Resistance to activated protein C (APC): mutation at ARG506 of coagulation factor V and vascular access thrombosis in haemodialysis patients

BACKGROUND.: Vascular access thrombosis represents a serious problem in haemodialysispatients. Therefore identification of relevant thrombotic riskfactors is clinically valuable. Resistance to activated proteinC (APC) was recently identified as a new thrombophilic defectwhich is caused by a single point mutation in the factor V gene.Whether this mutation predisposes to vascular access thrombosisis unknown. METHODS.: The presence of factor V Leiden (mutation at nucleotide position1691 of the factor V gene) was determined by polymerase chainreaction (PCR) analysis in 152 haemodialysis patients from allthree haemodialysis units of the University Hospital of Vienna.In 61 patients (54 without mutation, 7 with heterozygous mutation)resistance to APC was evaluated. Onehundredseven individualswithout renal failure (57 negative for factor V Leiden, 50 heterozygoussubjects) served as controls. Haemodialysis patients with heterozygousfactor V Leiden mutation were carefully investigated for thromboticcomplications of vascular access, other thromboembolic eventsand additional putative thromboembolic risk factors. RESULTS.: Seven of 152 (4.6%) patients were heterozygous carriers of factorV Leiden. The mean APC resistance ratio in heterozygous dialysispatients was 2.31; in the 50 heterozygous controls the ratiowas 2.02. The mean APC ratio in haemodialysis patients withoutmutation was 3.53 in contrast to 2.95 in the control group.Not one of the seven heterozygous haemodialysis patients sufferedfrom vascular access thrombosis of inexplicable origin. Threepatients remained totally free of access thrombosis from onsetof haemodialysis treatment. In four of seven patients nine eventsof thrombosis of the vascular access occurred, but were dueto anatomical stenosis in each case. In six permanent centralvenous catheters no episode of occlusion or reduced blood flowrequiring thrombolytic therapy was observed. Family historywith regard to thrombotic events was negative in all seven patients.No thromboembolic complication occurred during 13 periods ofimmobilization, in the course of six pregnancies and duringoral contraception. CONCLUSIONS.: The heterozygous carrier status for factor V Leiden does notappear to represent a risk factor for vascular access thrombosisin haemodialysis patients. This is possibly due to the factthat the functional APC activity is high and in heterozygoushaemodialysis patients APC resistance ratios are very closeto the normal range. However, it cannot be excluded that a homozygousfactor V mutation represents an increased risk for shunt thrombosis.Therefore patients suffering from repeated and/or inexplicableshunt thrombosis should be tested for the factor V mutationto evaluate the effect of a homozygous mutation.     

Homocyst(e)ine and vascular access complications in haemodialysis patients: insights into a complex metabolic relationship.

BACKGROUND: As elevated total homocyst(e)ine (tHcy) is associated with increased risk of vascular thrombosis, we hypothesized that the elevated levels of tHcy seen in patients on haemodialysis may be associated with an increased risk of thrombosis of native arteriovenous fistulae (vascular access failure). Our study was designed to investigate the relationship between tHcy and vascular access failure. The relationship between tHcy and mortality was explored as a secondary analysis. METHODS: The study comprised a cross-sectional analysis of 96 haemodialysis patients at a single university-affiliated hospital and a subsequent 9-month prospective follow-up of 88 of the 96 patients. RESULTS: Levels of tHcy (median 30 micromol/l) were elevated. In the initial cross-sectional sample, there was an inverse relationship between tHcy and history of vascular access failure which was not observed in the prospective study. Variables influencing the risk of vascular access failure in the prospective study included history of previous vascular access failure (RR=2.93, P=0.03), use of antiplatelet agents (RR=0.13, P=0.01), increased urea reduction ratio (RR=0.55 for a 5% increase, P=0.01) and increased weight (RR=0.61 for a 10 kg increase, P=0.02). Secondary analysis showed an unexpected inverse relationship between tHcy and mortality (RR=0.033 for 1 log increase in tHcy, P=0.006), such that the lower levels of tHcy were associated with an increased risk of death in short-term follow-up. CONCLUSION: We did not demonstrate a relationship between tHcy and risk of vascular access failure. Patients with the lowest levels of tHcy appeared to be at increased risk of death in this short-term follow-up. The relationship of tHcy to vascular access complications and death in haemodialysis patients appears complex and requires further study.     

