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E A Friedman

Publications and source records attributed to E A Friedman.

At least 73 records · Page 4Linked to original sources
PubMed1997

Overt malignancy in long-term hemodialysis patients.

We studied all 39 patients who were on maintenance hemodialysis for 10 years or more (range, 10 to 24 years) in three free-standing, not-for-profit hemodialysis units to determine the prevalence of malignancy. The three dialysis units have a total patient population of 470, all of whom are cared for by the same group of physicians. From the same dialysis units, we selected a control cohort of 37 patients matched for age, gender, race, and renal diagnosis who were on hemodialysis for 3 years or less (short-term patients). Control patients were selected by randomly choosing the next patient who filled the criteria for duration of dialysis from the roster of all patients at a facility. Clinically overt malignancy during dialytic therapy was determined by history, physical examination, Pap smear, mammogram, and colonoscopy in patients with gastrointestinal bleeding. The mean age (+/-SE) of the long-term patients was 51.8 +/- 1.9 years, and that of the control group was 51.5 +/- 2.4 years (P = .92). Thrice-weekly hemodialysis prescriptions were similar in both groups: long term, 3.5 +/- 0.02 hours; control, 3.4 +/- 0.02 hours (P = .27). No malignancy was detected in either the long-term or the short-term patients, and no patient of either group had a malignancy in the past. Colonic biopsy specimens of four long-term patients who had gastrointestinal bleeding were normal. The prevalence of malignancy was not increased in patients who were on maintenance hemodialysis for 10 years or longer.

Case-Control Studies↗
PubMed1996

Uninsured in the USA.

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Health Services Accessibility↗
PubMed1996

The effect of kidney size on cadaveric renal allograft outcome.

Chronic rejection is the commonest cause of long-term renal allograft loss. Though immunologic factors are thought dominant in its pathogenesis, nonimmunologic factors, in particular, hyperfiltration damage related to reduced renal mass, have also been proposed as factors in the causation of chronic allograft rejection. We assessed the influence of renal size on graft survival and function in all cyclosporine-treated cadaver donor adult renal allograft recipients engrafted at a single center between June 1989 and July 1994, whose grafts functioned for > or = to 3 months (n=169). Patients were divided into 4 groups based on the ratio of kidney volume to recipient body surface area (volume/BSA) (ml/m2), and outcome in groups compared by methods including Cox's proportional hazards and Kaplan-Meier analysis. No significant differences between groups existed for serum creatinine levels, presence of significant proteinuria, or 1- and 5-year graft survival. There was no correlation between volume/BSA and either serum creatinine or degree of proteinuria at 3, 6, 12, 36, and 60 months posttransplant. Volume/BSA was similar in patients with good or poor renal function (58 +/-21 vs. 56 +/- 28 ml/m2), with or without significant proteinuria (57 +/- 24 vs. 60 +/- 25 ml/m2) or in patients who lost their grafts to chronic rejection compared with those with stable allograft function (64 +/- 34 vs. 59 +/- 24 ml/m2). Volume/BSA was not a predictor of graft survival on multivariate regression. We conclude that donor kidney size has no apparent effect on cadaveric renal allograft outcome in the short and intermediate-term, suggesting that close matching of donor kidney size to recipient size is not presently indicated.

Adolescent↗
PubMed1996

The intensity of hemodialysis and the response to erythropoietin in patients with end-stage renal disease.

