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Biomedical subjects

C A Vaamonde

Publications and source records attributed to C A Vaamonde.

At least 19 recordsLinked to original sources
PubMed1992

The protection against gentamicin nephrotoxicity in the streptozotocin-induced diabetic rat is not related to gender.

Since gender can influence the renal toxicity of a drug in a given species, the present study was undertaken to evaluate the role of sex in the protection against gentamicin (G)-induced nephrotoxicity afforded by diabetes mellitus (DM) in the rat. We have compared the effects of administration of G (40 mg/kg/day, for 14 days) on male and female DM Sprague-Dawley rats. Non-diabetic animals of both sexes receiving identical doses of G served as controls. At the end of the experiment on day 14, both female (F) and male (M) control groups had similar and marked evidence of nephrotoxicity: elevation of plasma creatinine (F 1.7 +/- 0.7; M 2.8 +/- 0.6 mg/dl), decrease in endogenous 24-h creatinine clearance (Ccr) (F0.3 +/- 0.1; M 0.2 +/- 0.1 ml/min/100 g BW), and histological evidence of severe acute tubular necrosis. In marked contrast, the DM rats showed no functional or morphological evidence of renal damage throughout the study regardless of their gender (day 14: plasma creatinine: F 0.2 +/- 0.03; M 0.2 +/- 0.02; Ccr: F 1.2 +/- 0.1; M 1.6 +/- 0.1 ml/min/100 g BW), and they also accumulated less G in their kidney cortex than the C rats. The male controls exhibited higher renal cortex accumulation of G than the female controls (p < 0.05), whereas the opposite occurred in the DM groups (p < 0.01). Because the validity of using Ccr for the evaluation of GFR changes in experimental nephrotoxicity has been questioned, we have compared, in a separate experiment, three different methods of estimation of GFR (simultaneous short clearances of inulin and Ccr, and 24-h Ccr) in conscious female Sprague-Dawley rats undergoing the same treatment with G described above. At no time during the study did the method used for estimation of the GFR influence the results. We conclude that male and female Sprague-Dawley rats with diabetes are functionally and morphologically equally protected against G. Furthermore, no gender-related differences in the magnitude of G-induced nephrotoxicity was demonstrated in the non-diabetic control animals.

Animals↗
PubMed1990

Hepatitis C infection in two urban hemodialysis units.

We determined the prevalence of antibodies to the hepatitis C virus (anti-HCV) in 90 patients and 37 staff members of two hemodialysis units utilizing a recently developed anti-HCV recombinant based assay. Eleven patients (12%) were anti-HCV(+). Of these, eight (73%) had antibodies to the hepatitis B core antigen (anti-HBc) indicating prior hepatitis B infection; one patient was hepatitis B surface antigen (HBsAg)(+). All staff members were anti-HCV(-), although seven (19%) of them were anti-HBc(+). Alanine aminotransferase elevations were present at the time of the study in four anti-HCV(-) patients and in only one anti-HCV(+) patient. All anti-HCV(+) (mean 59 +/- 74; range 3 to 269 units) and 85% of anti-HCV(-) patients (mean 16 +/- 27; range 0 to 204 units) had received multiple blood transfusions (P = 0.348). Among 50 patients tested for human immunodeficiency virus (HIV), 43% of anti-HCV(+) as compared to only 7% anti-HCV(-) were positive (P = 0.003). There was a history of intravenous drug abuse (IVDA) in eight (72%) of the anti-HCV(+) patients and in only seven (9%) of the anti-HCV(-) group (P = 0.00001). The results of this serologic survey suggests that anti-HCV positivity is prevalent, although much less than anti-HBc, among our dialysis patients, whereas it was not detected among staff members. The prevalence rate of anti-HCV was statistically significantly higher among anti-HIV(+) and IVDA patients but not in multi-transfused patients.

Adult↗
PubMed1990

Influence of magnesium sulfate-induced hypermagnesemia on the anion gap: role of hypersulfatemia.