Increased prevalence of apolipoprotein E3/E4 genotype among Swedish renal transplant recipients.

There is increasing evidence that lipoproteins are involved in the progression of kidney diseases and in the deterioration of kidney transplant function, although the exact mechanism is still not known. Common polymorphisms of apolipoprotein E genotype associate with the variability of lipoprotein levels and composition. We have, therefore, determined the apolipoprotein E genotype in a group of 112 renal transplant patients, of whom 27 had had an episode of acute vascular rejection, while 85 had not. We found no difference in apolipoprotein E genotype distribution or in relative allele frequency in the vascular rejection group as compared with the group without vascular rejection. The apolipoprotein E genotype distribution in the transplant group was also compared with that in a group of 407 healthy Swedish individuals. The E3/E4 genotype occurred with a significantly increased frequency in the transplant group: 38.3 versus 16% in the control group (p < 0.001). The prevalence of individuals carrying the epsilon4 allele among the transplant group was also significantly higher (44%) as compared with the control group (30%; p < 0.01). This increase was entirely due to the predominant increase of E3/E4, as the E4/E4 genotype was less frequent in transplant recipients than in normal controls (3.5 vs. 10.6%; p < 0.05). The relative frequencies of epsilon2 (0.044), epsilon3 (0.716), and epsilon4 (0.238) alleles in the renal transplant group were not different from those of normal controls (0. 078, 0.718, and 0.202, respectively). With regard to the prevalence of E4/E4 in the two groups, the lack of difference in the relative frequency of the epsilon4 allele must be interpreted with caution. The results thus suggest that the E3/E4 genotype may be associated with the progression of kidney disease leading to renal insufficiency. However, the apolipoprotein E genotype does not seem to influence the risk of vascular rejection among transplant recipients.     

Pulmonary hypertension in chronic dialysis patients with arteriovenous fistula: pathogenesis and therapeutic prospective

PURPOSE OF REVIEW: End-stage renal disease patients receiving chronic haemodialysis via arteriovenous access often develop various cardiovascular complications, including vascular calcification, cardiac-vascular calcification and atherosclerotic coronary disease. This review describes recently published studies that demonstrate a high incidence of pulmonary hypertension among patients with end-stage renal disease receiving long-term haemodialysis via a surgical arteriovenous fistula. Both end-stage renal disease and long-term haemodialysis via arteriovenous fistula may be involved in the pathogenesis of pulmonary hypertension by affecting pulmonary vascular resistance and cardiac output. RECENT FINDINGS: Morbidity and mortality from cardiovascular disease are greatly increased in patients on maintenance haemodialysis therapy. Using Doppler echocardiography, we found a significant increase in cardiac output in 40% of chronic haemodialysis patients, probably related to the large arteriovenous access or altered vascular resistance as a result of the local vascular tone and function expressed by the imbalance between vasodilators such as nitric oxide, and vasoconstrictors such as endothelin-1. SUMMARY: We propose different potential mechanisms as explanations for the development of pulmonary hypertension. Hormonal and metabolic derangement associated with end-stage renal disease might lead to pulmonary arterial vasoconstriction and an increase in pulmonary vascular resistance. Pulmonary arterial pressure may be further increased by high cardiac output resulting from the arteriole-venous access itself, worsened by commonly occurring anaemia and fluid overload.     

Low-molecular-weight heparin (LMWH): influence on blood lipids in patients on chronic haemodialysis

A low-molecular-weight heparin (LMWH) has been compared to conventionalheparin in haemodialysis in a 12-month study. In a group of22 patients who had been on chronic haemodialysis for longerthan 12 months, the conventional, unfractionated heparin wasreplaced by a low-molecular-weight analogue (LMWH) (Fragmin,Kabi-Pharmacia Erlangen) for 6 months. Baseline values of lipoproteinprofile prior to the intervention were compared with resultsobtained after 2, 4 and 6 months of LMWH. Control values wereobtained 3 and 6 months after switching back to conventionalheparin. During the LMWH treatment total cholesterol decreasedsignificantly. This coincided with a significant decrease inLDL cholesterol and a minor decrease in total HDL cholesterol.There was no noticeable change in the HDL cholesterol subfractions.The decrease of LDL and HDL was accompanied by a distinct andcontinuous decrease of apolipoprotein B throughout the LMWHperiod while the apolipoprotein Al declined during the first2 months and then stabilized at this lower value. Triglyceridesincreased significantly during the first 2 months and then reboundedto the initial values by the end of the LMWH treatment period.After switching back again to conventional heparin the lipoproteinparameters returned to the starting values. We conclude thatthe long-term use of low-molecular-weight heparin instead ofconventional heparin for anticoagulation during dialysis maycontribute to a reduction of the cardiovascular risk factorsof haemodialysis patients.     

