Homocysteine and vascular access thrombosis in hemodialysis patients

BACKGROUND: Vascular access remains the Achilles' heel of successful hemodialysis, and thrombosis is the leading cause of vascular access failure. Hyperhomocystinemia is common in hemodialysis patients and is associated with venous and arterial thrombosis in patients without end-stage renal disease. SUBJECTS AND METHODS: In the study, 65 hemodialysis patients with native arteriovenous fistula were included. Two groups of patients were defined: group A including 45 patients with their vascular access either never or only once thrombosed, and group B including 20 patients with two or more thromboses of their vascular access. We determined serum concentrations of total homocysteine (immunoassay, Abbott) in our patients. RESULTS: In 63 (96.9%) patients, hyperhomocystinemia was presented. There was no statistically significant difference between group A and B regarding age, gender and duration of hemodialysis treatment. Total homocysteine concentrations were higher in group A (42.1 +/- 18.6 micromol/l) than in group B (36.1 +/- 18.1 micromol/l) patients but the difference was small and not statistically significant. CONCLUSION: We found no significant differences in total homocysteine concentrations between group A (thrombosis non-prone) and group B (thrombosis prone) patients. Our results suggest that thrombosis of native arteriovenous fistulas may not be caused by hyperhomocystinemia in these patients.     

Predictors of early vascular-access failure in patients on hemodialysis

Vascular access management is key and critical in the successful management of hemodialysis patients, and an arteriovenous fistula (AVF) is considered the access of choice. This study was conducted between January 2007 and October 2009 at the Military Hospital in Rabat. Data on 115 patients who underwent 138 AVFs were retrospectively studied. Wrist AVF was the most common site of use. The primary course was uncomplicated in 63% of the patients, while primary failure occurred in 23.9% of the patients. Presence of diabetes was the most important risk factor for primary failure.     

Homocysteine targeting of plasma proteins in hemodialysis patients

Hyperhomocysteinemia, an independent, modifiable risk factor for cardiovascular disease, is found in most patients with end-stage renal disease. In this issue, Perna et al. examine the extent of protein-S-linked and protein-N-linked homocysteinylation in uremic patients on hemodialysis and the effect of folate treatment on protein homocysteinylation. Their findings show that protein-N-linked homocysteinylation, but not S-linked homocysteinylation, can be normalized by folate therapy.     

Homocysteine in chronic kidney disease: Effect of low protein diet and repletion with B vitamins

BACKGROUND: Data are limited on the determinants of homocysteine (tHcy) and its relationship with nutritional indices, and dietary protein intake, in the earlier stages of chronic kidney disease (CKD). METHODS: Levels of tHcy were assayed at baseline (N= 804) and 1 year postrandomization (N= 678) in the Modification of Diet in Renal Disease (MDRD) Study [study A, glomerular filtration rate (GFR) 25 to 55 mL/min/1.73 m(2) and study B GFR 13 to 24 mL/min/1.73 m(2)]. Participants were randomly assigned to different blood pressure targets and protein diets and all subjects received a multivitamin supplement containing 1 mg of folic acid, 10 mg pyridoxal 5'-phosphate (PLP) and 6 mug of vitamin B(12). Multivariable analyses were used to evaluate determinants of tHcy at baseline and 1 year. RESULTS: The prevalence of hyperhomocysteinemia (tHcy >15 mumol/L) at baseline was 56% in study A and 85% in study B. Baseline tHcy was negatively correlated with measures of body fat and dietary protein intake. Folate, vitamin B(12), and GFR were the major determinants of tHcy levels. Of the patients with hyperhomocysteinemia at baseline, 49% and 24% reduced their tHcy levels at 1 year to < or =15 micromol/L in study A and study B, respectively. There was no association between dietary protein intake and odds of developing hyperhomocysteinemia at 1 year in study A (P= 0.94) or study B (P= 0.10). CONCLUSION: Hyperhomocysteinemia is partly amenable to correction by vitamin supplementation in CKD stages 3 and 4. There is insufficient evidence to suggest that low tHcy is associated with poor nutritional status in the MDRD Study cohort. B vitamins and GFR, but not dietary protein, are the major determinants of tHcy in this patient population.     

