole resistances (Ra and Re, respectively), SN filtration fraction (SNFF), ultrafiltration coefficient (Kf) were measured. Body weight, blood pressure and haematocrit were similar in the four groups. GFR was significantly reduced in group II (0.83 +/- 0.08 ml/min vs 1.29 +/- 0.01 in group I, 1.46 +/- 0.25 in group III, and 1.40 +/- 0.09 in group IV, P less than 0.05 vs all the groups), while no statistical difference was detected in urinary volume. SNGFR was significantly reduced in group II vs group I (18.7 +/- 1.8 nl/min vs 30.6 +/- 1.3, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Glomerular dynamics and salt balance in pregnant rats with renal hypertension.

These studies were aimed at investigating whether chronic hypertension in pregnancy causes changes both in salt excretion (NaE) and in glomerular hemodynamics. Metabolic and renal micropuncture studies were performed in pregnant (P) and Virgin (V) Munich-Wistar rats with normal blood pressure (N) and two-kidney Goldblatt hypertension (H). Mean NaE was higher in PN than VN (2.7 vs. 1.7 meq/day, P less than 0.01). Hypertension raised NaE both in P and V rats: in P and V rats with "benign" hypertension (blood pressure less than 180 mmHg) NaE averaged 3.2 and 2.6 meq/day, respectively (P less than 0.05); mean NaE was 5.9 and 3.8 meq/day, respectively (P less than 0.01), in P and V rats with "malignant" hypertension (blood pressure greater than or equal to 180 mmHg). Afferent arteriole resistance (Ra) averaged 1.73 and 3.50 10 dyn.s-1.cm5 in PN and VN, respectively (P less than 0.01). Hypertension raised Ra in V, but not in P rats (4.47 vs. 2.14 10 dyn.s-1.cm5, P less than 0.01). Thus glomerular plasma flow, glomerular capillary hydrostatic pressure, and single-nephron glomerular filtration rate were markedly higher in PH than VH rats: in PH rats single-nephron filtration fraction was significantly lower than in VH. These results show that in PH rats a marked rise in NaE is associated with glomerular vasodilation.

Animals↗
PubMed1988

Effects of furosemide therapy on free-water excretion in uremic patients.

To assess the intrinsic effects of treatment with furosemide on free-water excretion in patients with chronic renal failure, two groups of patients with and without replacement of diuretic-induced salt losses have been studied. Furosemide therapy was administered for 1 week during constant sodium intake (100 mEq/day). In neither of the groups did furosemide cause hyponatremia, while it did decrease the urine to plasma osmolality ratio, an effect lasting even when the diuretic effect was exhausted. During water diuresis, furosemide decreased the fractional sodium reabsorption in diluting segments but not the absolute rate of the free-water generation (CH2O). Presumably the expected decrease of CH2O was masked by the increased distal delivery of tubular fluid mainly due to an additional effect of the diuretic on the proximal tubule. The hypotonicity of urine after furosemide treatment may be secondary to the dissipation of medullary hypertonicity, caused by furosemide, in the condition of decreased water permeability of the collecting duct due to uremic disease.

Furosemide↗
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↗
PubMed1985

Mechanism of increased plasma urea after diuretic therapy in uraemic patients.

To clarify why diuretic therapy raises plasma urea in patients with chronic renal failure, three groups of uraemic subjects were treated with frusemide for 6 days. In group 1 (n = 9), frusemide significantly decreased body weight and increased average plasma urea from 18.7 mmol/l to 28.8 mmol/l (P less than 0.001). this rise in plasma urea was secondary to reduced urea excretion, which occurred in spite of an increase in urea filtration. In group 2 (n = 7), frusemide was associated with salt replacement, in order to prevent salt depletion; in these patients neither reduction in urea excretion nor increase in plasma urea occurred. In group 3 (n = 10), the marked diuretic-induced fall in urea clearance was found to be independent of enhanced proximal tubular reabsorption (measured in water diuresis). These results show that the rise in plasma urea is due to increased tubular reabsorption of urea, presumably in the distal part of the nephron, secondary to extracellular fluid (ECF) volume depletion.

Body Weight↗
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

A modified Payne technique with a personal antireflux valvular system in the surgical treatment of morbid obesity.

Reflux into the blind loop in end-to-side jejuno-ileal bypass is commonly considered the cause of weight loss failure, but the lower morbidity and mortality suggest that this procedure should be preferred to end-to-end bypass in the surgical treatment of morbid obesity, with the proper technical modifications to prevent the reflux. An antireflux single or double valvular system created 3-6 cm proximally to the anastomosis, with few introverting seroserous stitches, parallel and perpendicular to the ileal axis, is reported. This technique, as compared to others, is not time consuming, is easily feasible and does not interfere with the blind loop down-flow. Comparative clinical data and x-ray controls demonstrated the value of this procedure which is able to give excellent results in cases where other procedures (gastric operations, bilio-intestinal, bilio-pancreatic bypass etc.), are contraindicated.

Barium Sulfate↗
PubMed1983

Renal function in pregnant rats with two-kidney goldblatt hypertension.

This study was carried out in female Wistar-Münich rats with two-kidney, one-clip hypertension, using clipped normotensive rats as controls. Metabolic studies were performed in the first two weeks of pregnancy, consisting of daily measurement of systolic blood pressure (BP) (tail-cuff), body weight (BW), and salt and water balance. At the end of metabolic studies, glomerular dynamics were studied in the unclipped kidney by micropuncture. During pregnancy, urinary output of Na+ and water was greater in hypertensive than normotensive rats. The greater natriuresis accounted for a reduced Na+ retention and a lower increase in maternal BW. Micropuncture studies showed an impaired renal auto-regulation. These results show that hypertension in pregnancy causes a salt-losing tendency, that may be secondary to incomplete renal autoregulation.

Animals↗
PubMed1982

Effects of pregnancy on glomerular dynamics: micropuncture study in the rat.

Glomerular dynamics were investigated by micropuncture in 15-day pregnant Munich-Wistar rats. Female non-pregnant rats were used as control. In hydropenia, single nephron glomerular filtration rate (SNGFR) averaged 37.2 nl/min/g kidney weight in pregnant rats, and 26.2 nl/min/g kidney weight in controls (P less than 0.0005). During pregnancy, mean glomerular plasma flow (GPF) rose from 63.0 to 104.5 nl/min (P less than 0.0005), and glomerular capillary hydrostatic pressure (PG) from 44.8 to 50.6 mm Hg (P less than 0.0005). This rise in PG accounted for an increase in effective filtration pressure (EFP). Mean EFP at the efferent end of the glomerulus rose from near zero to 9.7 mm Hg, indicating filtration pressure disequilibrium. After extracellular fluid volume expansion with saline, GPF and EFP were still greater during pregnancy. A filtration pressure disequilibrium occurred also in non-pregnant rats, allowing calculation of definite values of the ultrafiltration coefficient (Kf). During pregnancy, mean Kf was reduced from 0.0332 to 0.0285 nl/(sec X mm Hg) (P less than 0.005). SNGFR was moderately, but not significantly, increased. These results show that during pregnancy glomerular dynamics is characterized by a rise in GPF and EFP, and by a reduction in Kf. Following these changes, a plasma-flow dependent rise in SNGFR occurs in hydropenia. After expansion, instead, SNGFR is unmodified because the dependence of ultrafiltration on plasma-flow declines while the influence of Kf increases at high values of GPF.

Animals↗