Aortic calcification in haemodialysis patients with diabetes mellitus.

BACKGROUND: Certain metabolic disorders, such as hyperphosphatemia induce vascular calcification in haemodialysis patients; it is unclear, however, whether these disorders contribute to aortic calcification in diabetic haemodialysis patients. This study examined the risk factors of aortic calcification in a large number of haemodialysis patients, and compared risk factors between diabetic and non-diabetic patients. METHODS: The subjects were 667 patients on maintenance haemodialysis: 184 with type 2 diabetes and 483 without. Aortic calcification was measured semi-quantitatively using a plain computed tomography image of the abdominal aorta, and an aortic calcification index (ACI) was calculated. RESULTS: The ACI of the diabetic subjects was significantly higher than that of those without diabetes (57.3+/-22.1 vs 44.8+/-28.3%, P < 0.0001), although the dialysis vintage of the former was significantly shorter (P < 0.001). Multiple regression analyses showed that diabetes was a significant independent risk factor for increased ACI. Multiple regression analyses, performed separately in diabetics and non-diabetics, revealed that advanced age, higher systolic blood pressure, smoking and longer haemodialysis vintage were common independent risk factors significantly associated with increased ACI in both patient groups (R2 = 0.296, P < 0.0001 for non-diabetics; R2 = 0.193, P < 0.0001 for diabetics). Higher serum phosphate concentration was not significantly associated with increased ACI in diabetic patients (P = 0.429), although it was a significant independent factor in non-diabetic patients (beta = 0.150, P < 0.0005). CONCLUSION: Aortic calcification in diabetic haemodialysis patients is more advanced, compared with non-diabetic patients, even with short haemodialysis vintage. Since disorders of mineral metabolism are not significantly associated with aortic calcification in diabetic haemodialysis patients, aortic calcification in these patients could be affected by metabolic abnormalities associated with the diabetic state per se, independent of other confounding factors; and aortic calcification may be advanced even before haemodialysis induction.     

Apolipoprotein E4 reduces risk of diabetic nephropathy in patients with NIDDM

Hypercholesterolemia is a major determinant of the decline of renal function in patients with diabetes. Apolipoprotein E polymorphism may influence the metabolism of lipoprotein in diabetic patients. The purpose of this study was to investigate the association between genetic polymorphisms in apolipoprotein E and the progression of diabetic nephropathy in patients with non-insulin-dependent diabetes mellitus over a 10-year period (13 to 37 years; median, 20 years). Subjects with a stable renal function without overt proteinuria had a higher cholesterol level, lower incidences of hypertension and proliferative diabetic retinopathy, and a higher frequency of the E4 allele than subjects with a decline in renal function (end-stage renal failure requiring dialysis treatment). In the diabetic patients, the apolipoprotein E4 carriers had a higher cholesterol level than did the noncarriers. The survival rate from renal disease in the apolipoprotein E4 carriers was higher than in the noncarriers among the diabetic patients. Apolipoprotein E polymorphism and hypertension were identified as independent risk factors for the progression to renal failure. Results indicate that apolipoprotein E polymorphism is associated with the progression of diabetic nephropathy. Presence of the apolipoprotein E4 allele is a protective factor, and other alleles are risk factors.     

