Characteristics and clinical relevance of chronic anemia in adult heart transplant recipients

BACKGROUND: Mild chronic anemia following heart transplantation (HTX), with hemoglobin (Hb) values of 10-14 g/dL in men and 10-12 g/dL in women, is frequent. It has continued to be of uncertain etiology yet clinical relevance. Nonetheless, therapeutic immunosuppression has been regarded as a major cause of chronic anemia in HTX patients. METHODS: Sixty outpatients were observed over a period of 5 yr after HTX. Laboratory values related to anemia such as Hb, erythropoietin (EPO), ferritin, transferrin, iron, and vitamin levels were obtained and analyzed monthly. Patients were divided into two groups retrospectively. Patients with persistent anemia for more than 1 yr were compared with non-anemic patients. RESULTS: Forty-three (72%) of the 60 patients were anemic. Anemia was normochromic, normocytic, and slightly anisocytic. Anemic and non-anemic patients showed EPO levels within the expected range as defined by Erslev (Erythropoietin. N Engl J Med 1991: 324: 1339). Reticulocyte counts were found to be normal in all patients. Iron deficiency and deficiency of vitamin B12 or folic acid were not observed. Patients with persistent anemia showed a significantly shorter survival period than non-anemic patients (p<0.02). CONCLUSIONS: Mild anemia following HTX shows the same characteristics as anemia in chronic diseases. Persisting mild anemia used to be associated with a shorter life expectancy. There is no evidence that standard immunosuppression causes anemia.     

Prevalence and etiology of anemia in renal transplant recipients

We aimed to define the prevalence of anemia and possible causes for it in a group of renal transplant recipients. A total of 229 recipients (65 women; age 36.1 +/- 11.8 years; minimum posttransplant duration, 3 years) were included. Patients with iron, vitamin B(12), and folic acid deficiencies were excluded. Patients were grouped according to number of posttransplant years completed with functioning grafts (3, 5, or 10 years). Demographic data, donor information, HLA mismatches, acute rejection episodes, biochemical parameters, and medications received during the 3 months before transplant and at 3, 5, and 10 years posttransplant were collected retrospectively. The anemia threshold was 13 g/dL for men and 12 g/dL for women. Anemia prevalence was 41.5%, 35.3%, and 93.2% at 3, 5, and 10 years, respectively. Anemic patients had higher creatinine levels for all years. In the anemic patients, hemoglobin values were lower in the pretransplant period than at 3 and 5 years. Anemic patients had higher HLA mismatches for the same years. Three-year hemoglobin levels were positively correlated with pretransplant hemoglobin and negatively correlated with creatinine levels and HLA mismatches. Five-year hemoglobin levels were positively correlated with pretransplant hemoglobin and albumin levels. Ten-year hemoglobin levels were positively correlated with pretransplant hemoglobin and albumin values but negatively correlated with creatinine levels and HLA mismatches. The prevalence of anemia in renal transplant recipients increases in parallel with posttransplant duration. Hemoglobin levels in these patients are closely related with pretransplant hemoglobin, follow-up creatinine levels, and HLA mismatches.     

Factor Deficiency in the Anemia of Renal Transplant Patients With Grade III-IV Chronic Kidney Disease: Baseline Results of the ARES Study

ARES is a multicenter, prospective study of the prevalence, management, and repercussions on the quality of life of anemia in renal transplant patients with a reduced renal function (creatinine clearance according to Cockcroft-Gault: ≤60 and >15 mL/min). The frequency of factor deficiency and its relationship with anemia were analyzed at the baseline time of the study. Of the 500 patients included in the main study, valid data were available for iron metabolism in n = 419 μg/dL; folic acid, n = 205 ng/mL; and vitamin B12, n = 210 pg/mL. Anemia was defined as hemoglobin ≤13 g/dL (men) or ≤12 g/dL (women) and/or use of erythropoietin (EPO). Anemic patients (59.4%) had less sideremia (73.4 vs 81.2 μg/dL; P = .008), but no significant differences were observed for transferrin saturation index (25.9% vs 25.5%), ferritin (167 vs 171 ng/mL), iron insufficiency (26.5% vs 36.2%), pronounced ferropenia (20.4% vs 20.1%), folic acid (7.5 vs 6.6 ng/mL), or vitamin B12 (486 vs 530 pg/mL). Treatment with oral or intravenous iron was much more frequent in anemic patients (31.6% vs 9.9%; P < .001). The logistic regression analysis of factors associated with anemia revealed that renal function and the use of angiotensin-converting enzyme (ACE) inhibitors were significant but not the degree of iron deficiency. In conclusion, iron deficiency in renal transplant patients with chronic nephropathy is frequent and insufficiently treated. Although it may be an aggravating factor, it was not shown to be a determining factor for the presence or absence of anemia in the patients as a group.     

An underappreciated problem in renal transplant recipients: anemia

PURPOSE: Posttransplant anemia (PTA) is associated with a higher risk of cardiac mortality, which is the most frequent cause of death among renal transplant recipients. In this study, we sought to determine the prevalence and causes of PTA among Turkish patients. PATIENTS AND METHODS: The study included 75 (52 male, 23 female) adults. Anemia was defined as an hemoglobin (Hb) level < or = 13 g/dL for men and < or = 12 g/dL for women. RESULTS: The prevalence of PTA was 49.3% at a mean duration of 60.45 months after renal transplantation. The most frequent causes of PTA were erythropoietin (EPO) and iron deficiency. The mean Hb level of 12.76 +/- 2.31 g/dL was significantly higher in male compared to female patients (13.26 +/- 2.31 g/dL vs 11.64 +/- 1.93 g/dL, P = .005). The Hb value was positively correlated with creatinine clearance and serum albumin level, and negatively correlated with serum creatinine level, the amount of proteinuria, and cyclosporine level. Creatinine clearance and serum albumin level were found to be an independent risk factors for PTA upon multivariate analysis. Only 12 of 37 anemic patients received treatment for anemia: 5 (13.5%) with EPO and 7 (18.9%) with iron preparations. CONCLUSION: PTA a common complication was unfortunately neglected in this setting. Impaired renal allograft function and decreased serum albumin were major risk factors for PTA. Increased cyclosporine levels were also correlated with decreased Hb concentrations.     

