Clinical practice guidelines in end-stage renal disease: a strategy for implementation.
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Clinical practice guidelines (CPGs) for end-stage renal failure (ESRD) were recently published, and represent a comprehensive review of available literature and the considered judgment of experts in ESRD. To prioritize and implement these guidelines, the evidence underlying each guideline should be ranked and the attributes of each should be defined. Strategies to improve practice patterns should be tested. Focused information for each high priority guideline should be disseminated, including a synopsis and assessment of the underlying evidence, the evidence model used to develop that guideline, and suggested strategies for CPG implementation. Clinical performance measures should be developed and used to measure current practice, and the success of changing practice patterns on clinical outcomes. Individual practitioners and dialysis facilities should be encouraged to utilize continuous quality improvement techniques to put the guidelines into effect. Local implementation should proceed at the same time as a national project to convert high priority CPGs into clinical performance measures proceeds. Patients and patient care organizations should participate in this process, and professional organizations must make a strong commitment to educate clinicians in the methodology of CPG and performance measure development and the techniques of continuous quality improvement. Health care regulators should understand that CPGs are not standards, but are statements that assist practitioners and patients in making decisions. (+info)
Recurrent "Flexispira rappini" bacteremia in an adult patient undergoing hemodialysis: case report.
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A blood culture from a 65-year-old febrile man undergoing hemodialysis revealed, 5 days after inoculation, an unusual gram-negative fusiform rod with darting motility. During another episode of fever 21 days later, this Campylobacter-like organism was again recovered from three blood cultures and subcultured under an H2-enriched microaerobic atmosphere. The organism was catalase negative and oxidase positive and hydrolyzed urea rapidly. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of whole-cell proteins was indistinguishable from that of "Flexispira rappini" LMG 8738 described by Archer et al. in 1988 (J. R. Archer, S. Romero, A. E. Ritchier, M. E. Hamacher, B. M. Steiner, J. H. Bryner, and R. F. Schell, J. Clin. Microbiol. 26:101-105, 1988). The analysis of the 16S ribosomal DNA sequence revealed a similarity of 99.3% between the two strains. The patient recovered completely after a 4-week course of meropenem therapy. This is the first reported case of a recurrent "F. rappini" bacteremia in an adult patient, which confirms that this organism may be an invasive pathogen in immunocompromised patients, like other newly described Helicobacter species. (+info)
Acute barium intoxication following ingestion of ceramic glaze.
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A case of deliberate overdose of barium sulphide in a psychiatric setting is presented, with resulting flaccid paralysis, malignant arrhythmia, respiratory arrest and severe hypokalaemia, but ultimately with complete recovery. The degree of paralysis appears to be related directly to serum barium levels. The value of early haemodialysis, particularly with respiratory paralysis and hypokalaemia, is emphasised. (+info)
A cholesteryl ester transfer protein gene mutation and vascular disease in dialysis patients.
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Among patients undergoing maintenance hemodialysis, a decreased high-density lipoprotein cholesterol (HDL-C) concentration is among the most common abnormalities of lipid metabolism and apparently is an independent risk factor for vascular disease. A common missense mutation of cholesteryl ester transfer protein gene, D442G (Asp 442 to Gly), increases HDL-C levels through the reduced activity of cholesteryl ester transfer from HDL to VLDL, but the mutation also may lead to reduced activity of reverse cholesterol transport. To investigate the effect of the D442G polymorphism on atherosclerotic complications in dialysis patients, the genotype and allele frequency of the polymorphism were determined in 414 unselected dialysis patients and 220 control subjects, and postprandial serum lipid levels were measured in the dialysis patients. A similar genotype distribution was found between hemodialysis patients and healthy control subjects, and in dialysis patients with and without vascular disease. Serum levels of total cholesterol and HDL-C did not differ between patients with and without the mutation and in patients with and without vascular disease. However, patients with sub-median HDL-C levels (<45 mg/dl) had an independent odds ratio of 1.8 for vascular disease (95% confidence interval, 1.04 to 3.2; P < 0.05). In this low-HDL-C subgroup, patients with the D442G mutation had a significantly higher prevalence of vascular disease than those with no mutation (54.5% versus 24.4%; P < 0.05), and an independent odds ratio of 4.9 (95% confidence interval, 1.05 to 22.65; P < 0.05). In conclusion, the D442G mutation is an independent risk factor for atherosclerotic complications in dialysis patients with HDL-C levels below 45 mg/dl. (+info)
Non-insulin-dependent diabetes mellitus and hypertriglyceridemia impair lipoprotein metabolism in chronic hemodialysis patients.
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Patients with diabetes mellitus undergoing chronic hemodialysis treatment have the worst outcome on dialysis due to an increased rate of cardiovascular complications. Nearly all patients present with dyslipidemia, a prominent vascular risk factor, probably responsible for the high rate of vascular injury. Since both uremia and diabetes predispose to hypertriglyceridemia, the present study was conducted to investigate the influence of diabetes mellitus and/or hypertriglyceridemia on lipoprotein metabolism in hemodialysis patients. LDL was isolated and characterized from hyper- and normotriglyceridemic diabetic and nondiabetic hemodialysis patients (n = 40; 10 in each group); also, LDL-receptor-dependent uptake and intracellular cholesterol metabolism were studied in HepG2 cells. In addition, scavenger-receptor-mediated uptake was examined in mouse peritoneal macrophages. LDL isolated from nondiabetic normotriglyceridemic hemodialysis patients exhibited impaired cellular uptake via the LDL receptor. Additionally, intracellular sterol synthesis was less inhibited and cholesterol esterification was reduced compared with LDL from healthy control subjects. Reduction of catabolic capacities was more marked in hemodialysis patients who were either diabetic or hypertriglyceridemic and even more pronounced in patients presenting with a combination of both diabetes and hypertriglyceridemia. Hypertriglyceridemic and diabetic patients showed reduced lipase activity and increased LDL oxidation. Furthermore, they accumulated a fraction of small, dense LDL, and LDL was predominantly taken up via the scavenger-receptor pathway in peritoneal macrophages. This study elucidates the distinct influence of diabetes and/or hypertriglyceridemia in hemodialysis patients on cellular LDL metabolism via specific and nonspecific metabolic pathways. Furthermore, it underscores the cumulative impact of these pathologic entities on impairment of lipoprotein metabolism and increase of cardiovascular risk. (+info)
Mortality in end-stage renal disease: a reassessment of differences between patients treated with hemodialysis and peritoneal dialysis.
