Renal artery stenosis: duplex US after angioplasty and stent placement.

PURPOSE: To evaluate the hemodynamic outcome of technically successful percutaneous transluminal renal artery angioplasty and stent placement (PTRAS) with duplex ultrasonography (US). MATERIALS AND METHODS: Eighteen patients who underwent PTRAS in 22 renal arteries were prospectively examined. All had abnormal preprocedural duplex US findings. Those who had significant renal artery stenosis (>70%) at angiography and underwent technically successful percutaneous interventions were enrolled. Standard intrarenal duplex US parameters (acceleration index [AI], acceleration time, waveform morphology grade, and resistive index) were compared before and after interventions. RESULTS: A significant AI increase occurred after PTRAS (9.02 m/sec(2) +/- 4.85 [SD]), as compared with before intervention (2.34 m/sec(2) +/- 2.03; P <.001). Acceleration time significantly decreased from 0.084 second +/- 0.049 to 0.032 second +/- 0.008 (P <.01). There was also a significant resistive index increase from 0.69 +/- 0.12 to 0.79 +/- 0.12 (P <.01). Abnormal waveform morphology (modified Halpern waveform grade 3-6) was present in 19 (86%) of 22 intrarenal arteries prior to intervention, as compared with one (5%) after PTRAS (P <.001). In the instance in which an abnormal waveform persisted after intervention, waveform morphology improved from grade 6 to grade 3, with a concomitant AI increase from 0.96 to 5.1 m/sec(2). CONCLUSION: The findings suggest an important potential role for duplex US in noninvasive assessment of the immediate hemodynamic outcome and long-term follow-up of PTRAS.

Predicting change in depression following renal transplantation: effect of patient coping preferences.

Improvement in patient quality of life is a central goal of renal transplantation. This study examined the hypothesis that change in depression following transplantation would vary as a function of patient coping preferences. Sixty patients were assessed with the Krantz Health Opinion Survey and the Beck Depression Inventory while on the waiting list for a cadaveric renal transplant. Patients were reassessed approximately 12 months later. Among the 33 patients receiving a transplant during the follow-up period, those with a high preference for health-related information exhibited a substantial reduction in depression. In contrast, patients low in preference for information showed a slight increase in depression. Among the 27 patients who were not transplanted during the follow-up period, preference for information had no effect on depression. Patient differences in preference for behavioral involvement did not exert a significant effect on depression.

Cynical hostility, powerful others control expectancies, and patient adherence in hemodialysis.

OBJECTIVE: The present study examined the joint role of cynical hostility and powerful others health locus of control expectancies in predicting regimen adherence in a sample of center hemodialysis patients. METHOD: Forty-eight hemodialysis patients completed the Cook-Medley Hostility (Ho) Scale and the Powerful Others Health Locus of Control (PHLC) scale. Adherence to the fluid-restriction and phosphorus reduction components of the treatment regimen was assessed by examining patients' interdialysis session weight gains and serum phosphorus (P) levels. RESULTS: In a hierarchical regression analysis, higher hostility was associated with significantly higher serum P levels indicating poorer dietary and medication adherence. The main effect for hostility was qualified by the interaction of hostility and PHLC. This pattern indicated that the deleterious effect of hostility on adherence was most pronounced among patients possessing the expectancy that positive health outcomes are not strongly contingent on the actions or advice of powerful others (eg. health care providers). Similar analyses failed to show significant effects for hostility or PHLC in the prediction of interdialytic weight gain. CONCLUSIONS: The present findings suggest that jointly assessing hostility and health-related expectancies may be useful in identifying chronically ill patients who are potentially at risk for difficulties in performing a prescribed regimen.

Monitoring attentional style and medical regimen adherence in hemodialysis patients.

Previous research involving individuals facing chronic health problems suggests that an attentional style characterized by pronounced monitoring of threat-relevant information is associated with poorer behavioral and emotional adjustment. This study examined the hypothesis that a pronounced monitoring style would be associated with poorer medical regimen adherence in a sample of 51 chronic hemodialysis patients. Hierarchical regression analyses (controlling for demographic factors and trait anxiety) revealed that "high monitors" exhibited higher interdialysis weight gains and higher serum K values reflecting poorer adherence to fluid-intake and dietary restrictions. However, monitoring was not associated with a measure of medication adherence. Partial support was found for a model suggesting that a lack of perceived control is responsible for the relationship between higher monitoring and poorer adherence.

