Vascular access malfunction due to upper extremity embolization in dialysis patients.

Acute occlusions of arteries such as those of the cerebral and peripheral circulation are usually due to thrombotic or embolic events. Emboli have not been previously reported to cause arteriovenous (AV) dialysis access malfunction. We describe in this report three patients with end-stage renal disease (ESRD) and atrial fibrillation (Afib) who developed acute ischemia of an arteriovenous access-bearing extremity due to embolization. The clinical manifestations mimicked thrombotic events, but the presence of symptoms and signs of limb ischemia distinguished these cases clinically. A timely diagnosis followed by an appropriate intervention can lead to limb and access salvage.

Withholding and withdrawing dialysis: the role of physician specialty and education and patient functional status.

Withholding and withdrawing dialysis are subjects of major concern to nephrologists, because both result in a significant number of end-stage renal disease (ESRD) patient deaths. The medical literature on withholding dialysis is extremely limited, and that on withdrawing dialysis consists mainly of retrospective studies from the 1980s. The present study was conducted to identify ways to improve dialysis decision making by providing a current understanding of how decisions to withhold or withdraw dialysis are being made and by examining whether some patients who might benefit from dialysis are not being referred. In 1995, 22 of 27 (82%) nephrologists practicing in West Virginia agreed to participate in a year-long prospective study in which they completed forms on each patient from whom they withheld or withdrew dialysis. Seventy-six of a random sample of 214 (36%) primary care physicians returned questionnaires describing their practice experience in 1995 with patients with advanced chronic renal failure. The nephrologists withdrew dialysis from 60 of 822 (7%) patients. Academic nephrologists who had received education in the ethics and law of stopping dialysis withdrew it from a greater percentage of patients than those in private practice (12% v 6%; P = 0.009). Patients who were withdrawn more often resided in nursing homes (37% v 2%; P < 0.0001). Twenty-one patients (37%) lacked decision-making capacity at the time the decision was made to withdraw dialysis. Advance directives were available for 13 of the 21 (62%) patients: eight of the 10 treated by academic nephrologists and five of the 11 treated by private practice nephrologists. Academic nephrologists found advance directives to be helpful in decision making to withdraw dialysis of incapacitated patients more often than nephrologists in private practice (70% v 9%; P = 0.004). Nephrologists withheld dialysis from 25 of 357 (7%) ESRD patients compared with 42 of 193 (22%) withheld by primary care physicians (P < 0.001). In deciding not to refer a patient for a dialysis evaluation, 25% of primary care physicians did not consult a nephrologist; 60% cited age as a reason not to refer. These findings suggest that dialysis decision making might be improved by educating nephrologists about the ethics and law of withdrawing dialysis and about how to implement successfully advance care planning so that advance directives will be present and helpful when decisions need to be made for incapacitated dialysis patients. Education of primary care physicians about when to refer patients with chronic renal failure for a dialysis evaluation might also result in more referrals for patients who will benefit from dialysis.

Torsades de pointes in two chronic renal failure patients treated with cisapride and clarithromycin.

Patients with chronic renal failure are often on multiple medications and are at risk for the development of adverse effects from drug interactions. Two cases of torsades de pointes that followed the initiation of clarithromycin therapy in patients receiving long-term cisapride therapy are being reported. Elevated cisapride levels while on this combination with return to therapeutic range while on cisapride only was documented in one of the patients. The role of the inhibition of cytochrome P-4503A4 in the occurrence of the arrhythmia is discussed.

Hyperkinetic borderline hypertension in Tecumseh, Michigan.

Of 691 healthy (untreated) villagers of Tecumseh, Michigan (average age 32.6 years), 99 had a clinical blood pressure exceeding 140/90 mmHg. Thirty-seven per cent of these borderline hypertensives had increased heart rate, cardiac index, forearm blood flow and plasma norepinephrine. These subjects had elevated self-determined home blood pressure (average of 14 measurements). The present hyperkinetic borderlines had elevated blood pressure at 5, 8, 21 and 23 years of age and their parents also had higher blood pressure. The prevalence of high blood pressure in Tecumseh, its long history, elevated blood pressure readings outside the physician's office and family background of hypertension, suggests that the hyperkinetic state is a significant clinical condition. Previous studies on hospital-based populations proved that the hyperkinetic state is caused by an excessive autonomic drive. The association of the hyperkinetic state with elevated norepinephrine in this study suggests that a sympathetic hyperactivity is present in a large proportion of unselected subjects with mild blood pressure elevation.

"White coat" versus "sustained" borderline hypertension in Tecumseh, Michigan.

During a survey of young subjects not receiving treatment for hypertension in Tecumseh, Michigan, clinic and self-monitored blood pressures taken at home (14 readings in 7 days) were obtained in 737 subjects (387 men, 350 women, average age 31.5 years). Hypertension in the clinic was diagnosed if the clinic blood pressure exceeded 140 mm Hg systolic or 90 mm Hg diastolic. In the absence of firm criteria for what constitutes hypertension at home, subjects whose average home blood pressure was in the upper decile of the whole population were considered to have hypertension at home. By these criteria, 7.1% of the whole population had "white coat" hypertension (i.e., high clinic but not elevated home readings). The prevalence of "sustained" hypertension (i.e., high readings in the clinic and at home) was 5.1%. Subjects with white coat and sustained borderline hypertension in Tecumseh were very similar. Both groups showed, at previous examinations (at ages 5, 8, 21, and 23 years), significantly higher blood pressure readings than the normotensive subjects. As young adults (average age 33.3 years), the parents of both hypertensive groups had significantly higher blood pressure readings than the parents of normotensive subjects. Both hypertensive groups had faster heart rates, higher systemic vascular resistance, and higher minimal forearm vascular resistance. Both hypertensive groups were more overweight, had higher plasma triglycerides, insulin, and insulin/glucose ratios than normotensive subjects. The white coat hypertensive group also had lower values of high density lipoprotein than the normotensive group. White coat hypertension is a frequent condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Sensitization of human alpha 1- and alpha 2-adrenergic venous responses by guanadrel sulfate.

