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Biomedical subjects

W J Stone

Publications and source records attributed to W J Stone.

At least 55 records · Page 3Linked to original sources
PubMed1985

Magnesium toxicity as a cause of hypotension and hypoventilation. Occurrence in patients with normal renal function.

Symptomatic hypermagnesemia usually requires both increased intake of the ion and abnormal renal function; however, we treated two patients with iatrogenic hypermagnesemia (10.4 and 13.2 mEg/L) who had normal renal function. One received ureteral irrigation with hemiacidrin (Renacidin) to dissolve a stone, and the other was treated for ingestion of an unknown toxin with large doses of magnesium sulfate. Therapy included ventilatory support, intravenous calcium, and fluids. Dialysis was not required, and recovery was complete.

Adult↗
PubMed1984

Severe allopurinol toxicity. Description and guidelines for prevention in patients with renal insufficiency.

A life-threatening toxicity syndrome consisting of an erythematous, desquamative skin rash, fever, hepatitis, eosinophilia, and worsening renal function in 78 patients receiving allopurinol is described. In a majority of cases, the development of this syndrome was associated with the use of standard (200 to 400 mg per day) doses of allopurinol in patients with renal insufficiency. In pharmacologic studies, it was demonstrated that the renal clearance of the major metabolite of allopurinol, oxipurinol, is directly proportional to the renal clearance of creatinine (oxipurinol clearance = 0.22 X creatinine clearance -2.87). An inverse linear relation was noted between the serum oxipurinol half-life and the renal creatinine clearance [( serum oxipurinol half-life in hours]-1 = 0.00034 X creatinine clearance in milliliters per minute + 0.0045). Long-term use of 300 mg per day of allopurinol was found to result in elevated steady-state serum oxipurinol concentrations in patients with renal insufficiency (serum oxipurinol concentration in micromoles per liter = -2.5 X creatinine clearance in milliliters per minute + 326). Avoidance of allopurinol or use of reduced doses in patients with renal insufficiency according to proposed guidelines should be adequate to inhibit uric acid production in most patients and may reduce the incidence of life-threatening allopurinol toxicity.

Adult↗
PubMed1984

Glucoheptonate measurement of differential renal function.

In previous studies using dogs whose renal function was rendered asymmetric by unilateral infarction or partial ureteral obstruction, the efficacy of technetium-99m diethylenetriamine pentaacetic acid and dimercaptosuccinic acid in the measurement of differential renal function was demonstrated. The present study was undertaken to determine if technetium-99m glucoheptonate could also be used to quantitate differential renal function in these conditions. Five dogs with partial ureteral obstruction, 4 with segmental infarction and 2 with ipsilateral combination of both were studied. Seven to 10 days following these interventions the animals were given a bolus injection of 10 mCi Tc-99m glucoheptonate. This was acquired in the posterior projection on a minicomputer at 2 seconds/frame for 3 minutes. Static images were obtained anteriorly and posteriorly between 3 and 5 hours postinjection. The following day iothalamate and creatinine clearances were measured by ureteral catheterization. There was good correlation between differential function calculated from the 1 to 3 minute portion of the bolus study and that determined by the ureteral catheter studies, r greater than 0.99. Correlations based on the static images were less satisfactory due to pelvic retention in the obstructed animals, r = 0.73. We conclude that technetium-99m glucoheptonate may be used to determine differential renal function.

Animals↗
PubMed1984

Mitral anular calcification in chronic renal failure.

In order to determine the incidence and pathogenesis of mitral anular calcification (MAC) in chronic renal failure, we analyzed biochemical, hemodynamic and echocardiographic data in 168 patients on long-term hemodialysis. Mitral anular calcification is more common in patients with chronic renal failure than in other patients of similar age. Its pathogenesis appears to be due to abnormal calcium-phosphorus homeostasis in the setting of secondary hyperparathyroidism. Hypertension did not appear to be an important etiologic factor in our patients. Meticulous control of hyperphosphatemia would appear to be the most important therapeutic measure in preventing this complication.

Adult↗
PubMed1983

Tularemia complicated by acute renal failure.

Acute renal failure has been a rare, uniformly fatal complication of infection with Francisella tularensis. The literature suggests that either acute tubular necrosis, interstitial nephritis, or glomerulonephritis may be responsible for this syndrome. We have described a patient with tularemia who had nonoliguric acute renal failure probably due to interstitial nephritis and who recovered slowly but spontaneously during antimicrobial therapy with doxycycline.

Acute Kidney Injury↗
PubMed1983

Plasma binding of pancuronium: effects of age, sex, and disease.