Lipoprotein Abnormalities in Chronic Haemodialysis Patients

Measurement of lipids, apolipoproteins A-I, A-II, B, C-III,Lp(a) and cholesterol, phospholipids, apo C-III in lipoproteinwith and without apolipoprotein B was made in 49 patients (18women and 31 men; mean age 50±15 years) undergoing maintenancehaemodialysis for chronic renal failure. A group of 49 healthypeople, matched for sex and age, acted as controls. In the haemodialysis group, special attention was placed uponthe comparison of patients who had evident cardiovascular alterations(n=17) with the residual group (n=32). The concentration ofapo C-III in apolipoprotein B containing lipoproteins was statisticallyhigher in the patients with arterial disease than in the remainingsub jects, whereas the ratio apo C-III from Lp no B/apo C-IIIfrom Lp B was decreased. Compared to controls, haemodialysispatients had significantly higher values of triglycerides, apolipoproteinsC-III, Lp(a), and apolipoprotein C-III from apolipoprotein B-containinglipoproteins (LpB); in contrast, concentrations of phospholipidsand cholesterol from lipoproteins without apolipoprotein B (Lpno B) and apolipoprotein A-II were significantly reduced inpatients. Discriminant analysis indicated that the levels ofapolipoprotein C-III and apolipoprotein C-III from LpB werethe best indicators of deranged lipid transport in patientswith chronic renal failure. Our data suggest that chronic haemodialysis patients tend toexhibit qualitative abnormalities of serum apolipoprotein-Btriglyceride rich particles containing apolipoprotein C-IIIor (a).     

Doxycycline may reduce the incidence of aneurysms in haemodialysis vascular accesses.

BACKGROUND: Doxycycline can prevent aortic aneurysms through the inhibition of enzymes that degrade vessel walls. We investigated whether haemodialysis patients who had received one or more courses of doxycycline were at less risk for aneurysms in their vascular accesses than those who had received other antibiotics. METHODS: Three hundred and eight patients undergoing chronic maintenance hemodialysis were evaluated for aneurysm formation after exposure to doxycycline or another antibiotic. Conditional forward logistical analysis using Cox proportional hazards test (SPSS) was performed to determine the potential significance of differences of aneurysm formation between the two groups. RESULTS: Patients who had received doxycycline appeared to be at lower risk than the control group, but the effect was most obvious in those patients with synthetic grafts. CONCLUSIONS: Doxycycline may have the ability to reduce aneurysm formation in haemodialysis vascular accesses and a large prospective study is warranted.     

Experience with the Hemasite device in haemodialysis and haemofiltration patients with vascular access problems

Multiple vascular access failure is a frequent problem and we report our experience with 32 Hemasite devices implanted in 28 patients with end-stage renal disease. All of the patients were on maintenance haemodialysis or haemofiltration with a range of treatment of 1-17 years. Their mean age was 58 +/- 14 years (range 28-72 years). The main indication for using this device as an alternative vascular access was the presence of high-risk patients with a high incidence of previous access failure (1-8 accesses per patient). The majority of the patients were considered as high risk, due either to old age (more than 60 years) (60%) or to the presence of diabetes mellitus (29%). The results of 5 years' experience and follow-up showed that the Hemasite device could be successfully used as a secondary vascular access in high-risk patients who have problems of multiple access failures. The 1-year cumulative survival of the device (55%) was affected by complications such as thrombosis and infection (47% and 16%) which were noted mostly among patients with diabetes mellitus. These complications are the major ones endangering the longevity of the Hemasite implant and were important causes of implant loss (31% and 6% respectively). Being needleless and painless, the Hemasite was well-accepted by the patients and it functioned well, with adequate blood flow. We conclude that the Hemasite device is a valuable alternative when vascular access becomes a problem in haemodialysis patients.     

Catheter-related bacteraemia in haemodialysis patients with HIV infection.