BACKGROUND: Anemia (characterized by a hematocrit of 30 percent or lower) persists in 40 to 60 percent of patients treated for end-stage renal disease with maintenance hemodialysis, despite concomitant erythropoietin (epoetin) therapy. We tested the hypothesis that inadequate dialysis is a key reason for the insufficient response to erythropoietin in patients with end-stage renal disease who are receiving hemodialysis. METHODS: We prospectively studied 135 randomly selected patients undergoing hemodialysis who had been receiving intravenous erythropoietin for at least four months. The adequacy of dialysis was assessed by measuring the percent reduction in the blood urea nitrogen concentration and the serum albumin concentration. The hematocrit was measured weekly for four weeks, transferrin saturation was measured, and coexisting illnesses were documented. To determine the effect of an increased level of dialysis on the hematocrit, the thrice-weekly schedule of dialysis was increased to raise the mean urea-reduction value from 60.7 to 72 percent for six weeks in 20 consecutive patients whose base-line urea-reduction value was less than 65 percent. The change in the hematocrit in these patients was compared with that observed in the next 20 patients who had an equivalent base-line urea-reduction value but whose level of dialysis was not altered. RESULTS: The mean hematocrit of the entire group was 29.2 +/- 4 percent, and the mean thrice-weekly dose of erythropoietin was 59 +/- 29 U per kilogram of body weight. The mean serum albumin concentration was 3.8 +/- 0.4 g per deciliter, the mean urea-reduction value was 62 +/- 4.8 percent, and the mean transferrin saturation was 20 +/- 9 percent. Multiple regression analysis revealed direct correlations between the hematocrit and the serum albumin concentration (P = 0.009) and between the hematocrit and the urea-reduction value (P = 0.012) after adjustment for other factors. A logistic-regression analysis indicated that an 11 percent increase in the urea-reduction value doubled the odds that a patient would have a hematocrit above 30 percent. After six weeks of increased intensity of dialysis in 20 patients with base-line urea-reduction values of less than 65 percent, the mean (+/- SE) hematocrit rose from 28.4 +/- 0.78 percent to 32.3 +/- 0.71 percent (P = 0.002); there was no significant change in a control group of 20 patients with equivalent base-line urea-reduction values in whom the dialysis level was not altered (28.2 +/- 0.84 percent to 26.3 +/- 0.85 percent; P = 0.175). CONCLUSIONS: In patients with end-stage renal disease, inadequate hemodialysis is associated with a suboptimal response to erythropoietin therapy. Increasing the intensity of dialysis in patients with anemia who are receiving inadequate dialysis results in a significant increase in the hematocrit.

Aged↗
PubMed1996

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Abbreviations as Topic↗
PubMed1996

Excess morbidity in patients starting uremia therapy without prior care by a nephrologist.

Many inner-city residents with progressive renal disease do not receive specialist care from a nephrologist, and often arrive in the emergency room manifesting life-threatening uremic symptoms requiring emergency rescue dialysis. We examined the relationship between the quality of medical care received during progression to end-stage renal disease, and the clinical condition and morbidity at initiation of renal replacement therapy. During a 5-year period (January 1990 to December 1994), we prospectively studied 139 consecutive inner-city residents with a confirmed diagnosis of chronic renal failure who were starting uremia therapy. At onset of study, subjects were sorted into one of three groups depending on the extent of medical care received during the 3 years immediately preceding initiation of hemodialysis: nephrologist, nonnephrologist (physician), or no medical care. Information obtained from each subject included length of hospital stay during the admission for initiation of dialysis therapy and the type of hemodialysis vascular access used for first dialysis treatment (permanent v temporary). Predialysis blood urea nitrogen concentration, serum creatinine concentration, serum albumin concentration, and serum bicarbonate concentration were measured once immediately before the first dialysis. The 139 study subjects (62 men and 77 women) comprised 116 blacks (83%), 15 Hispanics (11%), and eight whites (6%), and had a mean age of 56 +/- 15 years (+/-SD). Only 59 (43%) subjects received prior specialist nephrologist care, and their mean length of hospital stay (12 +/- 23 days) was shorter than that of subjects who received nonnephrologist care (n = 63 [45%]; 25 +/- 21 days) or those who received no prior medical care (n = 17 [12%]; 29 +/- 23 days) (P = 0.002). Temporary hemodialysis vascular access was used for the first dialysis in all 17 (100%) of the subjects with no prior medical care, in 56 (89%) of the 63 subjects who received prior care from a nonnephrologist, and in 21 (36%) of the 59 subjects who received prior care from a nephrologist (P = 0.0001). Subjects who received prior care from a nephrologist had a lower mean serum creatinine concentration at initiation of dialysis (11 +/- 4.4 mg/dL) than did either the subjects who received nonnephrologist care (13 +/- 5.4 mg/dL) or no medical care (16 +/- 5.7 mg/dL) (P = 0.003). In addition, subjects who received prior care from a nephrologist had less severe metabolic acidosis than the subjects in the other two groups (P = 0.04). We infer that initiation of uremia therapy is delayed in inner-city residents with progressive renal failure who do not receive specialist nephrologic care, and that as a consequence these patients suffer excess short-term morbidity.