Evaluation of hemodialysis patients treated with erythropoietin

We evaluated 20 hemodialysis patients who had been treated with erythropoietin (Epo). All patients had hemoglobin levels below 8.5 g/dL. They were randomized to receive either Epo (100 U/kg) or placebo three times per week for 12 weeks. All patients on Epo had a significant (P less than 0.001) elevation of hematocrit levels (19.7% v 35.7%). They also had a significant (P less than 0.05) increase in midweek predialysis blood urea nitrogen (BUN) levels, 27.8 versus 29.6 mmol/L (78 v 83 mg/dL), and serum phosphorus, 1.8 versus 2.1 mm/L (5.7 v 6.6 mg/dL). Protein catabolic rate also increased significantly (P less than 0.05). No changes were seen in the levels of serum creatinine and potassium, but episodes of hyperkalemia were more frequent in patients on Epo. No changes were seen in patients on placebo. When hematocrit increased, the clearance of blood-water for urea decreased 9%, and the clearance of creatinine, potassium, and phosphorus decreased 15%. Patients on Epo increased both their appetite and protein intake. More frequent episodes of hyperkalemia and elevated phosphorus level resulted from a combination of increased intake and decreased dialyzer clearance. We may need blood-water clearance to calculate Kt/V.     

Blood rheology and hypertension in hemodialysis patients treated with erythropoietin

Fifteen hemodialysis patients suffering from stable anemia were treated with recombinant human erythropoietin (r-HuEPO). Within 16 weeks, hematocrit values increased from 23.7 +/- 1.2 to 35.7 +/- 0.2%. Simultaneously, mean predialytic blood pressure rose significantly from 131/79 to 139/85 mm Hg. Three out of 15 patients developed frank hypertension and had to be put on antihypertensive therapy. When the hematocrit was lowered again from 36.3 +/- 1.8 to 30.5 +/- 1.2% in these 3 patients, blood pressure was attenuated and the antihypertensive medication could be reduced or abolished. With rising hematocrit values, whole blood viscosity increased at both low (+42%) and high shear rates (+33%) without reaching the values seen in healthy subjects. By contrast, plasma viscosity was already elevated in hemodialysis patients prior to r-HuEPO treatment and showed only a slight, but insignificant increase during r-HuEPO treatment. Since whole blood viscosity is one factor that determines vascular resistance, it is conceivable that the development of hypertension during correction of the renal anemia is, at least partly, due to an increment of blood viscosity.     

Selenium depletion in hemodialysis patients treated with polysulfone membranes

BACKGROUND/AIMS: Epidemiological, animal and human studies have indicated that selenium deficiency is a risk factor for death from malignant diseases. The mechanisms that could modify selenium status may, therefore, be of particular interest in hemodialysis patients, considering their high cancer mortality rates. We aimed at evaluating the effect of hemodialysis with polysulfone membranes on selenium status. METHODS: Twenty- eight chronically dialyzed patients and 32 age-matched healthy controls were enrolled in the study. Serum and dialysis fluid selenium concentrations, serum total protein, and hemoglobin concentrations and serum glutathione peroxidase activity were determined before and after the hemodialysis procedure. RESULTS: The (mean +/- SD) serum selenium and total protein concentrations and glutathione peroxidase activities were significantly (p < 0.05) higher in healthy controls (75.9 +/- 8.3 microg/l, 78 +/- 6 g/l, and 23.8 +/- 4.8 mU/20 microl, respectively) than in the patients. There was no significant difference between serum selenium concentration before (63.6 +/- 11. 6 microg/l) and after (64.4 +/- 11.4 microg/l) hemodialysis sessions, although hemoglobin and total serum protein concentrations and serum glutathione peroxidase activities increased (from 98.5 +/- 1.3 to 114.8 +/- 1.5 g/l, from 64 +/- 8 to 71 +/- 9 g/l, and from 16.8 +/- 1.8 to 18.9 +/- 1.9 mU/20 microl, respectively) significantly (p < 0.05) during hemodialysis, indicating hemoconcentration. The selenium concentration doubled, and protein appeared in the dialysates during dialysis session. The correlation of the selenium concentrations with the protein concentrations in the dialysate is significant (p < 0.01) with a Spearman R value of 0.97. CONCLUSION: The results of the present study suggest that selenium is lost through the pores of polysulfone membranes during hemodialysis which is associated with their protein permeability.     