Although hypermagnesemia purportedly lowers the anion gap (AG), we have shown previously that increases in the serum concentration of the unmeasured cation (UC) Mg due to therapeutic infusion of MgSO4 are not associated with AG reduction. To assess our hypothesis that increases in serum SO4 (unmeasured anion, UA) offset the effect of elevated serum Mg on the AG, we prospectively studied 11 patients receiving MgSO4 intravenously for toxemia of pregnancy. After 6 h of MgSO4 infusion, serum Mg increased by 2.1 +/- 0.2 (SE) mEq/l (p less than 0.001) without a significant decrease in the AG. Concomitantly, serum SO4 increased by 1.4 +/- 0.2 mEq/l. Comparison of the renal handling of SO4 versus Mg showed a higher fractional excretion of the former, probably accounting in part for the smaller increment of serum SO4 than of Mg. Comparison of the change in serum SO4 minus that of Mg indicated that, on the average, 70% of the observed 1.0 +/- 0.7 mEq/l reduction in AG was accounted for by the observed changes in the two pertinent unmeasured ions. A small decrement in serum Ca probably was a quantitatively minor factor tending to obviate a greater decrease in AG. We conclude that hypersulfatemia attenuates the reduction in AG that would otherwise accompany MgSO4-induced hypermagnesemia.

Acid-Base Equilibrium↗
PubMed1990

Effect of hypercalcemia on the anion gap.

It has been assumed, but not documented, that hypercalcemia induces an appreciable reduction in the serum anion gap (AG) because it represents an increase in the level of unmeasured cations. To test this question, we retrospectively compared the data of 59 hypercalcemic patients with malignancy [group 1, serum Ca 13.3 +/- SE 0.3 mg/dl] with those of 108 patients whose hypercalcemia was of parathyroid origin (group 2, serum Ca 12.1 +/- 0.1 mg/dl), and those of 51 control subjects (group 3, serum Ca 9.5 +/- 0.1 mg/dl). The AG of group 2 subjects (8.7 +/- 0.3 mEq/l) was significantly lower than that of the other two groups (p less than 0.001 for both) despite their higher serum albumin and lower serum Ca in comparison to group 1. The AGs of group 1 (11.1 +/- 0.4 mEq/l) and group 3 (11.1 +/- 0.3 mEq/l) were identical. There was no statistically significant correlation between the AG and serum Ca in the hypercalcemic patients. The major finding that the association of hypercalcemia with reduced AG is seen in hyperparathyroidism, but not in malignancy-related hypercalcemia, is not explained by differences in serum albumin, renal function, or acid-base status. Overlap of values between groups limits the diagnostic usefulness of the AG in an individual patient. Nevertheless, in the absence of multiple myeloma, the finding of an AG of 5 mEq/l or less in a hypercalcemic patient may be a helpful clue suggesting that malignancy is not the etiology.

Acid-Base Equilibrium↗
PubMed1989

The effects of administration of lithium salts and magnesium sulfate on the serum anion gap.

Whether or not an increased serum level of an unmeasured cation will reduce the anion gap (AG) depends on concomitant changes (or lack thereof) in serum unmeasured anions. In the present retrospective study, we sought to determine the effect of lithium carbonate or citrate and magnesium sulfate on the AG. Two groups of psychiatric patients whose average serum lithium levels were 0.6 and 1.0 mEq/L were studied. The AG in each group (10.2 +/- 0.3 [SE] and 9.0 +/- 0.4 mEq/L, respectively) was significantly (P less than 0.05) lower than that of a control group (11.1 +/- 0.3 mEq/L). Separately, we collected 87 pairs of AG and serum magnesium data of patients with toxemia of pregnancy. These included those of 15 patients evaluated both before and during magnesium sulfate infusion. Despite an average serum magnesium level of 4.1 +/- 0.2 mEq/L, the AG of the latter subjects tended to increase slightly from 10.8 +/- 0.5 to 11.7 +/- 0.7 mEq/L during magnesium infusion, instead of decreasing. The other data (72 determinations in the 55 patients without preinfusion values) revealed a mean AG of 11.0 +/- 0.3 mEq/L, coexisting with an elevated serum magnesium of 4.1 +/- 0.1 mEq/L. None of the above-mentioned three mean AG values differed significantly from that of the control group. We conclude that hypermagnesemia resulting from the administration of magnesium sulfate does not reduce the AG, probably because of a concomitant and proportional increase in serum sulfate. The present data reemphasize the need to assess the anion gap as the result of concomitant changes in both unmeasured anions and cations.

Acid-Base Equilibrium↗
PubMed1989

Phlorizin-induced glycosuria does not prevent gentamicin nephrotoxicity in rats.