Social support and conscientiousness in hemodialysis adherence.

Previous conclusions regarding the role of social support in hemodialysis adherence are inconsistent, suggesting that other factors may moderate this relationship. Using the Five-Factor Model of Personality, we examined the hypothesis that conscientiousness would interact with social support in predicting fluid-intake and medication adherence in a sample of 56 chronic hemodialysis patients. Hierarchical regression analyses (controlling for demographic, clinical, and other personality variables) revealed a significant interaction between social support and conscientiousness. However, inconsistent with prediction, high support among patients with low conscientiousness was associated with poorer fluid-intake adherence, while support had little effect on fluid-intake adherence among high conscientiousness patients. No main or interactive effects were found for support or conscientiousness on a measure of medication adherence.

Body consciousness, illness-related impairment, and patient adherence in hemodialysis.

Recent theory and evidence suggests that bodily self-focusing tendencies (e.g. private body consciousness) may be associated with medical regimen adherence among chronically ill patients. The present study examined the joint effects of private body consciousness and degree of illness-related physical impairment on treatment regimen adherence in a sample of 52 hemodialysis patients. It was predicted that the effect of PBC on adherence would vary as a function of patients' level of illness-related physical impairment. For patients experiencing more severe impairment, higher PBC scores were associated with poorer adherence to the prescribed medication and dietary regimen. In contrast, for patients experiencing a relatively low degree of disease-related physical impairment, higher private body consciousness was associated with more favorable adherence. Results are discussed in terms of self-focused attention and behavioral self-regulation theories. Implications for future research and clinical intervention are also discussed.

Coping with treatment-related stress: effects on patient adherence in hemodialysis.

With a modified version of the Ways of Coping Checklist, the relation of coping to adherence among 57 hemodialysis patients was examined. The association of a particular type of coping to adherence was predicted to depend on the specific type of stressful encounter being considered. As predicted, coping efforts involving planful problem solving were associated with more favorable adherence when used in response to stressors involving a relatively controllable aspect of the hemodialysis context. For less controllable stressors, coping efforts involving emotional self-control were associated with more favorable adherence. The seeking of informational support in response to an uncontrollable encounter was associated with poorer fluid-intake adherence. Confrontive coping was associated with poorer adherence for both high- and low-control situations.

Effect of dietary potassium on blood pressure, renal function, muscle sympathetic nerve activity, and forearm vascular resistance and flow in normotensive and borderline hypertensive humans.

We evaluated the effect of a low potassium diet on blood pressure in normotensive (NT) and in borderline hypertensive subjects (BHT). There were 11 BHT men (age, 24.6 +/- 1.2 years) and 10 NT men (age, 23.5 +/- 1.0 years). Subjects were studied while on both low potassium, high sodium (30 meq/day, 400 meq/day) diets and high potassium, high sodium (100 meq/day, 400 meq/day) diets, each taken for 6 days. During the low potassium diet, daytime ambulatory systolic blood pressure increased in both NT (123 +/- 5 mm Hg, low potassium, vs. 116 +/- 4 mm Hg, high potassium, p less than 0.01) and BHT groups (134 +/- 3, low potassium, vs. 124 +/- 3, high potassium, p less than 0.001). Mean blood pressure was not different in NT during the two diets but was significantly higher during the low potassium diet in BHT subjects (97 +/- 2 mm Hg low potassium, vs. 92 +/- 1 mm Hg, high potassium, p less than 0.05) without change in heart rate in BHT subjects during the two diets. Low potassium diet increased the postural rise in diastolic blood pressure when subjects changed from the supine position to quiet standing (standing diastolic blood pressure for NT: low potassium, 79 +/- 2 mm Hg vs. high potassium, 72 +/- 2 mm Hg; for BHT: low potassium, 89 +/- 2 mm Hg vs. high potassium diet, 83 +/- 2 mm Hg, p less than 0.01). The effects of low potassium diet on blood pressure were not related to marked changes in renal hemodynamics, in plasma renin activity, in aldosterone, or in norepinephrine, nor to increases in forearm vascular resistance or in muscle sympathetic nerve activity. In fact, muscle sympathetic nerve activity decreased in the BHT group during low potassium compared with high potassium diets (p less than 0.001) and did not change in the NT group. Sympathetic nerve activity was also higher in BHT compared with the NT group during high potassium and low potassium diets, p less than 0.001. In the NT group, the low potassium diet was associated with lower hematocrit levels, weight gain, and increased 24 hour urinary calcium levels. After the low potassium diet, serum potassium fell in both groups, and serum phosphorus fell significantly in the BHT group.(ABSTRACT TRUNCATED AT 400 WORDS)

Renal and hemodynamic effects of atrial natriuretic peptide in patients with cirrhosis.