Hyperhomocysteinemia in hemodialysis patients: effects of 12-month supplementation with hydrosoluble vitamins

BACKGROUND: High-efficiency hemodialysis may induce a deficiency in hydrosoluble vitamins. Supplementation with B-complex vitamins has been shown to lower serum homocysteine concentrations in several groups, but relatively few studies have concerned hemodialysis patients. Our objectives were to determine the status in B-complex vitamins in a large cohort of unsupplemented hemodialysis patients and to assess the effects of supplementation with hydrosoluble vitamins on serum homocysteine over one year. METHODS: Serum total homocysteine (tHcy), vitamin B12, folate, pyridoxal-5'-phosphate (P-5'-P; the active moiety of vitamin B6), as well as red blood cell folate concentrations, were measured in 168 chronic dialysis patients on three times weekly high-efficiency hemodialysis and not supplemented with hydrosoluble vitamins. Their methylenetetrahydrofolate reductase C677T (MTHFR) genotypes were also determined (homozygotes TT, heterozygotes CT, without mutation CC). All involved patients were then supplemented with hydrosoluble vitamins (once daily by mouth, DiaVite; R&D Laboratories, Minneapolis, MN, USA), and half of them were randomized to receive in addition 10 mg intravenously of folic acid posthemodialysis (30 mg intravenously per week). Serum tHcy was monitored after 6 and 12 months of supplementation in the 140 and 128 patients available for follow-up. RESULTS: At baseline, serum and red blood cell folate concentrations were within normal limits in all patients except for two with borderline serum folate (mean values of 21 +/- 8 and 1195 +/- 454 nmol/L), whereas serum vitamin B12 and P-5'-P were below normal in 11 and 65 patients, respectively (mean values of 327 +/- 215 pmol/L and 19 +/- 16 nmol/L for the 168 patients). Initial tHcy levels were increased in all patients (mean 33.3 +/- 16.6 for a normal below 11.8 +/- 1.5 micromol/L); tHcy significantly decreased to 23.5 +/- 7.6 micromol/L after six months (P < 0.0001 vs. baseline) and to 21.7 +/- 6.1 micromol/L after 12 months (P < 0.0001 vs. baseline) for the entire group, but was normalized in only four patients at 12 months. After six months, the mean reduction in tHcy was slightly but significantly greater for patients receiving intravenous folic acid (12.2 +/- 18.5 micromol/L) compared with patients not receiving it (8.3 +/- 9.8 micromol/L, P < 0.05). However, at 12 months, no difference between both subgroups persisted. When considering the different genotypes, tHcy at baseline tended to be higher for TT than CT and CC (39.8 +/- 30.9 vs. 31.4 +/- 10.5 vs. 31.6 +/- 11.8 micromol/L) and decreased to respective values of 21.1 +/- 6.9 versus 21.4 +/- 6.1 versus 22.2 +/- 5.9 micromol/L at 12 months. The impact of the addition of folic acid to DiaVite appeared particularly significant in TT patients at six months. CONCLUSIONS: (1) Hyperhomocysteinemia was present in 100% of our hemodialysis patients. (2) Nearly 40% of our unsupplemented hemodialysis patients were deficient in vitamin B6. (3) Supplementation with DiaVite(R) has resulted in significant tHcy reductions for all three genotypes. (4) The impact of the proposed supplementation protocol was found after six months and was maintained, but did not increase further after 12 months of the same regimen. (5) The addition of intravenous folic acid has been associated with a more pronounced decrease in tHcy in TT patients.     

Dietary intake of trace elements,minerals, and vitamins of patients on chronic hemodialysis

Purpose

We aimed to estimate dietary intakes of trace elements, minerals, and vitamins in hemodialysis patients (HDP) of three centers in one metropolitan and two urban areas of Italy.

Methods

Daily dietary intake was assessed using a 3-day diet diary in 128 HDP.

Results

Mean daily intakes of trace elements were as follows: zinc, 7.6 ± 5.4 mg; copper, 14.3 ± 11.8 mg; selenium, 28.3 ± 18.1 μg; and iron, 7.2 ± 4.1 mg (7.8 ± 2.6 mg in women, 6.9 ± 2.4 mg in men). The distribution of patients by daily intakes of trace elements showed most were under the recommended values, with the exception of copper intake, which was much higher. Mean daily intakes of minerals were as follows: magnesium, 174.4 ± 94.3 mg; phosphorus, 842.6 ± 576.8 mg; calcium, 371.8 ± 363.7 mg; potassium, 1,616.2 ± 897.3 mg; and sodium, 1,350 ± 1,281 mg. Mean daily intakes of vitamins were as follows: vitamin A, 486.1 ± 544.6 μg; vitamin B₁, 0.86 ± 0.7 mg; vitamin B₂, 1.1 ± 0.7 mg; vitamin B₃, 13.3 ± 8.1 mg; vitamin C, 47.8 ± 50.3 mg; and vitamin E, 9.5 ± 3.6 mg. The distribution of patients by daily intakes of vitamins showed most were under the recommended values. Daily intakes of trace elements and vitamins were similar among the three centers and did not differ between dialysis and non-dialysis days.