Because rats with streptozotocin-induced diabetes mellitus (DM) have a high solute diuresis (glycosuria of 10 to 12 g/day), we have suggested that this may in part be responsible for their resistance to gentamicin-induced acute renal failure (ARF). The protection from gentamicin nephrotoxicity was studied in non-diabetic rats with chronic solute diuresis induced by blockage of tubular glucose reabsorption with phlorizin (P). DM rats with mild glycosuria (similar in degree to that of the P treated animals) were also studied. Unanesthetized adult female, Sprague-Dawley rats were divided in four groups and studied for 15 days. Group 1 (P alone) received P, 360 mg/day, for 15 days; Group II (P + gentamicin); Group III (gentamicin alone) and Group IV (mild DM + gentamicin). Nephrotoxic doses (40 mg/kg body wt/day) of gentamicin were injected during the last nine days of study to the animals of groups II to IV. In Group I, P induced a moderate and stable glycosuria (3.9 +/- 0.1 g/day, SE), and no functional or morphologic evidence of renal dysfunction (baseline CCr 2.1 +/- 0.1 ml/min, undetectable lysozymuria) or damage (tubular necrosis score [maximum 4], zero). In Group II, P did not prevent gentamicin-ARF (maximal decrease in CCr at day 9.89%, P less than 0.001; peak lysozymuria, 1863 +/- 321 micrograms/day; and tubular necrosis score, 3.9 +/- 0.1). These values were not different from those of Group III: maximal decrease in CCr 73% (P less than 0.001); lysozymuria, 2147 +/- 701 micrograms/day; tubular necrosis score, 3.8 +/- 0.1.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1989

Acute and chronic renal effects of radiocontrast in diabetic rats. Role of anesthesia and risk factors.

The acute and chronic renal effects of the intravenous injection of meglumine diatrizoate sodium 76% (CM), 5 mL/kg body weight were studied in diabetic (DM) and age-matched normal (C) female Sprague-Dawley rats. In acute studies, the effect of anesthesia was assessed for 2 hours. Although anesthesia decreased 14C-inulin clearance (Cin) in both DM and C rats (P less than .001 vs. conscious values), there was no impairment of Cin in either group after administration of CM. In chronic studies, creatinine clearance (Ccr) was followed for 3-4 days after CM administration. Four protocols to assess risk factors in DM and C were used: adult rats with normal hydration (2A); old dehydrated rats with DM of long duration (2B); rats with prior decreased Ccr (remnant kidney, 2C); and DM rats treated with insulin (2D). No clear-cut nephrotoxicity was apparent in these studies, except that proteinuria increased with CM in Study 2C. A greater severity of renal dysfunction, renal disease, or the association of multiple risk factors may be necessary to induce CM-related nephrotoxicity in the experimental animal. The rat, diabetic or not, may have an inherent resistance to CM-induced renal injury.

Aging↗
PubMed1988

Effect of acute reversal of experimentally-induced ketoacidosis with sodium bicarbonate on the plasma concentrations of phosphorus and potassium.

To determine if ketoacidosis per se, or its reversal with NaHCO3, predisposes to hypophosphatemia, six conditioned dogs were infused for two hours with 3.0 mmol/kg body wt/hour of beta-hydroxybutyric acid, followed by 1.5 mmol/kg/hour of NaHCO3 for two hours. Acid infusion caused moderate decrements in blood pH and [HCO3], a 23 +/- 4% increase in plasma [P] (p less than 0.005), and a 15 +/- 3% decrease in plasma [K] (p less than 0.005). NaHCO3 administration returned blood pH and [HCO3] levels to or slightly greater than baseline. Plasma [P] decreased, but not below baseline, whereas plasma [K] remained below baseline, and underwent an additional small decline (p less than 0.01). We conclude that acute correction of experimental ketoacidosis with NaHCO3 reverses the characteristic hyperphosphatemia but does not induce hypophosphatemia. On the other hand, NaHCO3 administration appeared to contribute to the perpetuation of hypokalemia.

3-Hydroxybutyric Acid↗
PubMed1988

Blunted kaliuresis after an acute oral potassium load in diabetes mellitus.

