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J Uribarri

Publications and source records attributed to J Uribarri.

At least 55 records · Page 3Linked to original sources
PubMed1990

Prevention of myelinolysis in rats by dexamethasone or colchicine.

The purpose of the present investigation was to determine whether dexamethasone, an agent known to preserve the blood-brain barrier, and colchicine, an agent that impairs mobilization of macrophages, can prevent demyelinating lesions associated with rapid correction of hyponatremia in the experimental animal. Hyponatremia was induced in rats with Pitressin and water. After 4 days hyponatremic rats received hypertonic saline alone or hypertonic saline plus dexamethasone or colchicine. All of the 9 rats that received only 5% NaCl developed demyelinating disease, while 3 of 6 rats treated with dexamethasone and 5 of 15 rats treated with colchicine showed no CNS abnormality. The results of our investigation might help understand the pathogenetic mechanism of central pontine myelinolysis in humans, a disease attributed to rapid correction of hyponatremia.

Animals↗
PubMed1989

The first kidney stone.

The proper approach to diagnosis and management in patients with a first episode of a calcium-containing kidney stone is controversial, and we have reviewed the literature in a search for objective information. Six large retrospective studies show the "natural cumulative recurrence rate of renal stones" to be 14% at 1 year, 35% at 5 years, and 52% at 10 years. Randomized studies of the use of either thiazides or allopurinol suggest a modest beneficial effect of about 35% over placebo. Considering that the risk of this specific therapy is about 5%, the morbidity associated with renal stones is limited, and relatively less invasive procedures can often replace nephrolithotomy, we conclude that use of specific drug therapy, namely thiazides or allopurinol, is not warranted in patients with a first kidney stone and, therefore, that extensive metabolic evaluation is unnecessary.

Allopurinol↗
PubMed1989

Danger of central pontine myelinolysis in hypotonic dehydration and recommendation for treatment.

Isotonic saline is the fluid most commonly used for treatment of asymptomatic hypotonic dehydration, but as shown in the case presented in this article, rapid increase in serum sodium may follow administration of isotonic saline, leading to the development of central pontine myelinolysis (CPM). Because the necessity of rapid correction is less, whereas the risk of CPM is greater with chronic asymptomatic hyponatremia than with acute hyponatremia, use of a half normal saline might be more appropriate than normal saline for treating certain patients with hypotonic dehydration with asymptomatic hyponatremia. The calculations indicate that half normal saline will expand the extracellular volume quite effectively, but the rate of increase in serum sodium will be considerably slower than that with normal saline.

Dehydration↗
PubMed1986

Acidosis-induced osteomalacia: metabolic studies and skeletal histomorphometry.

The pathogenesis of osteomalacia was investigated in three patients with chronic metabolic acidosis. Serum levels of parathyroid hormone and vitamin D metabolites were measured, and bone biopsy specimens were analyzed after double tetracycline labeling. Parathyroid hormone concentrations were normal in patients 1 and 3 and slightly elevated in patient 2. Vitamin D metabolism was undisturbed. Static indicators of bone remodeling substantiated the diagnosis of osteomalacia in each case. In patient 1 fluorescent microscopy revealed no evidence of tetracycline uptake. In patients 2 and 3 active mineralization was evident at all osteoid seams, but because double labels were rare, the mineral apposition rate appears to have been substantially reduced in most bone-forming units. Our results indicate that acidosis-induced osteomalacia, unlike that due to vitamin D deficiency, may be associated with mineral deposition at every possible site. Nevertheless, like other causes of osteomalacia, metabolic acidosis prevents mineral apposition at a normal rate even if mineral deposition is ubiquitous. We suggest that titration of newly deposited phosphate causes the observed impairment of mineral apposition and ultimately leads to osteomalacia.

Acidosis↗
PubMed1985

Metabolic utilization and renal handling of D-lactate in men.

This study was carried out to investigate the renal handling of d- and l-lactate and the extent of their metabolism in men. Ten healthy male subjects were given an intravenous (IV) infusion of a racemic mixture of d- and l-lactate. At an infusion rate of 1.0 to 1.3 meq/kg body weight of each isomer, d-lactate achieved a concentration in plasma of 1.7 to 3.0 meq/L, and l-lactate 2.8 to 4.2 meq/L. At these levels, fractional excretion of d-lactate ranged from 40% to 65%, while fractional excretion of l-lactate was always less than 5%. At a higher infusion rate, 1.8 to 2.0 meq/kg/h, plasma concentrations of d- and l-lactate reached 4.5 to 6.0 meq/L, and 4.0 to 6.7 meq/L, respectively. Fractional excretion of d-lactate then ranged from 61% to 100%, while that of l-lactate ranged from 9% to 30%. At plasma concentrations of d-lactate less than 3.0 meq/L, reabsorption of l-lactate was nearly complete, but when plasma d-lactate exceeded 3.0 meq/L, reabsorption of l-lactate was considerably impaired. Similarly, for a given concentration of plasma d-lactate, its reabsorption was more efficient when the plasma l-lactate concentration and fractional excretion of l-lactate were low than when they were high. At an infusion rate of d-lactate of 1.0 to 1.3 meq/L, about 90% of the infused lactate was metabolized, and at a higher infusion rate, still more than 75% of the infused lactate was metabolized.(ABSTRACT TRUNCATED AT 250 WORDS)

Creatinine↗
PubMed1985

A mechanism of hypoxemia during hemodialysis. Consumption of CO2 in metabolism of acetate.