The effects of anaritide, a 25-amino-acid synthetic analogue of ANP, were evaluated in 28 patients with cirrhosis complicated by ascites and/or edema. Each patient received two doses of the agent, as well as an infusion of placebo. Six different doses were tested ranging from 0.015-0.300 microgram/kg/min. The infusions lasted for 2 hours and were flanked by both baseline and recovery periods. There was a significant effect of placebo on urinary sodium and chloride excretion rates but no effect on urine flow rate. In response to anaritide, the urine flow rate increased at 0.03, 0.06, 0.075, and 0.100 microgram/kg/min. The sodium and chloride excretion rates increased at all doses except the highest dose. There was no definite effect of anaritide on urinary potassium, calcium, and phosphate excretion rates. There was also no significant effect on creatinine clearance. The mean arterial pressure decreased in response to the 0.060, 0.075, and 0.100 microgram/kg/min doses. In addition, five of the patients receiving the highest dose (0.300 microgram/kg/min) had decreases in their systolic pressures to 90 mm Hg or less. In conclusion, anaritide is natriuretic and diuretic in patients with cirrhosis complicated by ascites and/or edema. Its effect, however, on arterial pressure may limit its therapeutic potential in this patient population.

Elevated sympathetic nerve activity in borderline hypertensive humans. Evidence from direct intraneural recordings.

Reports of elevated plasma catecholamine levels and augmented responses to autonomic blockade suggest increased sympathetic tone in borderline hypertension. It is not known if this reflects greater sympathetic neural outflow. We directly recorded muscle sympathetic nerve activity (microneurography) in 15 normotensive and 12 borderline hypertensive age-matched men to determine whether borderline hypertensive individuals have elevated sympathetic nerve activity. Supine heart rate, blood pressure, plasma norepinephrine, and efferent muscle sympathetic nerve activity (peroneal nerve) were measured after 6 days of both low and high dietary sodium intake (10 and 400 meq sodium/24 hr). Sympathetic nerve activity was elevated significantly in borderline hypertensive individuals on both low (37 +/- 1 in borderline hypertensive individuals vs. 29 +/- 1 bursts/min in normotensive individuals; p less than 0.01) and high (25 + 1 in borderline hypertensive individuals vs. 16 +/- 1 bursts/min in normotensive individuals; p less than 0.01) sodium diets. The borderline hypertensive group had higher systolic (p less than 0.01) and diastolic (p less than 0.05) blood pressures independent of sodium intake. Across both groups, high sodium intake reduced muscle sympathetic nerve activity (p less than 0.001), plasma norepinephrine (p less than 0.001), diastolic blood pressure (p less than 0.02), heart rate (p less than 0.002), and increased weight (p less than 0.005). A significant (p less than 0.05) group-by-diet interaction was observed for plasma norepinephrine levels. Specifically, compared with the normotensive group, plasma norepinephrine levels in the borderline hypertensive group tended to be higher on low sodium diet (p = 0.08) and lower on high sodium diet (p = 0.23).(ABSTRACT TRUNCATED AT 250 WORDS)

Dietary salt produces abnormal renal vasoconstrictor responses to upright posture in borderline hypertensive subjects.

We studied the effect of high and low NaCl diets in normotensive and borderline hypertensive subjects to determine if a high NaCl diet produces abnormal renal vasoconstriction during the stress of upright posture in borderline hypertensive subjects. We studied 13 normotensive young men with diastolic blood pressures below 85 mm Hg and nine borderline hypertensive young men defined by diastolic blood pressures intermittently above 90 mm Hg. The subjects achieved comparable sodium balance during 6 days of low NaCl (10 mEq Na, 40 mEq Cl, 100 mEq K) and high NaCl (400 mEq Na, 400 mEq Cl, 100 mEq K) diets. In the normotensive subjects, standing for 30 minutes resulted in a tendency for diastolic blood pressure to fall during both diets. In contrast, during standing borderline hypertensive subjects showed no change in diastolic blood pressure during the low salt diet and a tendency for diastolic blood pressure to increase after the high salt diet. Standing reduced renal plasma flow in both groups during both diets. However, only during the high NaCl diet did the absolute decrease and percent decrease in renal plasma flow during standing differ significantly (p less than 0.05 and p less than 0.01, respectively) between the borderline hypertensive (-151 +/- 24 ml/min/1.73m2; -29 +/- 4%) and normotensive subjects (-79 +/- 17 ml/min/1.73m2; -15 +/- 3%). The resultant increase in the renal vascular resistance index with standing did not differ between the two groups during the low NaCl diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Low sodium diet corrects the defect in lymphocyte beta-adrenergic responsiveness in hypertensive subjects.