Conclusions

Many HDP have daily dietary intakes of trace elements and vitamins below the recommended values, whereas the intake of copper is much higher.     

Concentrations of vitamin C, vitamin B12 and folic acid in patients treated with hemodialysis and on-line hemodiafiltration or hemofiltration

OBJECTIVE: Uncertainty has arisen as to whether vitamin supplements are needed by dialysis patients, in particular those treated by means of hemofiltration or hemodiafiltration using highly permeable (high-flux) filters. We therefore measured the concentrations of vitamin C, cobalamin (vitamin B12) and folic acid in conventional (low-flux) dialysis patients and in those receiving on-line treatment (hemofiltration or hemodiafiltration). MATERIAL AND METHODS: Plasma (P-)ascorbate, serum (S-)cobalamin and S-folate concentrations were measured before and after a treatment session in 15 patients treated with low-flux hemodialysis and in 14 treated with on-line hemofiltration or hemodiafiltration. The patients' vitamin supplementations were also recorded. RESULTS: P-ascorbate concentrations were lowered by 51% and 53% in the hemodialysis and on-line groups, respectively after treatment and this reduction was significant (p<0.001). Concentrations below the reference values were found in 12/14 patients not receiving vitamin C supplementation. S-cobalamin did not decrease in the hemodialysis or on-line groups. S-folates did not change significantly in the hemodialysis or filtration groups. Patients without folacin supplementation had low values. CONCLUSIONS: P-ascorbate was reduced by both dialysis and filtration treatments. Neither S-cobalamin nor S-folate were reduced by dialysis or filtration treatments.     

Homocysteine lowering with folic acid and B vitamins in people with chronic kidney disease--results of the renal Hope-2 study.

BACKGROUND: Elevated plasma homocysteine levels are reported to be associated with higher rates of vascular diseases. Plasma homocysteine increases in chronic kidney disease (CKD) and could contribute to the increased cardiovascular risk in CKD. METHODS: Participants aged 55 years or older with CKD, defined as estimated GFR<60 ml/min and at high cardiovascular risk, were randomly assigned to the combination of folic acid, 2.5 mg, vitamin B6, 50 mg and vitamin B12, 1 mg (n = 307) or placebo (n = 312) daily for 5 years. The primary outcome was a composite of death from cardiovascular causes, myocardial infarction and stroke. RESULTS: Mean baseline plasma homocysteine was 15.9 +/- 7.3 micromol/l in the active treatment group and 15.7 +/- 5.7 micromol/l in placebo group and decreased to 11.9 +/- 3.3 micromol/l (P < 0.001) on active treatment (15.5 +/- 4.5 on placebo). Primary outcome events occurred in 90 participants (29.3%) on active therapy and in 80 (25.6%) on placebo (relative risk, 1.19; 95% confidence interval, 0.88-1.61; P = 0.25). There were no significant treatment benefits on death from cardiovascular causes (1.24; 0.84-1.83), myocardial infarction (1.10; 0.76-1.61) and stroke (1.00; 0.54-1.85). More participants in the active treatment group were hospitalized for heart failure (1.98; 1.21-3.26; P = 0.007) and for unstable angina (1.70; 1.02-2.83; P = 0.04). Incidence of primary outcome increased with decreasing GFR. CONCLUSIONS: Active treatment with B vitamins lowered homocysteine levels in participants with CKD but did not reduce cardiovascular risk.     

Homocysteine, vitamin B12, serum and erythrocyte folate in peritoneal dialysis patients