The extent of pancuronium binding in plasma in controversial due to a lack of definitive studies in human plasma. The degree of pancuronium binding in human plasma and the concomitant effects of age, sex, and renal disease on drug binding were determined by equilibrium dialysis using [3H]pancuronium. The free fraction of pancuronium was 93.2 +/- 1.6% in male subjects and 88.9 +/- 2.5% in adult nonpregnant female subjects, indicating that pancuronium is not highly protein bound. The free fraction in newborns and their mothers was 91.0 +/- 1.8% and 89 +/- 1.3%, respectively. There were no significant differences between the plasma binding of pancuronium in men, nonpregnant women (whether on oral contraceptives or not), pregnant women, or neonates. The free fraction of pancuronium was unaltered (90.7 +/- 2.1%) in patients with severe renal disease. We therefore conclude that the binding of pancuronium in human plasma is very low and that age, sex, oral contraceptives, pregnancy, and renal disease do not influence the plasma binding of this drug.

Adult↗
PubMed1982

Massive upper extremity edema with arteriovenous fistula for hemodialysis. A complication of previous pacemaker insertion.

A 50-year-old patient with chronic renal insufficiency developed massive edema of the left upper extremity following placement of an elective radial artery-cephalic vein fistula for future hemodialysis. Subclavian vein thrombosis was diagnosed by radionuclide venography and was undoubtedly caused by prior transvenous pacemaker insertion. Ablation of that fistula relieved the edema. Investigation of the circulation of extremities used for previous pacemaker insertion is advised prior to their employment as vascular access for hemodialysis.

Arm↗
PubMed1981

Ceforanide kinetics in renal insufficiency.

Ceforanide (500 mg) was infused intravenously over 30 min into six normal subjects, 10 nondialysis patients with renal insufficiency, and six hemodialysis patients. Dialysis patients received two ceforanide infusions, one immediately before dialysis and another during an interdialysis period. Sequential plasma samples over 24 to 72 hr were assayed for ceforanide. Peak ceforanide levels (mean = 69 +/- 12 micrograms/ml) and volumes of distribution did not vary with creatinine clearance (Clcr, ml/min/1.73 m2) and both plasma clearance and renal clearance decreased linearly as Clcr decreased. Mean nonrenal clearance (4.6 +/- 1.8 ml/min/1.73 m2) did not vary with Clcr. Mean half-life was 3 hr in the normal subjects, increasing to approximately 25 hr in patients with severe renal insufficiency. Hemodialysis resulted in a removal of approximately 21% of the dose of ceforanide. Dosing recommendations for patients with renal insufficiency are provided.

Adult↗
PubMed1981

Simultaneous assay of immunoreactive beta-lipotropin, gamma-lipotropin, and beta-endorphin in plasma of normal human subjects, patients with ACTH/lipotropin hypersecretory syndromes, and patients undergoing chronic hemodialysis.

We have studied the relative concentrations of the human immunoreactive (IR) peptides gamma-lipotropin (hgammaLPH, [1-58]hbetaLPH), beta-lipotropin (hbetaLPH), and beta-endorphin (hbetaEND, [61-91]hbetaLPH) using gel exclusion chromatography together with a specific radio-immunoassay (RIA) for hgammaLPH and a RIA that (because hbetaEND is the COOH-terminus of the hbetaLPH molecule) measures both hbetaEND and hbetaLPH on an equimolar basis. In normal subjects, basal plasma IR-hgammaLPH was often undetectable (<12.5 fmol/ml), but ranged up to 21 fmol/ml, and IR-hbetaEND/hbetaLPH was 10.8+/-0.7 fmol/ml; previous studies by others suggest that most of the IR-hbetaEND/hbetaLPH was probably hbetaLPH. Both IR-hgammaLPH and IR-hbetaEND/hbetaLPH were significantly elevated (P < 0.001) in patients undergoing chronic hemodialysis (101.5+/-12.7 and 23.8+/-2.0 fmol/ml, respectively). Their IR-hgammaLPH coeluted with standard hgammaLPH as a single peak, and IR-hbetaEND/hbetaLPH coeluted with hbetaLPH; no distinct peak of IR-hbetaEND was observed. In patients with ACTH/LPH hypersecretion due to Addison's disease, Nelson's syndrome, or ectopic ACTH syndrome, IR-hgammaLPH and IR-hbetaEND/hbetaLPH were both elevated, and IR-hbetaEND/hbetaLPH eluted as two peaks, one coeluting with hbetaLPH and the other with hbetaEND. The molar concentrations of all three peptides were significantly correlated with one another. The lower concentrations of endogenous IR-hbetaEND observed may be due in part to its apparent shorter plasma half-life, as estimated in an Addison's patient given a cortisol infusion. The biologic significance of these three peptides in circulating blood is still unknown. The increased levels of hbetaLPH and hgammaLPH in plasma of patients with chronic renal failure suggest that the kidney may be an important organ for their metabolism.

ACTH Syndrome, Ectopic↗
PubMed1980

Massive propranolol metabolite retention during maintenance hemodialysis.