To determine the role of dietary sodium intake in the reduction in beta-adrenergic sensitivity in hypertension, lymphocyte beta-receptors from 8 borderline hypertensive and 16 normotensive subjects were studied after 5 d on a high sodium diet (400 meq/d) and also following a low sodium diet (10 meq/d). During the high sodium diet, lymphocyte beta-receptor-stimulated adenylate cyclase activity, expressed as the relative increase over basal levels stimulated by the beta-agonist isoproterenol, was significantly (P less than 0.025) decreased in hypertensive (24 +/- 5%, mean +/- SE) compared with normotensive (42 +/- 4%) subjects. Neither beta-receptor density nor the proportion of nonsequestered beta-receptors differed between groups. A low sodium diet significantly increased beta-receptor-stimulated adenylate cyclase activity in hypertensives (low sodium, 51 +/- 7%; high sodium, 24 +/- 5%, P less than 0.025) to a level not different than that of normotensives (46 +/- 5%). Thus, reduced lymphocyte beta-receptor responsiveness in hypertensive subjects is not due to beta-receptor sequestration and is corrected on a low sodium diet. Dietary sodium may be an important factor in the beta-receptor defect in early hypertension.

Local and systemic effects of orally applied sodium salts.

This study determines whether the oral application of a baking soda-3% hydrogen peroxide dentifrice and a nearly saturated sodium chloride mouthwash, as a home care method for treating periodontal disease, creates a sodium burden for human subjects. The dietary intake and urinary excretion of sodium and potassium were monitored in participating subjects. Urinary sodium did not increase in subjects using the method. Desquamative gingival lesions, however, were seen in all treated subjects. Further study is needed to determine safe salt concentrations for this home care regimen.

Effects of aldosterone on urinary kallikrein and sodium excretion during fetal life.

The present study was designed to investigate the effect of acute (2 h) and chronic aldosterone (4 days) infusion on urinary kallikrein excretion rate and on renal handling of Na+ and K+ in chronically catheterized fetal lambs less than 115 days gestation (n = 6) and greater than 125 days gestation (n = 7). Chronic aldosterone infusion decreased plasma renin activity in both groups of fetuses. Both acute and chronic aldosterone infusion produced significant decreases in UNa + V in fetuses greater than 125 days and in the majority of fetuses less than 115 days gestation (five of six). Aldosterone infusion did not increase K+ excretion in either group of fetuses. It is also demonstrated that chronic aldosterone infusion induced an increase in urinary kallikrein excretion rate in both groups of fetuses. Taken together, these results demonstrate that aldosterone has antinatriuretic but no kaliuretic effects during fetal life, but produces a rise in urinary kallikrein excretion rate during the last trimester of gestation in fetal lambs.

Urinary kallikrein response to acute saline or water loads in hypertensive and normal humans.

Urinary kallikrein excretion during acute water or saline loading was studied in normal and hypertensive humans after chronic Na+ depletion and Na+ loading to answer the following questions. 1. Is urinary kallikrein a natriuretic or diuretic substance? 2. During acute water or saline loading, does the underlying Na+ balance influence (a) the urinary kallikrein response? or (b) the relationship between urinary kallikrein and renal Na+ or water handling? 1) Urinary kallikrein did not change during a 1.2 liter water load given to nine white hypertensive and five white normal men. Urinary kallikrein was significantly decreased, however, in five white hypertensive and five white normal subjects during and after 1 hour of isotonic saline infusion (30 ml/kg). In sodium-depleted hypertensive patients kallikrein excretion was decreased from 19.8 to 9.5 mEU /min, and in Na+-depleted normal subjects it was decreased from 15.7 to 12.6 mEU /min (p = 0.003). The response in hypertensive patients was not different from normal subjects. In all Na+-loaded subjects, kallikrein excretion was also significantly decreased during isotonic saline infusion (p = 0.01). Urinary kallikrein did not change in three other subjects given hypertonic saline. 2(a) The underlying state of Na+ balance influenced the baseline level of kallikrein excretion, but not the directional decline in kallikrein during isotonic saline. (b) In Na+-restricted hypertensives given isotonic saline, urinary kallikrein was inversely related to the fractional excretion of Na+ (r = -0.54, p less than 0.01) and the tubular reabsorption of H2O (TcH2O/GFR; r = -0.50, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Renal and adrenal responses to converting-enzyme inhibition in fetal and newborn life.

