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G de Arriba

Publications and source records attributed to G de Arriba.

At least 19 recordsLinked to original sources
PubMed2004

[Minimal changes nephrotic syndrome associated to penicillamine treatment].

We describe three patients with minimal change nephrotic syndrome associated with penicillamine treatment. Two patients had systemic sclerosis and one had rheumatoid arthritis. Cumulative dose of D-penicillamine was similar in all cases, and nephrotic syndrome appeared after 15-33 months of treatment. The drug was stopped and nephrotic syndrome disappeared in 2-4 months, suggesting a possible causal relationship between penicillamine and minimal change disease.

Adult↗
PubMed2003

Antioxidant nutrients protect against cyclosporine A nephrotoxicity.

The immunosuppressive drug cyclosporine A (CsA) has been successfully used in several diseases with immunological basis and in transplant patients. Nephrotoxicity is the main secondary effect of CsA treatment. Although the mechanisms of nephrotoxitity are not completely defined, there is evidence that suggests the role of reactive oxygen species (ROS) in its pathogenesis. It has been demonstrated in numerous in vivo and in vitro experiments that CsA induced renal failure and increased the synthesis of ROS, thromboxane (TX) and lipid peroxidation products in the kidney. Furthermore, CsA modified the expression and activity of several renal enzymes (ciclooxygenase, superoxide-dismutase, catalase and glutathione-peroxidase). Antioxidant nutrients (e.g. Vitamins E and C) can neutralize some of the effects that CsA produced in the kidney. Thus, Vit E inhibited the synthesis of ROS and TX and the lipid peroxidation process induced by CsA in kidney structures. Antioxidants can also improve renal function and histological damage produced by CsA administration. Although there are few data in humans treated with CsA, the possibility exists that antioxidants can also neutralize CsA nephrotoxicity and LDL oxidation. Thus, antioxidant nutrients could have a therapeutic role in transplant patients treated with CsA.

Animals↗
PubMed1998

Cyclosporine increases local glomerular synthesis of reactive oxygen species in rats: effect of vitamin E on cyclosporine nephrotoxicity.

BACKGROUND: We report an investigation of the effects of cyclosporine (CsA) on kidney function, the glomerular synthesis of reactive oxygen species, the peroxidation of lipids, and the levels of thromboxane B2 (TXB2). The effect of the simultaneous administration of the antioxidant vitamin E (Vit E) and CsA in rats was also evaluated. METHODS: Adult male Wistar rats were treated for 30 days with CsA (30 mg/kg/day), with Vit E (0.05 mg/ml), with CsA plus Vit E, or with the vehicle used for administration of CsA, namely 12.6% ethanol. RESULTS: CsA induced kidney failure and increased the glomerular synthesis of superoxide anion, H2O2, malonyldialdehyde, and TXB2. Vit E minimized the adverse effects of CsA on kidney function and the glomerular synthesis of these compounds. CONCLUSIONS: Our results suggest that the acute decrease in glomerular filtration rate induced by CsA might be mediated by the synthesis of reactive oxygen species and subsequent peroxidation of lipids, which increases the levels of TXB2. Treatment with Vit E prevented these effects, suggesting a possible role for antioxidants in the prevention of CsA nephrotoxicity.

Animals↗
PubMed1998

Cyclosporine A nephrotoxicity: role of thromboxane and reactive oxygen species.