Plasma homocysteine (tHcy) is an important risk factor for atherosclerosis in dialysis patients. Few data were reported on the prevalence and severity of hyperhomocysteinemia in peritoneal dialysis (PD) patients. In addition, little attention was paid to the search of factors possibly involved in the pathogenesis of hyperhomocysteinemia in these patients. A cross-sectional study was performed in 107 stable PD patients. None of them was given folate or vitamin B12 supplementation before or during the study. Plasma tHcy, serum vitamin B12, serum and erythrocyte folate were measured by immunoenzymatic methods. Genetic analysis of the methylentetrahydrofolate-reductase thermolabile mutation (tMTHFR) was performed in 61 patients. 97% of patients had tHcy levels higher than normal. tHcy was not different between men and women, patients with or without malnutrition, with or without clinically evident atherosclerotic vasculopathy, with or without anemia. tHcy levels were significantly higher in homozygotes for the tMTHFR mutation than in patients carrying the wild type form. Significant univariate correlation was found between hyperhomocysteinemia and time since the start of dialysis, serum and erythrocyte folate and vitamin B12. The best fitted model equation was log tHcy = 108.53 + 0.1606 (duration of dialysis) -1.1053 (s-F) -0.7980 (age) 0.0215 (vitamin B12). Our results agree with those reported by other authors in hemodialysis patients. Despite the large number of PD patients with normal serum vitamin B12 and folate status, the relation between tHcy and vitamin B12 or folate suggests that the supplementation of these vitamins could be useful irrespective of their serum levels, especially in younger patients or in those treated for a long period of time with peritoneal dialysis.     

Hemoglobin cycling in hemodialysis patients treated with recombinant human erythropoietin

BACKGROUND: Treatment with recombinant human erythropoietin (rHuEPO) has been a major advance for the management of anemia in patients on hemodialysis. Therapy, however, is often observed to be associated with recurrent cyclic fluctuations in hemoglobin levels. The purpose of this analysis was to describe the phenomenology of hemoglobin cycling during rHuEPO treatment. METHODS: Data were analyzed for 281 hemodialysis patients treated at Winthrop-University Hospital Dialysis Centers between 1998 and 2003. Eligible patients' first full 1-year period with less than 10 hospital days was studied. Hemoglobin cycling (cycles with amplitude >1.5 g/dL and duration >8 weeks) and excursions (half of one full cycle) were analyzed. RESULTS: Greater than 90% of patients experienced hemoglobin cycling. The mean number of hemoglobin excursions was 3.1 +/- 1.1 per patient/year. The mean amplitude per hemoglobin excursion was 2.51 +/- 0.89 g/dL. The mean duration of hemoglobin excursions was 10.3 +/- 5.1 weeks. Factors associated with initiation of up excursions included increases in rHuEPO dose (84%), intravenous iron treatment initiation or increase in dose (27%), posthospital discharge (36%), factors associated with down excursions included rHuEPO dose hold (15%) or dose reduction (62%), infection (6%), discontinuation of intravenous iron therapy (5%), and hospitalization (14%). Patients with frequent hemoglobin cycling (>two full cycles per year) were characterized as being more responsive to rHuEPO [index of EPO responsiveness (ERI) 1036 +/- 659 compared to 1992 +/- 701 for other patients] (P = 0.02). CONCLUSION: Hemoglobin cycling is a common occurrence in rHuEPO-treated hemodialysis patients. It is most closely associated with frequent rHuEPO dose changes, hospitalization, and iron treatment practices.     

Improvement of brain function in hemodialysis patients treated with erythropoietin

To evaluate the effects of recombinant human erythropoietin (rHuEPO) on brain function, 15 chronic hemodialysis patients were studied by event-related P300, stimulus-related evoked potentials, and trailmaking before (hematocrit 22.7%) and after rHuEPO (hematocrit 30.6%). P300 peak latency elicited by a tone discrimination paradigm improved (391 before vs. 366 ms after; Cz = vertex; P less than 0.01) confirming beneficial effects on cerebral cognitive processing. P300 amplitude (13.6 vs. 15.8 microV; P = 0.06) and trailmaking tended to improve (55 vs. 43 s). P300 measures were influenced by low hemoglobin levels before rHuEPO (P less than 0.01), suggesting that severe anemia may contribute to uremic brain dysfunction. Furthermore, decrease of stimulus-related auditory brainstem I-V interpeak latency (4.28 before vs. 4.17 ms after; P less than 0.05) and increase of somatosensory N20/P25 amplitude (4.8 vs. 7.0 microV; P less than 0.05) pointed to improvement of sensory pathways by mechanisms unrelated to cognition. Brain dysfunction in chronic hemodialysis patients may, beside other factors, in part be caused by severe anemia and can be improved by rHuEPO treatment.     