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Recent registry studies comparing mortality between peritoneal dialysis (PD) and hemodialysis (HD) patients show conflicting results. The purpose of this study is to determine whether previously published results showing higher mortality for patients treated with PD versus HD in the United States continue to hold true over the period 1987-1993. National mortality rates for PD and HD were extracted from the U.S. Renal Data System (USRDS) annual reports for the cohort periods: 1987-1989, 1988-1990, 1989-1991, 1990-1992, and 1991-1993. Using Poisson regression, death rates per 100 patient years were compared between PD and HD for each cohort period controlling for age, gender, race, and cause of end-stage renal disease (diabetes versus nondiabetes). When incident patients and patients with a prior transplant were included in the analysis, starting with the 1989-1991 cohort, we found little or no difference in the relative risk (RR PD:HD) of death between PD and HD (1987-1989: RR = 1.17, P < 0.001; 1988-1990: RR = 1.12, P < 0.001; 1989-1991: RR = 1.06, P = NS; 1990-1992: RR = 1.06, P = NS; 1991-1993: RR = 1.08, P = 0.043). After a test for goodness-of-fit, separate analyses for diabetic patients and nondiabetic patients were done to examine unexplained variation in death rates. For nondiabetic patients, there was less than a 1% difference in the adjusted 1-yr survival between PD and HD from 1989-1993 (1989-1991: RR = 1.05, P = NS; 1990-1992: RR = 1.04, P = NS; 1991-1993: RR = 1.07, P < 0.01). Among diabetic patients, the PD:HD death rate ratio varied significantly according to gender and age. For the average male diabetic patient, there was little or no difference in risk between PD and HD from 1989-1993 (1989-1991: RR = 1.02, P = NS; 1990-1992: RR = 1.05, P = NS; 1991-1993: RR = 1.08, P < 0.01). For diabetic patients under the age of 50, those treated with PD had a significantly lower risk of death than those treated with HD (1989-1993: 0.84 < or = RR < or = 0.89, P < 0.005). Over the same period, female diabetic patients treated with PD had a higher risk, on average, than HD (1.18 < or = RR < or = 1.19, P < 0.001) as did diabetic patients over the age 50 (1.28 < or = RR < or = 1.30, P < 0.001). Unlike previously published results that were restricted to prevalent-only patients, this national study of both prevalent and incident patients found little or no difference in overall mortality between PD and HD. The recent trends in mortality likely reflect the inclusion of incident patients, but they may also reflect changes in case-mix differences and/or improved PD practice. Additional incident-based studies that allow for additional case-mix adjustments are needed to better compare outcomes between HD and PD. (+info)
Assessment of dry weight in hemodialysis: an overview.
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Fluid balance is an integral component of hemodialysis treatments to prevent under- or overhydration, both of which have been demonstrated to have significant effects on intradialytic morbidity and long-term cardiovascular complications. Fluid removal is usually achieved by ultrafiltration to achieve a clinically derived value for "dry weight." Unfortunately, there is no standard measure of dry weight and as a consequence it is difficult to ascertain adequacy of fluid removal for an individual patient. Additionally, there is a lack of information on the effect of ultrafiltration on fluid shifts in the extracellular and intracellular fluid spaces. It is evident that a better understanding of both interdialytic fluid status and fluid changes during hemodialysis is required to develop a precise measure of fluid balance. This article describes the current status of dry weight estimation and reviews emerging techniques for evaluation of fluid shifts. Additionally, it explores the need for a marker of adequacy for fluid removal. (+info)
Managing progressive renal disease before dialysis.
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OBJECTIVE: To enhance awareness of issues affecting patients with chronic renal failure and to provide guidance for primary care practitioners managing such patients. QUALITY OF EVIDENCE: Randomized trials establish the efficacy of blood pressure control and angiotensin-converting enzyme (ACE) inhibition in slowing the progression of chronic renal disease. Some randomized trials and many prospective studies address management of anemia, hyperparathyroidism, and multidisciplinary predialysis care. The benefits of lipid lowering are suggested by randomized trials among patients without renal disease. MAIN MESSAGE: Progression of renal failure, particularly in patients with proteinuria, can be slowed by lowering blood pressure. Angiotensin-converting enzyme inhibitors are more beneficial than other antihypertensives in this situation. Partial correction of anemia with iron, erythropoietin, or androgens can improve quality of life and potentially prevent cardiac disease. Renal bone disease and secondary hyperparathyroidism can be prevented in part by early dietary phosphate restriction, use of calcium-containing phosphate binders, and activated vitamin D. Correction of acidosis could improve protein metabolism and bone and cardiovascular health. Treatment of hyperlipidemia might reduce cardiovascular disease. Early involvement of a nephrology-based multidisciplinary team has the potential to reduce morbidity and costs, enhance patients' knowledge of their condition, and prolong the period before dialysis is required. CONCLUSIONS: Care of patients with progressive renal failure is complex and requires attention to detail. Family doctors play a vital role in these efforts and should be involved in all aspects of care. (+info)