It is unknown whether diabetic patients without renal failure or aldosterone deficiency respond normally to potassium administration. Acute oral potassium-loading was carried out in eight diabetic patients with modestly reduced creatinine clearance (Ccr) and in 11 diabetic patients and 13 controls with normal clearances. Only one diabetic patient manifested an inappropriately low upright plasma aldosterone level (6 ng/dL). The percentage of potassium excreted in 4 hour by both groups of diabetic patients was significantly less than that of the controls (decreased Ccr:21% +/- 6%, normal Ccr:36% +/- 5%, controls:54% +/- 5%; p less than 0.01 and 0.05 respectively). On the other hand, the estimated amount of potassium translocated intracellularly tended to be greater in the diabetic patients (18 +/- 3 mmol; 11 +/- 3 mmol) than controls(7 +/- 2 mmol; p less than 0.005 and 0.1 respectively), and the ratio of the increase in plasma (K) to the amount of potassium retained, was lower in diabetic patients, probably indicating enhanced intracellular potassium translocation. The authors conclude that diabetic patients with normal or only slightly reduced renal function (and no aldosterone deficiency) may have a reduced capacity to excrete an acute potassium load but an enhanced capacity to transfer potassium intracellularly.

Adult↗
PubMed1988

The stability of pH, PCO2, and calculated [HCO3] of urine samples collected under oil.

In order to determine the stability of directly measured pH and PCO2, and calculated [HCO3] in stored urine, 11 alkali-loaded normal subjects provided 33 spot and sixteen 24-hour mineral oil-covered, thymol-preserved, refrigerated urine samples. For the spot samples, pH and PCO2 were measured immediately and again at 4 and 24 h. In addition, immediately after voiding, 24 of the spot samples were split into oil-covered and no-oil moieties and analyzed immediately and again at 4 and 24 h. pH and PCO2 measurements of the 24-hour collections were carried out immediately after completion and again 24 h later. The results demonstrated the importance of using oil to limit the escape of CO2 from stored urine. Thus, after 24 h the oil-uncovered subgroup of 24 spot urine samples sustained a 82% decline in PCO2 and 20% fall in [HCO3]. In contrast, the corresponding percentage decrements in the oil-covered samples were 16 and 1%, respectively. The results also indicated that even with oil there is loss of CO2, which increases with time and which shows a statistically significant direct correlation with the baseline level of PCO2. Nevertheless, modest loss of CO2 usually produces only slight decrements in [HCO3] because of the countervailing influence of the resultant increase in pH. We conclude that the use of mineral oil is necessary in order to obtain adequate stability of PCO2, pH and [HCO3] in refrigerated urine requiring several hours or more of storage.

Bicarbonates↗
PubMed1988

Comparison of the effects of sodium bicarbonate versus sodium citrate on renal acid excretion.

Citrate is used commonly as an alkalinizing agent and in the management of nephrolithiasis, but its quantitative effect on acid-base homeostasis, as judged by changes in renal net acid excretion, has not been delineated. We therefore administered 61 mEq of sodium citrate/day for 4 days to 10 normal volunteers and compared the results to those obtained in 10 normal subjects (4 of whom also participated in the citrate protocol) given 60 mEq/day for 4 days of sodium bicarbonate, the prototypical alkalinizing agent. We found that the sodium citrate group experienced an average reduction in net acid excretion (45.5 +/- 7.2 mEq/day) that was very similar to that (42.0 +/- 7.2 mEq/day) induced by the same amount of sodium bicarbonate. In both groups, the reduction in net acid excretion was equivalent to approximately 70% of the alkali administered. The latter appeared to relate to an average negative hydrogen ion balance of approximately 15 mEq/day, since there was an increase in blood [HCO3] in each group of about 2.5 mEq/l. We conclude that the findings demonstrate that the short-term effects of sodium citrate on acid-base homeostasis in normal subjects are indistinguishable from those of sodium bicarbonate.

Acids↗
PubMed1986

Effect of routine doses of antacid on renal acidification.

Ten healthy volunteers took a magnesium and aluminium hydroxide antacid for 4 days, and their urinary acid excretion was measured. During antacid ingestion, blood bicarbonate levels did not change significantly, but there were highly significant rises in urine pH and bicarbonate excretion and falls in the 24 h excretion of titratable acid, ammonium, and net acid; the average change in net acid excretion was 41 +/- 4 mmol (72 +/- 9%) per 24 h. This large reduction in net acid excretion appears to result from neutralisation of more hydrochloric acid than sodium bicarbonate in the gastrointestinal tract rather than from absorption of exogenous alkali. Although metabolic alkalosis does not occur with their use in normal individuals, these antacids should not be termed "non-systemic". They might cause important changes in renal drug handling, solubility of excreted substances, or acid-base status in patients at risk.