The main adverse effect of cyclosporine A (CyA) is nephrotoxicity. CyA increases urinary concentrations of thromboxane A2 (TXA2), a potent vasoconstrictor that can be involved in kidney failure induced by CyA. Furthermore, it has been postulated that a relationship exists between oxygen free radicals and the synthesis of arachidonate metabolites in experimental models of CyA nephrotoxicity. We studied the effect of vitamin E (VitE), an oxygen free radical scavenger, on renal function, on glomerular synthesis of thromboxane B2 (TXB2), and on free radicals in rats treated with CyA. Four groups of male Wistar rats were studied: (1) a control group; (2) a group given VitE at 0.05 mg/dl in drinking water for 25 days; (3) a group given CyA at 50 mg/kg body weight/day orally for 10 days; and (3) a group given Vit E + CyA, in which rats were provided with drinking water containing VitE for 15 days and afterwards were treated with VitE and CyA for 10 days. Renal function parameters and glomerular synthesis of TXB2, superoxide anion (02.-), malondialdehyde (MDA), and hydrogen peroxide (H202) were evaluated. CyA decreased body weight, caused deterioration of kidney function and increased glomerular synthesis of TXB2, O2.-, MDA, and H202. Pretreatment with VitE prevented the effects of CyA on kidney function and decreased glomerular synthesis of these mediators. In conclusion, CyA induced glomerular synthesis of reactive oxygen species (ROS) and TxB2. Pretreatment with VitE inhibited acute renal failure induced by CyA, probably by scavenging free radicals and by inhibiting the synthesis of TXB2.

Animals↗
PubMed1998

Cyclosporin A-induced hydrogen peroxide synthesis by cultured human mesangial cells is blocked by exogenous antioxidants.

Cyclosporin A (CsA) is the immunosupressor most widely used in transplanted patients for preventing organ rejection, but it has some toxic side effects in vascular beds and kidney. The purpose of this work was to study if H2O2, a reactive oxygen species, is involved in the CsA-induced toxic effects on kidney in vitro. Human mesangial cells (HMC) in culture were incubated in presence of CsA (10[-5]-10[-8]M) and H2O2 was measured by flow cytometry. The specificity of the probe used in this method was demonstrated as fluorescence was not detected when superoxide anion generated through a Xanthine-Xanthine oxidase system was present, but fluorescence was noted when H2O2 was present in the incubation medium, both directly and after addition of superoxide dismutase to the medium thus promoting H2O2 synthesis. CsA induced a significant dose and time-response increased H2O2 synthesis by cultured HMC. This increase appeared 5 min after CsA addition, being maximal between 15-45 min at CsA concentration of 10(-7)M. When HMC were preincubated with antioxidants as vitamin E or selenium, the CsA-induced H2O2 production was partially blocked. In addition, selenium also induced an increased activity of glutathion peroxidase in HMC after 24 hours of incubation, suggesting that it exerted its H2O2 scavenging action through the modulation of the activity of this enzyme.

Antioxidants↗
PubMed1990

[Treatment of anemia with recombinant human erythropoietin and the bone marrow response in uremic patients undergoing periodic hemodialysis].

Treatment of anemia with human recombinant erythropoietin (EPO-R) and its effect on bone marrow was studied in 10 anemic patients on periodic hemodialysis (HD). Blood transfusion was not required once treatment started. Hemoglobin (Hb) levels normalized at six months in all patients (7.2 +/- 0.2 vs 12.4 +/- 3 g/dl, p less than 0.01). Serum ferritin levels decreased progressively as Hb increased (r = -0.5609), and six patients needed iron supplement since the third month. Bone marrow iron deposits decreased significantly (p less than 0.001), together with an increase of cellularity and improvement of erythrodysplasia. EPO-R was associated with worsening hypertension in previously hypertensive patients, although it could be controlled with more aggressive treatment. Thrombotic events either systemic or at the vascular access, were not observed. EPO-R corrects the anemia in uremic patients undergoing HD. Iron stores and blood pressure in hypertensive patients on treatment with EPO-R must be monitored regularly.

Adult↗
PubMed1989

[Prolactin response to acute administration of growth hormone releasing hormone in patients with uremia].

