Predictors of mortality in end-stage renal disease patients with mitral annulus calcification.

OBJECTIVE: Mitral annulus calcification (MAC) is an independent predictor of cardiovascular mortality in the general population. The purpose of the current historical cohort study is to assess risk factors for long-term mortality in end-stage renal disease (ESRD) patients with MAC (n = 30; age, 62 +/- 2 yr), as compared to ESRD patients without MAC (n = 30; age, 63 +/- 2 yr). Additional analysis compared ESRD patients with MAC to non-ESRD patients with MAC (n = 32; age, 66 +/- 2 yr). METHODS: The groups included age-matched male patients followed at a single center. Long-term survival was assessed by Kaplan-Meier analysis. Regular and stepwise Cox proportional hazards models were used to determine risk factors for mortality. RESULTS: There was a similarly high prevalence of cardiovascular complications, including hypertension, coronary artery disease, left ventricular hypertrophy, atrial fibrillation, and congestive heart failure, in all three groups. Median survival time was significantly longer in non-ESRD patients (90 months), compared with the ESRD with MAC (45 months) and ESRD without MAC (45 months) patients (log-rank test; P < 0.001). With stepwise Cox proportional hazards model, including ESRD patients with MAC and ESRD patients without MAC, increased calcium x phosphate product, decreased serum creatinine concentration, and the presence of coronary artery disease and lower extremity amputations were independent predictors of mortality for patients with ESRD. With stepwise Cox proportional hazards model, including ESRD patients with MAC and non-ESRD patients with MAC, the presence of ESRD, atrial fibrillation, diabetes, aortic valve calcification, coronary artery disease, and tricuspid regurgitation were independent predictors of mortality. CONCLUSION: The mortality rate was high in ESRD patients, approximately 15% per year. After accounting for baseline cardiovascular disease and traditional risk factors, the presence of MAC did not confer additional risk for mortality.

Influences on renal function in chronic spinal cord injured patients.

PURPOSE: The optimal method of bladder management in the spinal cord injured population remains controversial. We determined the significance of bladder management and other factors on renal function in this population. MATERIALS AND METHODS: We retrospectively reviewed the medical records and upper tract imaging studies of 308 patients with a mean followup of 18.7 years since injury. Renal function was assessed by serum creatinine, creatinine clearance and proteinuria measurement, and by upper tract abnormalities on renal ultrasound and nuclear medicine renal scan. Independent variables evaluated for an influence on renal function included patient age, interval since injury, injury level and completeness, vesicoureteral reflux, history of diabetes mellitus and bladder management method. RESULTS: Mean serum creatinine plus or minus standard deviation in patients on chronic Foley catheterization, clean intermittent catheterization and spontaneous voiding was 1.08 +/- 0.99, 0.84 +/- 0.23 and 0.97 +/- 0.45 mg./dl. (analysis of variance p = 0.05, Student's t test p = 0.10), and mean creatinine clearance was 91.1 +/- 46.5, 113.4 +/- 39.8 and 115 +/- 49 ml. per minute, respectively (analysis of variance and Student's t test p <0.01), respectively. Proteinuria was present in 19 patients (6.2%) in the Foley catheterization, 3 (1%) in the clean intermittent catheterization and 4 (1.3%) in the spontaneous voiding group (chi-square test p <0.01), while there were upper tract abnormalities in 56 (18.2%), 20 (6.5%) and 24 (7.8%) patients, respectively (chi-square test p <0.01). Multiple regression analyses revealed no significant predictors of serum creatinine, although older patient age and Foley catheterization significantly predicted low creatinine clearance. Additional logistic regression analyses showed that Foley catheterization was associated with proteinuria and vesicoureteral reflux was associated with upper tract abnormalities. CONCLUSIONS: While renal function may be preserved by all forms of bladder management, chronic indwelling catheters may contribute to renal deterioration.

Risk factors for development of proteinuria in chronic spinal cord injury.