BACKGROUND: Tunnelled catheters are used for dialysis in over 25% of haemodialysis (HD) patients and are a major risk factor for bacteraemia. HIV-positive patients may be at particularly increased risk of catheter-related bacteraemia (CRB) due to their immunocompromised state. The present case-controlled study compared catheter-related bacteraemia with HIV-positive and HIV-negative haemodialysis patients. METHODS: Using a prospective computerized vascular access database, we identified 33 HIV-positive haemodialysis patients who had a tunneled dialysis catheter placed during a 6.5-year period. Their catheter outcomes were compared with those observed in 55 age-, sex- and access date-matched control haemodialysis patients. RESULTS: The two groups were similar in terms of age, sex, diabetes, hypertension and peripheral vascular disease, but the HIV patients were more likely to be black (94 vs 76%, P=0.03). CRB occurred in 52% of the HIV patients and 49% of the controls (P=0.83). The median infection-free catheter survival was similar in HIV-positive and negative patients (165 vs 119 days, P=0.12). Among patients with CRB, the likelihood of a Gram-negative infection was similar in both groups (18 vs 30%, P=0.37). However, polymicrobial CRB was more likely in HIV patients (41 vs 15%, P=0.049). HIV-positive patients were more likely to be hospitalized for treatment of CRB than HIV-negative patients (29 vs 7%, P=0.05). CONCLUSION: CRB is equally likely in HIV-positive and control haemodialysis patients. However, CRB is likely to be more severe in HIV-positive patients, as judged from the greater likelihood of polymicrobial infection and of hospitalization.     

Nutritional vitamin D supplementation in haemodialysis: A potential vascular benefit?

Aim: Vitamin D deficiency is highly prevalent in end‐stage renal disease and has been associated with atherosclerosis, endothelial dysfunction and left ventricular hypertrophy. Although activated vitamin D has shown to be cardioprotective, the cardiovascular benefits of nutritional vitamin D (i.e. ergocalciferol or cholecalciferol) have not been explored in the dialysis population. The aim of this investigation was to evaluate the effect of ergocalciferol therapy on vascular adhesion molecules, markers of inflammation and atherosclerosis among haemodialysis patients. Methods: This was a pilot study of matched haemodialysis patients. For every patient enrolled taking ergocalciferol, an age and race matched control was recruited. Predialysis blood samples were collected and assayed for adhesion molecules (soluble vascular cell adhesion molecule‐1 (sVCAM‐1), soluble intercellular adhesion molecule‐1 (sICAM‐1), E‐selectin and P‐selectin), inflammatory cytokines (interleukin‐6 (IL‐6) and tumour necrosis factor‐α (TNF‐α)), oxLDL‐β₂GPI and IgG anticardiolipin. Results: A total of 40 haemodialysis patients were studied (20 on ergocalciferol therapy, 20 not receiving ergocalciferol therapy). Patients taking ergocalciferol had higher 25‐hydroxyvitamin D levels compared with those not taking ergocalciferol. Even though doxercalciferol usage and dosing was similar between groups, plasma sVCAM‐1, sICAM‐1 and P‐selectin concentrations were lower among ergocalciferol treated patients. No significant differences in E‐selectin, IL‐6, TNF‐α, oxLDL‐β₂GPI or anticardiolipin antibody levels were observed. Conclusion: Patients receiving ergocalciferol had lower plasma levels of vascular adhesion molecules despite equivalent use of activated vitamin D therapy. Future investigations should confirm the role of nutritional vitamin D therapy, in addition to activated D therapy, in haemodialysis patients and the potential vascular benefits of these agents.     

Cerebral amyloid angiopathy associated with hemorrhage: immunohistochemical study of 41 biopsy cases.

The relationship between cerebral amyloid angiopathy and hemorrhage was investigated by an immunohistochemical study of biopsy cases to characterize the involvement of amyloid beta-protein, apolipoprotein E, and cystatin C in cerebral amyloid angiopathy associated with hemorrhage. The amyloid-laden vessels were examined in biopsy specimens from 41 surgical cases of sporadic cerebral amyloid angiopathy (36 cases with hemorrhage and 5 cases without hemorrhage), using immunohistochemical staining with antibodies against amyloid beta-protein, apolipoprotein E, cystatin C, and alpha-smooth muscle actin. The relationship between the occurrence, recurrence, and enlargement of the hemorrhage, and the semiquantitative estimation of the cerebrovascular amyloid-related protein deposition was analyzed using Fisher's exact test. Severe amyloid beta-protein (p < 0.013) and apolipoprotein E (p < 0.013) immunoreactivity were risk factors for the occurrence of the hemorrhage. Severe cystatin C immunoreactivity was a risk factor for the occurrence (p < 0.002) and enlargement (p < 0.014) of the hemorrhage, and tended to induce recurrent hemorrhage (p < 0.103). In addition, loss of the vascular smooth muscle was observed in the intensely amyloid-laden vascular walls that showed cystatin C-immunoreactivity. The present study indicates that intense amyloid beta-protein deposition with cystatin C deposition weakens the cerebrovascular walls, and that cystatin C deposition is a strong predictor of hemorrhage in cerebral amyloid angiopathy.     