Anemia↗
PubMed1996

Bowel as a kidney substitute in renal failure.

Maintenance peritoneal dialysis and hemodialysis sustain the lives of approximately 250,000 uremic patients in industrialized nations worldwide. The cost of uremia therapy, however, exceeds health care budgets in developing countries. As a consequence, most of those alive today have no chance of effective treatment should their kidneys fail. Extraction, modification, or recycling of nitrogenous wastes by the gastrointestinal tract is a potentially low-cost means of substituting for missing renal function. Multiple approaches to the bowel as a substitute kidney have been attempted. Direct removal of nitrogen-containing compounds by an external gut fistula, gastric, ileal, or colonic gavage (dialysis) or induced diarrhea extract water and urea but only minimal amounts of larger molecules such as creatinine. Binding of nitrogen compounds to inert orally administered sorbents such as charcoal or oxystarch has been pursued in advanced uremia. Modification of nitrogen compounds by ingesting enzymes derived from soil bacteria or packaged in artificial cells is an approach that, although exciting, is incompletely evaluated. Evidence indicates that strains of bacteria can be induced to synthesize enzymes that recycle urea and other nitrogen compounds retained by uremic individuals. Clinical trials to substantiate uncontrolled trials of bowel substitution in renal failure will, if positive, accelerate development of a practical regimen to extend life where no other means are possible.

Animals↗
PubMed1996

Renal syndromes in diabetes.

Renal disorders attributed to diabetes mellitus are increasingly recognized as the dominant feature of long-term management. Renal failure in diabetic patients is the most commonly recognized cause of irreversible uremia in the United States, Europe, and Japan. Treating hypertension and normalizing hyperglycemia slows the previously thought inexorable progress of renal insufficiency in diabetes. Once end-stage renal disease has developed, either dialytic therapy or a renal transplant affords life extension, often with excellent rehabilitation.

Blood Pressure↗
PubMed1996

Correlates of vascular access and nonvascular access-related hospitalizations in hemodialysis patients.

Four hundred and thirty randomly selected hemodialysis patients, aged 20 years and over, were studied to identify risk factors for vascular access and nonvascular access-related hospitalizations in the immediately preceding 1 year. Risk estimates for hospitalization were assessed using a multinominal logistic analysis model. We measured functional status, utilizing a 14-point Karnofsky scale, and in a separate analysis of covariance, in which Karnofsky score was the outcome, we examined the relationships of age, gender, ethnicity, renal diagnosis, and hospitalization. Individual comparisons were adjusted for multiple comparison bias by Tukey's Honest Difference method. There were a total of 508 hospitalizations of which 322 (63%) lasted > or = 1 week. Two hundred and sixty (60%) patients were hospitalized at least once; 105 (24.4%) for access problems only, 115 (27%) for a nonaccess problem only, and 40 for access and nonaccess-related problems. Access-related problems, accounted for 48% of all hospitalizations. The risk of hemodialysis vascular access morbidity was increased in women (p < 0.028) and white (p < 0.048) hemodialysis patients. Neither diabetic nor elderly hemodialysis patients were at greater risk for access hospitalization than their respective counterparts, though a greater proportion of the access hospitalizations in the elderly (> or = 64 years) lasted > or = 1 week (p < 0.0006). More access-related hospitalizations in blacks (64.5%), lasted for > or = 1 week than in whites (40.6%) (p < 0.001). Hispanics (p < 0.043), whites (p < 0.002), and the older patients (p < 0.054) were at greater risk for nonaccess hospitalization than blacks and younger patients, respectively. Even after adjusting for age, race, and diabetes, each decrease of one unit in the modified Karnofsky score was associated with a 3-4% increased risk for all types of hospitalization (p < 0.001)--poor functional status is associated with increased risk for all hospitalizations. We conclude that the risk for hemodialysis vascular access morbidity is increased in women and white hemodialysis patients. Poor functional status is associated with increased risk for all hospitalizations.