Acid-Base Equilibrium↗
PubMed1986

Morphological alterations in distal and collecting tubules of the rat renal cortex after aminoglycoside administration at low doses.

Ultrastructural alterations in the cortical, distal and collecting tubules have been examined in female Sprague-Dawley rats treated with various aminoglycosides in clinical use. Gentamicin, dibekacin (10 mg/kg X day), netilmicin, tobramycin (4 or 10 mg/kg X day) or amikacin (37.5 mg/kg X day) were administered intraperitoneally twice a day over different periods of time, extending from 4 to 14 days. The kidney cortex was examined after 4, 7, 10 or 14 days of aminoglycoside administration by light (semithin sections) and electron microscopy. After 7 or more days of treatment, lysosomes in collecting tubular cells (and to a lesser extent in distal tubular cells) contained concentric lamellar material (myeloid bodies), an ultrastructural alteration typical of drug-induced lysosomal phospholipidosis. Although this alteration appeared qualitatively similar to that observed in proximal tubular cells, it was less conspicuous and occurred later during treatment. In addition, distal tubular cells occasionally showed marked vacuolization and disruption of the basal cell architecture. The possible relationship between these alterations and the urine hypo-osmolality characteristic of aminoglycoside-induced renal dysfunction is discussed.

Aminoglycosides↗
PubMed1979

Impaired renal bicarbonate reabsorption in the hypothyroid rat.

We previously demonstrated a decrease of sodium reabsorption in the proximal superficial nephron of the hypothyroid rat. The present clearance studies were designed to examine the renal handling of bicarbonate in hypothyroid rats. Hypothyroidism was induced by the intraperitoneal injection of Na131I and the animals were studied 10 or more wk thereafter under anesthesia and compared to their age-matched litter-mates. As is characteristic of hypothyroid animals, insulin clearance was lower and fractional urine flow and sodium excretion rates were higher than in the control rats. At the peak of the bicarbonate diuresis and at similar blood pH, PCO2, and bicarbonate levels, fractional renal bicarbonate excretion was significantly higher in the hypothyroid animals: 22 +/- 2 vs. 15 +/- 1%, P less than 0.02. This perturbation of bicarbonate reabsorption of the hypothyroid rats was independent of the influence of extracellular fluid volume expansion and appears closely related to the impaired sodium reabsorptive capacity characteristic of experimental hypothyroidism.

Animals↗
PubMed1979

The effect of acute metabolic acidosis on plasma cortisol, renin activity and aldosterone.

The effect of metabolic acidosis on the renin-aldosterone system remains unclear. In the present study anesthetized mongrel dogs (n = 19) were infused at similar rates with 0.45% NaCl (controls), HCl or NH4Cl (2.5mEq/kg) for 1--3 h. The induced metabolic acidosis in the two experimental groups was not associated with increases in plasma renin activity. Plasma cortisol (as a marker for ACTH secretion) and serum potassium concentration increased in both HCl- and NH4Cl-treated animals. Plasma aldosterone increased after 30 min in the HCl group and 60 min in the NH4Cl group and did not change in controls. These findings demonstrate that metabolic acidosis induced by HCl or NH4Cl is associated with increased aldosterone production without concomitant changes in plasma renin activity.

Acidosis↗
PubMed1979

Circulating levels of vasoactive intestinal polypeptide in liver disease.

In animals, the effects of vasoactive intestinal polypeptide (VIP) include peripheral vasodilation, hyperdynamic circulation, hyperglycemia, and hyperventilation. Because these phenomena are noted in patients with cirrhosis, it has been postulated that VIP might be escaping hepatic inactivation and entering the systemic circulatory system and contributing to these abnormalities. The major purpose of this study is to establish whether or not VIP levels are elevated in patients with cirrhosis. Additional goals are to determine if VIP levels are elevated in acute liver disease and in chronic illnesses with secondary liver involvement. The data demonstrate that patients with cirrhosis and those with acute liver disease or chronic illnesses with secondary hepatic involvement have a wide range of VIP levels with mean values significantly above that of normal individuals and patients with chronic illness and no liver involvement.

Acute Disease↗