The present study is an investigation of the role of acetate metabolism in dialysis-induced hypoxemia and of the relative roles of acetate metabolism, bicarbonate loss, and CO2 gas (g) loss in causation of hypoxemia. The loss of CO2 (g) measured in 23 patients during acetate dialysis was found to be negligible (0.21 +/- 0.01 mmol/min). The HCO-3 loss was substantial (3.4 +/- 0.5 mmol/min), but its predicted effect on dialysis hypoxemia was modest. The infusion of acetate at 4 mmol/min into 6 normal volunteers decreased the respiratory exchange ratio (R) from 0.83 +/- 0.06 to 0.71 +/- 0.06 with constant O2 consumption (VO2) and reduced net CO2 production (VCO2). In another experiment, the infusion of sodium acetate into 9 normal volunteers resulted in a similar reduction in R (from 0.82 +/- 0.04 to 0.71 +/- 0.04) and arterial pO2 (from 92.3 +/- 1.1 to 78.3 +/- 1.7 mm Hg). The results indicate that acetate metabolism can lead to reduction in R and hypoxemia and suggest that the same mechanism is responsible for hypoxemia during hemodialysis using acetate dialysate.

Acetates↗
PubMed1985

Bartter's syndrome due to a defect in salt reabsorption in the distal convoluted tubule.

Bartter's syndrome is generally attributed to a primary defect in salt reabsorption either in the ascending limb of Henle's loop or in the proximal tubule. 2 siblings presented here have all the clinical and biochemical features of Bartter's syndrome but seem to have defective salt reabsorption in the distal convoluted tubule. A surreptitious use of diuretics was ruled out. Free water clearance was reduced in both patients and also was low after the addition of furosemide when compared with controls. Urine osmolalities following overnight dehydration were 883 and 1,000 mosm/l. The reduced maximal free water clearance argues against a proximal defect, and the normal urine concentration against a Henle's loop defect. Low free water clearance after furosemide suggests a defect in the distal convoluted tubule.

Absorption↗
PubMed1985

Minoxidil in a once-a-day step-3 antihypertensive program.

Convenience of medicine-taking and lack of side effects are two major factors that favor compliance. Using a simple and convenient once-a-day regimen of minoxidil, nadolol, and chlorthalidone, we treated successfully 30 patients with moderate to severe hypertension. All patients were previously taking at least three medications, usually three to four times a day. Treatment was started with nadolol (160 mg) and chlorthalidone (50 mg) once daily. If diastolic blood pressure remained above 90 mmHg, minoxidil was added at a starting dose of 2.5 mg/day and increased weekly until blood pressure was controlled or the maximum dose of 100 mg/day was reached. The average blood pressure decreased from 170.9/107.0 mmHg (sitting) and 174.1/110.8 mmHg (standing), before the addition of minoxidil, to 138.8/86.7 mmHg (sitting) and 140.0/89.5 mmHg (standing), at the third month of minoxidil therapy. At the sixth month of minoxidil therapy, the figures were 140.9/86.3 and 141.9/89.8 mmHg. With this single-dose program, smooth blood pressure control throughout 24 hours was documented by 24-hour ambulatory blood-pressure monitoring. Hypertrichosis was common but was bothersome only to women patients. Pericardial effusions occurred in five patients, but they were all small and asymptomatic. Subjective side effects of the regimen were usually so mild that all patients who completed the study decided to remain on the same regimen.

Chlorthalidone↗
PubMed1983

Osmometry of CO2 in gas samples.

Measurement of solute concentrations in biologic fluids by an osmometric technique has been described previously. Here, we describe an osmometric technique for measuring CO2 in gas samples. A solution of NaOH is injected into a graduated syringe containing the gas sample and CO2 is trapped in the reaction: 2NaOH + CO2 leads to Na2CO3 + H2O. The decrease in osmolality of the NaOH solution allows estimation of pCO2 in the original gas sample.

Blood Gas Analysis↗
PubMed1982

Pseudohypoaldosteronism following kidney transplantation.

A 56-year-old woman received a kidney transplant and presented subsequently with evidence of volume contraction, hyponatremia and hyperkalemia. Urinary sodium excretion was inappropriately high for the degree of volume contraction and urinary potassium excretion inappropriately low for the degree of hyperkalemia. Marked elevation of plasma renin activity and plasma aldosterone suggested that the renal tubules were unresponsive to mineralocorticoids. The defect was shown to be transient. The mechanisms leading to the defect are discussed.

Aldosterone↗
PubMedDate not supplied

Hyperkalemia in diabetes mellitus.

Potassium filtered at the glomerulus is almost completely reabsorbed before the distal tubule; it must therefore be secreted into the collecting duct. The rate of potassium secretion is determined by a number of factors, notably aldosterone, distal sodium delivery, and serum potassium. Normal serum potassium is maintained by the interplay of passive leak of potassium from the cells and its active return to the cells. Transmembrane potassium distribution is influenced largely by acid-base equilibrium and hormones including insulin and catecholamines. In the diabetic with ketoacidosis hyperkalemia, in the face of potassium depletion, is attributable to reduced renal function, acidosis, release of potassium from cells due to glycogenolysis, and lack of insulin. Chronic hyperkalemia in diabetics is most often attributable to hyporeninemic hypoaldosteronism but other conditions including urinary tract obstruction may also contribute. A variety of clinical situations (e.g., volume depletion) and drugs (e.g., nonsteroidal antiinflammatory agents, and heparin) may acutely provoke hyperkalemia in susceptible individuals.

Diabetes Complications↗
PubMedDate not supplied

Acidosis in chronic renal insufficiency.

In this article we deal with three aspects of acidosis in patients with chronic renal insufficiency: clinical characteristics, pathophysiology, and therapeutic approach.

Acid-Base Imbalance↗