Adult↗
PubMed1996

Hemodialysis immediately after acute myocardial infarction.

Acute myocardial infarction (AMI) is common in patients who have end-stage renal disease. However, the prudent interval after AMI until resuming hemodialysis is unknown. Also incidence and severity of intradialytic morbid events during the initial dialysis treatment after AMI have not been determined. We conducted a retrospective analysis of the course of hemodialyses performed immediately after AMI in 13 maintenance hemodialysis patients (group 1) hospitalized with AMI over the 5-year period 1988-1992. For comparison, the incidence of intradialytic morbid events (hypotension--systolic blood pressure < 90 or diastolic blood pressure < 60 mm Hg or a fall in systolic or diastolic blood pressure of > 30 mm Hg--with and without symptoms, arrhythmias, and unplanned termination of hemodialysis was extracted from the charts of 9 maintenance hemodialysis patients (group 2) admitted during the same period with angina but no AMI, and in 13 stable ambulatory hemodialysis patients (group 3) dialyzed during the same period who had no evidence of heart disease. Patients in groups 1 and 2 were sorted by time interval from onset of chest pain to initiation of hemodialysis (< 12, 12-24, and > 24 h). In group 1, we examined the relationship of anatomic location of AMI, number of antihypertensive medications, predialysis left ventricular systolic ejection fraction, and various other clinical and laboratory parameters to the incidence intradialytic morbid events. The mean (+/- SD) age of the study subjects was 67 +/- 7.5 years in group 1, 57 +/- 3.7 in group 2, and 60 +/- 11 years in group 3 (p = 0.6). Arrhythmias and early termination of dialysis did not occur in any patient. Intradialytic hypotension (IDH) was recorded in 5 (38%) of 13 patients in group 1, in 3 (33%) of 9 in group 2, and in 2 (15%) of 13 patients in group 3 (p = 0.47). 4 (80%) of 5 patients in group 1 had multiple episodes of IDH. There were 0.92 +/- 1.4 episodes of IDH per patient in group 1 as compared with a rate of 0.44 +/- 0.68 per patient in group 2, and of 0.15 +/- 0.36 per patient in group 3 (p = 0.2). IDH responded to 0.9% normal saline replacement in all cases. Group 1 patients who had IDH (n = 5) were older (68 +/- 3 vs. 58 +/- 7 years, p = 0.01), had a lower diastolic blood pressure at the start of hemodialysis (59 +/- 13 vs. 83 +/- 13 mm Hg; p = 0.01), had a lower post-AMI left ventricular systolic ejection fraction (42 +/- 19 vs. 62 +/- 10%; p = 0.04), and also had a lower predialysis serum albumin level (3.6 +/- 0.4 vs. 4.1 +/- 0.4 g/dl; p = 0.09) than those who did not have IDH (n = 8). All 5 group 1 patients who had IDH (100%) had had prior AMI as compared with 2 (25%) of 8 of those who did not have IDH (p = 0.02). AMI involved the inferior myocardial wall in more (4 of 5; 80%) of the group 1 patients who had IDH as compared with those who did not have IDH (2 of 8; 25%; odds ratio = 9.5; p = 0.08; 95% confidence interval = 0.7-341.0). In group 1 patients, the time from onset of chest pain to hemodialysis did not affect the risk of IDH (p = 0.4). We conclude that a low diastolic blood pressure at onset of hemodialysis prior myocardial infarction, inferior myocardial wall involvement, advanced age, and a low predialysis serum albumin level are risk factors for the development of hypotension during the first hemodialysis session after AMI.

Aged↗