Eight outpatients on long-term hemodialysis receiving propranolol therapy were studied on a nondialysis day, 11 +/- 1 hr after the last dose. Steady-state daily dosage of propranolol averaged 225 +/- 36 mg (range, 80 to 400). Plasma concentrations of propranolol and three of its metabolites were measured by gas chromatography--mass spectrometry (x +/- SEM): propranolol, 47 +/0 17 ng/ml; propranolol glucuronide, 2.119 +/0 597 ng/ml; 4-hydroxypropranolol glucuronide, 789 +/- 149 ng/ml; and naphthoxylactic acid, 4,357 +/- 727 ng/ml. The plasma levels of these metabolites were 18, 20, and 29 times, respectively, as high as in patients with normal renal function and correlated well with the dose of propranolol. The total concentration of these metabolites exceeded the concentration of propranolol to 239 times (range 74 to 476). Four long-term hemodialysis patients on propranolol were hospitalized to ensure compliance. Plasma levels of propranolol and of the three metatolites were followed during a dosage interval. Plasma propranolol correlated well with dose (r = 0.94) and declined with approximately normal half-lifes of 3.2 to 5.4 hr. There was little variation in the extremely high plasma levels of the three metabolites during a dosage interval. The total metabolite to propranolol plasma concentration ratio in these four patients ranged from 109 to 705. The correlation between total metabolite concentrations and propranolol dose was striking (r = 0.997). Massive retention of propranolol metabolites occurs uniformly in uremia, is highly predictable from the dose, and could have important clinical implications.

Adult↗
PubMed1980

Propranolol disposition in renal failure.

1 Previous studies of propranolol disposition in renal failure have been conflicting. 2 Using simultaneous administration of [3H]-propranolol intravenously and unlabelled propranolol orally the principal determinants of drug distribution were calculated in normals, patients with severe renal impairment (creatinine clearance 14.5 +/- 2.8 ml/min) but not on haemodialysis and patients on haemodialysis (creatinine clearance less than 5 ml/min). 3 The effect of haemodialysis on propranolol binding and free fraction was also examined. The percentage of propranolol unbound rose from 7.1% to 9.9%. (P less than 0.001) 20 min following heparinization and beginning haemodialysis. This was accompanied by a large rise in free fatty acids from 0.567 +/- 0.059 to 3.326 +/- 0.691 mumol/ml (P less than 0.005). 4 The blood to plasma concentration ratios of propranolol were significantly higher in patients with renal failure (P less than 0.02) and on haemodialysis (P less than 0.001) and were significantly negatively correlated (P less than 0.001) with the haematocrit. 5 Although the half-life propranolol was significantly shortened in the patients with renal failure (P less than 0.02), there was no change in the apparent liver blood flow, extraction ratio or the principal determinants of steady-state drug concentrations in blood namely oral and intravenous clearance from blood. 6 There is, therefore, no pharmacokinetic basis to adjust the dosage of propranolol in patients with renal failure.

Administration, Oral↗
PubMed1979

Hemodialysis hypotension is not the result of uremic peripheral autonomic neuropathy.

Five chronic hemodialysis patients with persistent hypotension during dialysis (MAP: 74.2 +/- 3.1 mm Hg) were given a number of standard tests of autonomic nervous system function and compared with eight normotensive hemodialysis patients (MAP: 96.4 +/- 3.4 mm Hg). Tests of efferent sympathetic nerves were normal in both groups, as were plasma catecholamine levels and the cold pressor test. The response to Valsalva maneuver and the venoconstriction reflex were generally abnormal and did not differentiate between the two groups. When adjusted for age and MAP, the baroreceptor slope to a high-pressure stimulus was diminished only in the hypotensive subjects. This result reinforces the previously described finding that many uremic patients do not develop a normal cardioacceleration during hypotension. Although reduced baroreceptor sensitivity may be a factor in the chronic hypotension of some hemodialysis patients, autonomic dysfunction alone is not a sufficient explanation of this phenomenon.

Adult↗
PubMed1979

Grand rounds: Nashville VA Hospital--Vanderbilt University. Saturday conference: renal disease in the juvenile diabetic.

Renal disease, particularly glomerulosclerosis, is a major cause of morbidity and mortality in patients with juvenile-onset diabetes mellitus. Signaled by the onset of proteinuria after 15 or more years of insulin therapy, progressive renal insufficiency due to glomerulosclerosis terminates in uremia within five years. Although some patients have benefited from chronic dialysis programs, the outcome in uremic diabetics has been considerably better if successful renal transplantation can be accomplished. Extrarenal complications of diabetes mellitus and recurrence of diabetic lesions in transplanted kidneys have hampered the recovery and rehabilitation of transplant recipients. Other renal diseases encountered in juvenile diabetics are reviewed.

Acute Kidney Injury↗
PubMed1979

Hemodialysis and renal transplantation in progressive systemic sclerosis: report of 2 cases.

Renal failure is a common cause of death in patients with progressive systemic sclerosis (PSS). The present paper describes two patients with chronic renal failure secondary to PSS whom we have treated by a combination of chronic hemodialysis and renal transplantation. Also reviewed are reports of six additional patients who have undergone renal transplantation. We conclude that chronic hemodialysis and renal transplantation are successful life-sustaining treatment modalities in some patients with end-stage renal disease due to PSS.

Adult↗