IgM-anticardiolipin antibody and vascular access thrombosis in chronic hemodialysis patients

AIM: Vascular access failure is a major cause of morbidity in chronic hemodialysis (HD) patients. Elevated immunoglobulin-M anticardiolipin antibody (IgM-aCL) titer is associated with stenosis of vascular access in HD patients. The clinical significance of elevated IgM-aCL titer relative to recurrent vascular access thrombosis (VAT) in patients with HD is less clear. However, little information has been available until now about the clinical influence of elevated IgM-aCL titer with recurrent VAT in HD patients from Western countries, and no report exists for Taiwan. This study attempted to determine whether elevated IgM-aCL titer was associated with recurrent VAT in HD patients. METHODS: This study enrolled 483 patients undergoing HD. IgM-aCL titer and hepatitis C marker were measured for all subjects. RESULTS: Elevated IgM-aCL titer was present in 17.4% (84/483) of patients. There was no association recurrent VAT between elevated and normal IgM-aCL titers (P=0.90). Presence of hepatitis C had significant differences between elevated and normal IgM-aCL titers (P=0.027). CONCLUSIONS: We found no significant differences in recurrent VAT between elevated and normal IgM-aCL titer in chronic HD patients. Our results suggest recurrent VAT of synthetic or native fistula may not be caused by elevated IgM-aCL titer in these patients. Presence of hepatitis C may be a cofactor.     

Homocysteine and vascular access thrombosis in a cohort of end-stage renal disease patients

BACKGROUND: Maintaining successful hemodialysis services is dependent upon an access to circulation that is reliable and stable. Complications of vascular access such as dysfunction, thrombosis, or infection are major causes of hospitalization with thrombosis being the most common reoccurring problem. Initial prospective evidence supports an independent association between total homocysteine (tHcy) levels and access thrombosis. The purpose of this study was to determine if significant associations exist between tHcy, age, gender, and vascular access thrombosis in patients with end-stage renal disease (ESRD). SUBJECTS AND METHODS: One hundred eighty-five (N=185) patients undergoing dialysis were selected as subjects. The retrospective sample was divided into a one or less vascular access thrombosis (VAT) (VAT) group (n= 133) and more than one (VAT II) VAT group (n= 52). The data was collected during a 16-month period (January 2000 to April 2002). Additional subgroup analyses included gender and age. RESULTS: The Mann-Whitney U nonparametric t-Test for variance between groups revealed no significant difference in tHcy values between VAT groups (U=1841.50, p=0.284). A two-sample t-Test for variance between tHcy and age revealed no significant differences (F-ratio = 0.832, p = 0.32). A chi-square analysis revealed no significant differences in gender and VAT groups (chi2=0.246, p=0.62). A Kolmogorov-Smirnov test for normality was calculated for tHcy with a p-value of 0.859 revealing insufficient evidence that the distribution is not normal. Spearman Rank Correlations were calculated, revealing low to moderate associations among variables. CONCLUSIONS: While some studies have demonstrated a relationship between tHcy and VAT, this study found that chronically high homocysteine levels in patients with ESRD were not associated with incidence of VAT. There were no significant differences in the number of VATs across additional variables of age and gender.     

Challenges in blood pressure measurement in patients treated with maintenance hemodialysis

The association between blood pressure and cardiovascular outcomes in patients undergoing hemodialysis remains controversial. This may relate in part to the technique and device used and the timing of the blood pressure measurement in relation to the hemodialysis procedure. Emerging evidence indicates that standardized hemodialysis unit blood pressure measurements or measurements obtained at home, either by the patient or using an ambulatory blood pressure monitor, may offer advantages over routine hemodialysis unit blood pressure measurements for determining cardiovascular risk and treatment. This review discusses the available evidence and implications for clinicians and clinical trials.     

Depression in end-stage renal disease patients treated with hemodialysis: tools, correlates, outcomes, and needs

Depression has been thought to be the most common psychiatric abnormality in hemodialysis (HD) patients. There are few data using psychiatric diagnostic criteria and a lack of large, well-designed epidemiologic research studies in patients with end-stage renal disease (ESRD) that can render definitive results on this topic. The prevalence of major depression or a defined psychiatric illness in ESRD patients is unknown, but is probably between 5% and 10%. The prevalence of increased levels of depressive affect is greater. Estimates of the prevalence will vary according to the screening techniques used. Depression could affect medical outcomes in ESRD patients through several mechanisms. Correlational analyses suggest stressors and protective factors play roles in mediating the level of depressive affect and associated outcomes. Although early studies suggested a deleterious effect of depression on survival in ESRD patients, more recent studies had failed to confirm such findings. The use of longitudinal analyses and larger samples has confirmed an association of depressive affect and morbidity and mortality in more contemporary ESRD populations. The importance of depressive affect compared with the presence of a defined psychiatric syndrome in mediating clinically important outcomes in patients with chronic kidney disease has not been determined. Studies of interventions designed to reduce levels of depressive affect in ESRD patients are urgently needed.