Lipoprotein (a) and the kidney

Summary: Cardiovascular disease is the main cause of death in chronic renal failure patients. Lipoprotein (a) [Lp(a)] is an independent risk factor for development of vascular disease in non-renal and renal populations. the atherogenicity of Lp(a) is thought to relate to the structural homology between its apolipoprotein moiety [apo(a)] and plasminogen. Raised low-density-lipoprotein (LDL) cholesterol concentrations increase the atherogenic potential of Lp(a). Normally Lp(a) level is genetically determined but in renal disease positive correlations with urinary protein loss and peritoneal dialysate protein loss have been found. Levels are highest in nephrotic patients and chronic renal failure patients treated with peritoneal dialysis but are also increased in pre-dialysis and haemodialysis patients. Lipoprotein (a) falls following renal transplantation but cyclosporine therapy may adversely affect post transplant cardiovascular risk profile. Treatment with antiproteinuric drugs (converting enzyme inhibitors or non-steroidal anti-inflammatory agents) has been shown to reduce Lp(a) (and total cholesterol) concentrations. Most lipid-lowering drugs do not affect Lp(a) concentration but lowering LDL-cholesterol alone may significantly reduce the atherogenic effect of Lp(a). Routine measurement of Lp(a) concentration is not recommended but antiproteinuric therapy should have favourable effects on cardiovascular risk profile.     

Homocysteine and lipid peroxidation in haemodialysis: role of folinic acid and vitamin E.

BACKGROUND: Cardiovascular diseases are the leading cause of death in haemodialysis patients. Hyperhomocysteinaemia is an independent risk factor. Basic research has provided strong evidence that oxidation of low-density lipoprotein (LDL) plays an important role in the pathogenesis of atherosclerosis. Oxidative stress, lipid metabolism alterations, and hyperhomocysteinaemia observed in haemodialysis patients could induce increases in LDL oxidation. This study was designed to determine the effect of folinic acid on hyperhomocysteinaemia and to assess the antioxidant efficacy of folinic acid. The antioxidant effect of folinic acid was compared with that of vitamin E. METHODS: Sixteen stable patients (11 men, five women; mean age 54.3+/-6.32 years) on standard haemodialysis received 400 mg of vitamin E, orally, at the end of each haemodialysis session for 3 months. After a 1-month wash-out, they received 10 mg of folinic acid, intravenously, at the end of each haemodialysis session for an additional 3 months. Blood samples were drawn in the morning after an overnight fast and before dialysis. Plasma vitamin E was analysed by high-pressure liquid chromatography. Malondialdehyde (MDA) was determined using a fluorimetric method and plasma copper oxidized anti-LDL antibodies (Ab-LDLox) were measured with an ELISA method using native LDL and oxLDL as antigens. Plasma homocysteine was determined by an FPIA method. RESULTS: Folinic acid supplements significantly reduced hyperhomocysteinaemia (-44%), MDA concentrations (-40%), and IgG-LDLox titres (-13%). CONCLUSIONS: Treatment with folinic acid lowers plasma homocysteine levels and, like vitamin E, affords antioxidant protection, which prevents lipid peroxidation. This lowering of lipid peroxidation may reduce the risk of atherosclerosis and prevent or delay cardiovascular complications in HD patients.     

Anticardiolipin antibodies in children on chronic haemodialysis

IgG and IgM anticardiolipin antibody (Ab) concentrations weredetermined in serum samples of 48 children with end-stage renaldisease (ESRD) on haemodialysis using ELISA technique in anattempt to analyse their possible role in the occurrence ofthrombosis of the vascular access. Ten normal healthy childrenwere studied as a control group. The positivity of anticardiolipinAb isotypes both IgM and IgG was high in children with ESRDon haemodialysis. Children with positive anticardiolipin Abhad significantly higher incidence of prior thrombosis of vascularaccess. Also, these antibodies should be considered as markersof high risk for fistula thrombosis.     