The renal and adrenal responses to a continuous infusion of the angiotensin-converting enzyme (ACE) inhibitor captopril were studied in 27 chronically catheterized sheep fetuses (less than 120 days gestation, n = 15, and greater than 130 days gestation, n = 12; term being 145 days) and in 12 newborn lambs between 8 and 21 days of age. Total renal blood flow did not change during ACE inhibition. However, the renal vascular resistance decreased significantly in newborn lambs (-21.8 +/- 5.7%) and in fetuses greater than 130 days (-21.7 +/- 4.7%) but not in fetuses less than 120 days. A significant decrease in filtration fraction (-19.2 +/- 6.5%) was observed in newborn lambs. No changes in urinary kallikrein and prostaglandin excretion rate were observed during ACE inhibition in any group of animals. ACE inhibition produced similar declines in blood pressure in both groups of fetuses (-10.2 +/- 3% in fetuses less than 120 days and -9.5 +/- 4.6% in fetuses greater than 130 days) and in newborn lambs (-13.4 +/- 2.1%). The percent changes in plasma renin activity were similar in all groups of animals. However, a significant decline in plasma aldosterone concentration was observed only in newborn lambs (from 130 +/- 31 to 64 +/- 9 pg/ml). These results suggest that the renin-angiotensin system might have physiological significance during maturation, but that this role seems to be more important in near-term fetuses (greater than 130 days) and postnatally than early in gestation.

Fludrocortisone suppression of sympathetic nervous activity.

Fludrocortisone depressed plasma norepinephrine in normal subjects but to a lesser degree than it depressed renin activity or urinary aldosterone excretion. Sympathetic nervous reactivity (defined as upright/supine plasma norepinephrine) was decreased more than supine plasma norepinephrine. Pretreatment supine plasma norepinephrine (but not plasma renin activity or aldosterone excretion) correlated with blood pressure changes during fludrocortisone dosing, which suggests participation of the sympathetic nervous system in the blood pressure elevations reported during exogenous steroid administration or primary aldosteronism. Suppression of sympathetic nervous activity and reactivity by fludrocortisone tends to explain its limited usefulness in patients with autonomic dysfunction and postural hypotension.

Developmental aspects of the renal kallikrein-like activity in fetal and newborn lambs.

The ontogeny of the renal kallikrein-like activity and the interrelationships between this enzyme and the renin-angiotensin-aldosterone and prostaglandin systems were studied in 43 chronically catheterized sheep fetuses between 104 and 142 days of gestation (term, 145 days) and in 8 chronically catheterized newborn lambs between 5 and 23 days of age. Urinary kallikrein (UKall) excretion rate expressed in absolute values (mEU/hr) or corrected for kidney weight (mEU X hr-1 X gKW-1) or glomerular filtration (mEU X hr-1 X ml GFR-1) increased significantly during fetal maturation and after birth. The rise in UKall during fetal and newborn life was not dependent on an increase in urinary flow rate (r = 0.06). The increase in fetal UKall (mEU X hr-1 X gKW-1) correlated closely with the rise in plasma aldosterone concentration for values above 35 pg/ml (r = 0.72, P less than 0.001). A significant negative correlation was found between UKall (mEU X hr-1 X gKW-1) and log of individual urinary sodium excretion values (r = -0.78, P less than 0.001). No correlation was found between UKall and urinary prostaglandins (PGE, PGF2 alpha) excretion during fetal and newborn life, but UKall correlated closely with the rise in renal blood flow during maturation (r = 0.87, P less than 0.001). The present data suggest that aldosterone is an important regulator of UKall release early during development. It is also suggested that conceptional age is an important factor which may modulate the renal sensitivity to aldosterone-stimulated UKall excretion.