The alpha 1- and alpha 2-adrenergic venoconstriction in dorsal hand veins of normal subjects was determined by infusion of phenylephrine or clonidine. Oral administration of prazosin reduced the constriction response to phenylephrine but not to clonidine. Subjects were treated for 3 weeks in a randomized crossover design with placebo or guanadrel sulfate. Guanadrel reduced sympathetic tone (i.e., plasma norepinephrine and norepinephrine release rate), whereas venous responses to phenylephrine and clonidine were both augmented during guanadrel treatment. The effect on phenylephrine responses was primarily attributable to a decrease in the median effective concentration with a small increase in maximum response. Clonidine showed a markedly increased maximum response with a small increase in the median effective concentration. Platelet alpha 2-adrenergic receptors increased slightly but there was no change in the amount of platelet pertussis toxin substrate during guanadrel treatment. Thus reduction in sympathetic tone in normal young men results in increased venous responses to both alpha 1- and alpha 2-agonists.

Recovery from end-stage renal disease.

To evaluate the rate and associated factors for recovery of renal function in patients labeled by their nephrologists as having end-stage renal disease (ESRD), the data base of the Michigan Kidney Registry was used. All patients reported as starting treatment for ESRD between 1976 and 1985 (N = 7,404) were evaluated, excluding patients with acute tubular necrosis (ATN) or transplantation cases. While patients with ESRD due to diabetes and cystic diseases had lower recovery rates than average, patients with glomerulonephritis associated with a systemic illness, vasculopathies, and crescents had threefold to fourfold higher recovery rates. White race, older age, and later year of ESRD were associated with significantly higher recovery rates. Recovery rates did not differ substantially for patients receiving peritoneal dialysis or hemodialysis. Recovery occurred within 6 months of ESRD in approximately 48% of those recovering, 74% within 1 year, and lasted at least 1 year in 75% of the cases. The authors conclude that caution should be applied when the diagnosis of ESRD is made; the possibility of recovery should be sought and assessed, especially when early renal transplantation is considered.

Behaviour and hypertension: a pathophysiological puzzle.

Patients with borderline hypertension typically show enhanced sympathetic and decreased parasympathetic tone, characteristic personality traits (submissiveness, hostility) and hyperreactivity to mental stress. It has been proposed that the hypertensive personality results in a persistent 'defence reaction', enhancing sympathetic outflow from the central nervous system and reactivity to stress. But evidence from pharmacological intervention trials suggests that blood pressure reactivity is controlled independently of average baseline blood pressure. A study comparing the effects of the centrally-acting alpha 2-agonist, clonidine, and the selective beta 1-blocker, atenolol, demonstrated that both drugs had a comparable antihypertensive action on baseline blood pressure. However, neither agent affected stress responses to mental arithmetic, submaximal isometric handgrip exercise or cold pressor testing. We conclude that studies of stress reactivity, while of interest to students of circulatory control, are unlikely to yield insights into the causes of human hypertension.

Antihypertensive and hypotensive effects of atrial natriuretic factor in men.

Synthetic atrial natriuretic factor (ANF) was administered in ascending doses (0.03, 0.20, 0.45 microgram/kg/min) to eight mildly essential hypertensive men on high (200 mEq/day) or low (10 mEq/day) sodium diets. Responses of blood pressure, heart rate, urinary volume and electrolyte excretion, renin, and aldosterone were measured. For the entire group, ANF lowered blood pressure and increased heart rate during the 0.20 and 0.45 microgram/kg/min infusions, and the antihypertensive effect of the peptide persisted for at least 2 hours after the infusions ended. Four patients (2 at 0.20 microgram/kg/min and 2 at 0.45 microgram/kg/min) experienced sudden bradycardia and hypotension at the end of or shortly after completion of ANF infusion. Renal excretion of water, sodium, chloride, calcium, and phosphorus increased in a dose-dependent fashion in response to infused ANF. Patients on the 200 mEq/day sodium diet had greater increases in urinary volume (11.1 +/- 2.8 vs 3.0 +/- 2.0 ml/min; p less than 0.05), sodium (870 +/- 134 vs 303 +/- 27 microEq/min; p less than 0.05), and chloride (801 +/- 135 vs 176 +/- 75 microEq/min; p less than 0.02) compared with patients on the low sodium diet. The apparent direct suppressive effect of a 0.03 microgram/kg/min infusion of ANF on renin and aldosterone levels was overcome at higher doses by counterregulation provoked by the depressor action. Renin was slightly (-12%) suppressed during the 0.03 microgram/kg/min infusion of ANF but increased at the 0.20 (+50%) and 0.45 microgram/kg/min (+90%; p less than 0.03) rates. Aldosterone declined significantly during the 0.03 microgram/kg/min infusion (-45%; p less than 0.01) of ANF but not during the two higher dose infusions.(ABSTRACT TRUNCATED AT 250 WORDS)