Prevalence of hepatitis C, hepatitis B and HIV infection among haemodialysis patients in Ibn-Rochd university hospital, Casablanca

The viral infections are frequent in haemodialysis patients, notably those due to the hepatitis C virus (HCV), the hepatitis B virus (HBV) and the human immunodeficiency virus (HIV). The objective of this study is to determine the prevalence of the hepatitis C, the hepatitis B, the HIV infection in haemodialysis patients and the main risk factors for hepatitis C in the chronic haemodialysis patients treated in haemodialysis unit of Ibn Rochd University Hospital in Casablanca. This retrospective study was performed in 186 chronic haemodialysis patients and showed a high prevalence of HVC infection (76%), the prevalence of HBV infection was at 2%, none of the patients had detectable antibodies of HIV. Among the patients infected by the HCV, the mean duration of dialysis was 8,7 years. The mean number of blood units transfused was 16,5. Seventeen patients (11%) had no history of blood transfusion. In conclusion, the blood transfusion is not considered to be a like a major risk factor of the HCV infection in haemodialysis patients and this since the systematic detection of the anti-HCV antibodies in the blood donors. The nosocomial transmission of HCV seems to be the main risk factor HCV infection in the haemodialysis units requiring a strict adherence to infection control procedures for prevention of HVC infection in haemodialysis patients.     

Presence of apolipoprotein E epsilon4 allele in cerebral palsy

The apolipoprotein E gene, which is located on chromosome 19, has three alleles (epsilon2, epsilon3, and epsilon4). Several recent publications associate the presence of the apolipoprotein E epsilon4 allele with the occurrence of neurologic diseases, and consider it a risk factor for the development of central nervous system affections. A group of 40 patients with cerebral palsy was studied and compared to a control group of 40 subjects, and higher occurrence of the allele epsilon4 in the group of subjects with cerebral palsy was observed. A significantly higher risk of developing cerebral palsy was demonstrated among those subjects with the apolipoprotein E epsilon4 allele.     

The elderly population on haemodialysis: evaluation, prevention and treatment of cognitive decline

Epidemiological data suggest a large prevalence of cognitive impairment in elderly patients on haemodialysis. They are frequently exposed to pathologies that affect the brain, and hold a plurality of risk factors for neurodegenerative and vascular dementia. Cognitive dysfunctions, because of their medical and socio-economical consequences, may led to discuss the indication for haemodialysis and its profit for the elderly patient. These facts highlight the advantage of a regular assessment of cognitive functions in this population. They also suggest the need in the future of a multidisciplinary intervention for these patients, for a better evaluation of interventions aimed on primary and secondary prevention of cognitive decline in the elderly group.     

Cardiac high-sensitivity troponin T measurement: A layer of complexity in managing haemodialysis patients

Aim: To determine: (i) the proportion of stable asymptomatic haemodialysis patients with elevated troponin; (ii) stability of troponin values after dialysis and over a 2‐week interval; and (iii) whether high‐sensitivity troponin T (hsTnT) was associated with higher prevalence of cardiovascular risk factors or cardiovascular disease in these patients. Methods: We measured hsTnT and the fourth generation troponin I before and after dialysis in 103 stable in‐centre haemodialysis patients without ischaemic symptoms. Patients were divided into quartiles to test for associations with established cardiovascular risk factors or disease. Results: hsTnT was above the 99th percentile for the general population in 99% of haemodialysis patients compared with only 13% elevation for the troponin I assay (P < 0.001). Median pre‐dialysis hsTnT concentrations were unchanged after a 2‐week interval (69 vs 69 ng/L, P = 0.55) but fell slightly immediately following dialysis (69 vs 61 ng/L, P < 0.001). Established coronary artery disease (59% vs 22%), peripheral vascular disease (38% vs 4%) and diabetes (18% vs 7%) were more prevalent (P < 0.05) in those in the highest quartile for hsTnT compared with those in the lowest quartile. Conclusion: Almost all in‐centre haemodialysis patients have elevated troponin T in their baseline stable state and this appears unchanged over a 2‐week interval. Such a high rate of baseline elevation of hsTnT may lead to confusion in managing acute coronary syndrome in this group of patients, particularly when symptoms are atypical. We recommend that if Troponin I assay is unavailable then baseline hsTnT concentrations are measured periodically in all haemodialysis patients.