A retrospective, case-control study was performed to investigate the risk factors that may contribute to the development of proteinuria in patients with chronic spinal cord injury (SCI). During an 18-month period, 31 subjects with a 24-hour protein excretion of 1.0 g or greater were identified. Three control subjects with SCIs with a 24-hour urinary protein excretion of less than 1.0 g during the same time period were randomly selected for each study subject with proteinuria. Clinical data, including level and duration of injury, age, presence of indwelling bladder catheter, number of decubitus ulcer procedures, serum albumin and creatinine concentrations, hematocrit, creatinine clearance, and the presence of hypertension and diabetes mellitus, were obtained from medical records. Subjects with proteinuria had other evidence of renal dysfunction with greater serum creatinine concentrations and reduced creatinine clearances, serum albumin concentrations, and hematocrits. Proteinuric subjects were older, had a longer duration of injury, had undergone a greater number of decubitus ulcer procedures, and were more likely to have hypertension and indwelling bladder catheters. The independent predictors for the development of proteinuria using logistic stepwise multiple linear regression analysis were the use of chronic indwelling bladder catheters, number of decubitis ulcer procedures, presence of hypertension, and older age. These data suggest that inflammatory complications associated with complications of chronic SCI, rather than SCI per se, contribute to the development of proteinuria. SCI patients with proteinuria have more impaired renal function and increased mortality compared with SCI patients without proteinuria.

Hemodynamic response to vasopressin in dehydrated human subjects.

BACKGROUND: Despite the known potent vasoconstrictor effects of vasopressin, the role of this hormone in the maintenance of blood pressure is incompletely understood. In studies performed in animals with increased plasma vasopressin concentrations, several complex cardiovascular effects have been noted, including decreases in heart rate and cardiac output, which may account for a lack of effect on arterial pressure despite the vasopressin-induced increase in total peripheral resistance. Only a few studies have been done to assess the cardiovascular effects of vasopressin in human subjects, and most of these have been limited to measurement of heart rate and arterial pressure only. The present study was designed to identify more fully the cardiovascular effects of vasopressin when plasma vasopressin concentrations are increased by osmotic stimulation without the superimposition of major nonosmotic stimuli associated with severe volume depletion. METHOD: Studies were performed on 11 normal human subjects in supine and erect posture before and after 24 hours of fluid deprivation, and following administration of a selective V1 receptor antagonist, [d(CH2)5Tyr(ME)]AVP, after dehydration. Cardiovascular parameters were measured noninvasively by thoracic electrical bioimpedance cardiography and blood samples for measurements of plasma concentrations of vasopressin and other hormones affected by dehydration and differences in posture were collected for subsequent analysis. RESULTS: After 24 hours of fluid restriction, plasma osmolality was increased from 287 +/- 0.9 to 294 +/- 0.7 mosm/kg H20 and plasma vasopressin concentrations (Pavp) were increased in both supine and erect posture. Mean arterial (MAP) and systolic blood pressure (SBP) were reduced by fluid restriction but were higher in erect than in supine posture both before and after fluid restriction. Heart rate (HR), diastolic blood pressure (DBP), and systemic vascular resistance (SVRI) were also higher in erect than in supine posture, while cardiac index (CI), stroke index (SI), end-diastolic index (EDI), and an index of total thoracic fluid content (TFC) were all reduced in erect posture, both before and after dehydration. Plasma renin activity (PRA) and plasma norepinephrine concentrations (Pne) were increased in erect posture, both before and after dehydration, but there was no effect of erect posture on plasma vasopressin concentrations (Pavp), either before or after dehydration. Administration of the V1 receptor antagonist after dehydration had no effect on hemodynamic parameters other than small reductions in DBP and cardiac preload. CONCLUSION: It is concluded from these studies that small increases in Pavp associated with moderate dehydration do not play a role in the maintenance of arterial pressure in normal human subjects in either supine or erect posture.