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J L Monteiro

Publications and source records attributed to J L Monteiro.

12 recordsLinked to original sources
PubMed1997

L-Arginine and allopurinol protect against cyclosporine nephrotoxicity.

The role of nitric oxide (NO) and oxygen free radicals in cyclosporine (CsA) nephrotoxicity was investigated using L-arginine, an NO substrate, and allopurinol, a xanthine oxidase inhibitor (involved in the formation of oxygen radicals) in an experimental model with Wistar rats. CsA, administered at 15 mg/kg/body weight (BW) subcutaneously for 10 days, caused a decrease in glomerular filtration rate, with inulin clearance of 0.33+/-0.04 vs. 1.11+/-0.06 ml/min/100 g BW (P<0.01 vs. control). L-Arginine, 1.5% in drinking water 5 days before and during CsA administration, partially protected the animals against this fall in glomerular filtration rate, with inulin clearance of 0.68+/-0.03 ml/min/100 g BW (P<0.01 vs. CsA). Allopurinol, at 10 mg/kg/BW by gavage, also had a protective action, with inulin clearance of 0.54+/-0.04 ml/min/100 g (P<0.01 vs. CsA). CsA caused an elevation in NO production, as assessed by urinary excretion of its metabolites, nitrite and nitrate (NO2 and NO3; 0.836+/-0.358 vs. 0.107+/-0.019 nmol/microg creatinine). NO production was as much as threefold higher in the L-arginine group (1.853+/-0.206 nmol/g creatinine). This CsA effect is probably related to its vasoconstrictive stimulus. Supplementation with L-arginine, which provides more substrate for NO formation, may enhance vasodilatation and consequently reduce the impairment of renal function. The protection provided by allopurinol may be related to the reduced formation of oxygen radicals, preventing the deleterious effects of lipid peroxidation.

Allopurinol↗
PubMed1994

Effect of amphotericin B on water and urea transport in the inner medullary collecting duct.

The clinical usefulness of amphotericin B (AMP-B) is limited by its nephrotoxicity, as characterized by decreased RPF, decreased GFR, impaired urinary acidification, and potassium excretion defects. Defects of renal concentrating ability have been noted, but the mechanisms responsible for them have not been investigated. The chief objective of this research was to analyze directly the effect of AMP-B on arginine-vasopressin (AVP)- or dibutyrl cAMP (DcAMP)-stimulated water and urea transport of the inner medullary collecting duct (IMCD) obtained from rats by the in vitro microperfusion technique. AMP-B (10(-5) M) added to the bath fluid in the absence of AVP did not impair the hydraulic conductivity (Lp) and the urea permeability (Pu) of rat IMCD. AMP-B (10(-5) M) added to the bath fluid decreased the AVP-stimulated Lp (x 10(-6) cm/s.atm) of rat IMCD from 19.41 +/- 2.19 to 10.00 +/- 1.39 (P < 0.001), and the reversibility of its action was observed during a third period when Lp increased to 19.80 +/- 2.19 (P < 0.001) after the initial conditions were restored. In addition, AMP-B reduced DcAMP-stimulated Lp from 20.95 +/- 1.75 to 10.52 +/- 0.71 (P < 0.01) in a reversible manner when the drug was withdrawn from the bath. AMP-B also decreased AVP-stimulated Pu (x 10(-5) cm/s) when added to the bath fluid from 36.60 +/- 2.05 to 29.88 +/- 1.36 (P < 0.001), and this effect was reversible after AMP-B was withdrawn from the bath (37.40 +/- 1.36; P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Amphotericin B↗
PubMed1989

Effect of potassium depletion on ischemic renal failure.

The present study was carried out to examine the effect of potassium depletion in rat kidneys subjected to a temporary ischemic event produced by clamping of left renal artery. The postischemic kidneys of rats on a normal diet with adequate potassium intake showed an increase in H2O, Na and K excretion, with no change in inulin clearance whereas significant differences were found in potassium-deprived rats. Potassium depletion was brought about by dietary K deprivation for 10 days. K-depleted rats (serum K = 2.5 +/- 0.1 mEq/l) had a decrease in inulin clearance of the postischemic kidney from 1.01 +/- 0.10 to 0.43 +/- 0.05 ml/min (p less than 0.01), and a greater increase in fractional excretion of H2O, Na and K when compared to normal rats. The postischemic kidney from both normal and hypokalemic rats showed a decrease in Na-K-ATPase of the inner stripe of the outer medulla. These data indicate that short-term ischemia produces polyuria, increases natriuresis and kaliuresis, associated, at least in part, with a decrease in Na-K-ATPase in the inner stripe of the outer medulla (probably the thick ascending limb of Henle) and that K depletion potentiates ischemic renal failure.

Acute Kidney Injury↗
PubMedDate not supplied

[Renal regulation of sodium excretion in experimental heart failure: study of hemodynamics and renal tubular function].

This study was designed to evaluate the role of the kidney on sodium retention in congestive heart failure by clearance and hemodynamic studies. Twenty seven dogs were studied during hydropenia and aqueous diuresis 96 hours after the construction of a bilateral femoral A-V fistula, in 3 periods: 1) with open fistulae; 2) with closed fistulae and 3) with reopened fistulae. The animals retained sodium and water and developed edema during the first period when the fistulae were opened. Closure of the AV fistulae produced an enhanced diuresis and natriuresis associated with an increase in phosphaturia and distal sodium delivery, suggesting a diminished proximal sodium reabsorption. However, when the fistulae were reopened, sodium retention was observed in the presence of an increase in free-water clearance corrected by distal sodium delivery, indicating an increase in sodium reabsorption by distal segments. These findings were not associated with alterations in cortical distribution of renal blood flow. In conclusion, the sodium and water retention in congestive heart failure produced by A-V fistula is due to an increase in sodium reabsorption by the distal nephron segments, and it is not associated to a redistribution of the cortical renal blood flow.

Animals↗
PubMedDate not supplied

[Acute nephrotoxicity caused by amphotericin B in the dog].

Amphotericin-B is the drug of choice for the treatment of serious systemic fungal infections. The major limitation for the use of this drug is its potential nephrotoxicity. The chronic and acute administration causes both a reduction of renal blood flow and glomerular filtration rate, determining a fall of renal concentrating ability. Our study was designed to determine the acute effects of Amphotericin-B on dogs renal function, during hydropenia and water diuresis. In addition a hemodynamic study, with the measurement of intrarenal blood flow by the microsphere method was performed. The hydropenic dogs received the drug directly into the left renal artery. There was a significant decrease in creatinine clearance, urinary osmolality, and urinary solute excretion, in the left kidney only. Amphotericin-B was infused into the aorta above the renal arteries in the group in which the water diuresis was induced. This acute infusion produced intense fall in creatinine clearance and in the free water formation, as well as in absolute excretion of sodium. The hemodynamic study showed that the reduction of creatinine clearance may be due to the decrease in renal blood flow, and the alterations in the urinary excretion of water and sodium could not be correlated with the distribution of cortical blood flow to the deep nephrons. These findings suggest that the effects of Amphotericin-B may be attributed, at least in part, to its ischemic action.

Amphotericin B↗