The Growth Hormone Releasing Hormone (GH-RH) constitutes the most potent and specific stimulus for Growth Hormone secretion. Nevertheless, in some pathologic situations a Prolactin (PRL) response to GH-RH stimulus is also observed. In order to evaluate the possible effect of GH-RH over seric levels of PRL in uremic patients we carried out a study in a group of ten male patients on hemodialysis (HD), who were given an acute stimulus of GH-RH (an IV 50 mcg. bolus) immediately before and after the HD session, with blood extractions at times -15, 0, 15, 30, 45, 60, and 90 minutes for PRL determinations. The same procedure was carried out in 8 healthy controls. Basal PRL levels in the HD group (14 +/- 3.2 micrograms/L) were significantly greater (p less than 0.01) than control group (3.8 +/- 1.4 micrograms/L). There was no PRL response to GH-RH either in uremic patients before or after HD or in healthy controls. Our results show that there is a significant increase in PRL levels in uremic patients both before and after dialysis with a GH-RH response comparable to healthy subjects.

Adult↗
PubMed1988

Atrial natriuretic peptide inhibits angiotensin II-induced contraction of isolated glomeruli and cultured glomerular mesangial cells of rats: the role of calcium.

We examined the contractile effect of angiotensin II on isolated rat glomeruli and cultured glomerular mesangial cells, as well as the possible involvement of calcium in this contraction. In addition, the effect of rat atrial natriuretic peptide (ANP) on angiotensin II-induced contraction was studied. Computer-assisted image analysis was used to measure glomerular cross-sectional area and planar mesangial cell surface area in several experimental conditions. Angiotensin II induced a decrease in glomerular cross-sectional area and planar mesangial cell surface area that was both time and dose dependent. This effect was partially blocked by preincubation with verapamil or TMB-8, the latter compound being more effective. Incubation with ANP prevented angiotensin II-induced reduction of glomerular cross-sectional area and planar mesangial cell surface area and reversed contraction in mesangial cells. Incubation with TMB-8 impaired the effect of ANP. These data suggest that angiotensin II could exert part of its physiologic effects in the kidney through calcium-dependent mesangial and glomerular contraction. ANP inhibited this contraction, possibly explaining some of its renal effects.

Angiotensin II↗
PubMed1987

Adenosine induces a calcium-dependent glomerular contraction.

Glomeruli isolated from rat kidney cortex were incubated with adenosine in the presence or absence of verapamil and calcium and their change in cross-sectional area was recorded. Adenosine induced a 10% decrease in glomerular cross-sectional area. This decrease was blocked by verapamil or a calcium-free medium. The results suggest that the effect of adenosine in the kidney could be due to glomerular constriction, and that this constriction depends on the entry of calcium into glomerular cells.

Adenosine↗
PubMed1987

Changes in glomerular cross-sectional area induced by platelet activating factor.

Isolated glomeruli from normal rats were incubated with platelet-activating factor 10(-6) M at variable incubation times (8, 15, 30 and 45 min) and with different concentrations (0 to 10(-6) M) for 20 min. In addition, the platelet-activating factor effect (10(-6) or 10(-8) M, 20 min) was tested in the presence of BN-52021 (10 or 50 micrograms/ml), verapamil (10(-5) M), acetylsalicylate of lysine (10(-3) M), and in a free-calcium media with EGTA 2 mM. Glomerular microphotographs were taken before and 20 min after adding the substances, and glomerular cross-sectional area was measured using a computerised technique. Platelet-activating factor induced a significant time-dependent reduction in glomerular cross-sectional area, from a concentration of 10(-8) M. BN-52021, verapamil, and the free-calcium media inhibited platelet-activating factor-induced reduction of glomerular cross-sectional area, but acetylsalicylate of lysine did not. Platelet-activating factor-induced reduction in glomerular cross-sectional area seems to be dependent on the interaction of platelet-activating factor with a specific glomerular receptor, with a subsequent modification of the intracellular concentration of calcium. Arachidonic acid metabolites from the cyclo-oxygenase pathway do not seem to be involved in these phenomena. Results suggest that platelet-activating factor could modulate glomerular filtration rate not only by inducing changes in systemic or intrarenal haemodynamics, but also by modifying the filtration surface, thus reducing the Kf.

Animals↗