Anemia in pediatric hemodialysis patients: results from the 2001 ESRD Clinical Performance Measures Project

BACKGROUND: Despite improvements in dialysis care, anemia remains a problem in pediatric hemodialysis patients. METHODS: To assess possible explanations for the anemia, clinical data were obtained from the Centers for Medicare and Medicaid Services on all hemodialysis patients ages 12 to <18 years between October and December 2000. Complete data were available for 435 of the 516 patients (84%). RESULTS: A total of 160 (37%) patients had a mean hemoglobin of <11 g/dL (anemic). The mean (+/- SD) age for these patients was 15.5 +/- 1.8 years compared to 15.9 +/- 1.5 years for the target hemoglobin patients (P < 0.05). Mean time on chronic dialysis was similar for both the anemic and target hemoglobin patients (>/=100 g/dL) ( approximately 3 years) but patients on dialysis <6 months were more likely to be anemic (67%). While nearly all patients were treated with erythropoietin, anemic patients received greater weekly erythropoietin doses (intravenous, anemia 374 +/- 232 units/kg/week vs. target hemoglobin 246 +/- 196 units/kg/week, P < 0.001; and subcutaneous, 304 +/- 238 units/kg/week vs. 167 +/- 99 units/kg/week, P < 0.05). A total of 59% of anemic patients had a mean transferrin saturation (TSAT) >/=20% compared to 71% of patients with a target hemoglobin (P < 0.01). A mean serum ferritin >/=100 ng/mL was present in approximately two thirds of the anemic and target hemoglobin patients. Approximately 60% of all children were treated with intravenous iron. The mean Kt/V values were lower for anemic patients (1.46 +/- 0.4 vs. 1.53 +/- 0.3, P < 0.05). Anemic patients were less likely to have a normal serum albumin (29% anemic vs. 52% target hemoglobin patients, P < 0.001). CONCLUSION: In the final multivariable regression model, dialyzing <6 months, a low albumin, and a mean TSAT <20% remained significant predictors of anemia in children.     

Anemia in pediatric renal transplant recipients

The aim of this study was to establish the prevalence of anemia in stable pediatric renal transplant recipients and to examine the association of anemia with renal function, immunosuppressants, angiotensin converting enzyme inhibitors, and growth, as well as iron, vitamin B₁₂, and folate stores. This is a cross-sectional study of the 50 renal transplant recipients currently followed at our center. Patient data were collected regarding hematological parameters, growth, medications, renal function, underlying renal disease, delayed graft function, episodes of rejection, and iron or erythropoietin therapy post transplantation. The mean hemoglobin level (Hb) was 110 g/l and the overall prevalence of anemia was 60%, including 30% who were severely anemic (Hb<100 g/l). There was a high rate of iron deficiency (34%) and serum iron was the parameter of iron metabolism most closely associated with anemia. Hb in patients with low serum iron was 90.7 g/l versus 114.4 g/l in those with normal serum iron (P<0.01). Both univariate and multiple linear regression determined tacrolimus dose and creatinine clearance to be significant factors associated with anemia. Tacrolimus dose correlated with a 10 g/l reduction in Hb for every increase of tacrolimus dose of 0.054 mg/kg per day (P=0.001). The dose of mycophenolate was positively correlated with Hb, but this was likely to be confounded by our practice of dose reduction in the setting of anemia. Angiotensin converting enzyme inhibitor use was not associated with anemia. Severely anemic patients tended to be shorter, with a mean Z-score for height of –1.8 compared with –0.9 for those with normal Hb (P=0.02). Anemia is a significant and common problem in pediatric renal transplant patients. Deteriorating renal function is an important cause, but other factors like iron deficiency and immunosuppression are involved. Definition of iron deficiency is difficult and serum iron may be a valuable indicator. Medication doses, nutritional status, need for erythropoietin and iron, as well as poor graft function and growth require systematic scrutiny in the care of the anemic renal transplant recipient.     

Folic acid deficiency modifies the haematopoietic response to recombinant human erythropoietin in maintenance dialysis patients.

BACKGROUND: While folic acid deficiency causes macrocytic anaemia in non-renal patients, the relevance of altered folate metabolism in anaemia of end-stage renal disease and its response to rHu-EPO is less clear. METHODS: Ten haemodialysis patients with macrocytic anaemia due to dietary folic acid deficiency were compared to 10 matched (age, duration of dialysis, degree of anaemia) patients with normocytic normochromic anaemia. Nineteen patients received erythropoietin-alpha intravenously thrice weekly. The study design was a prospective crossover (ABA) comparison of the effects of intravenously administered high doses of folic acid on haemoglobin levels and EPO doses, with 6 months active supplementation (B) and two periods of 6 months duration each without folic acid supplementation (A). RESULTS: The two patient groups did not differ at recruitment. Red blood cell folate levels were normal in patients with normocytic anaemia, but they were subnormal in all patients with macrocytic anaemia. Compared to the first period without folic acid supplementation, patients with macrocytic anaemia had significantly higher haemoglobin levels despite lower EPO doses after 6 months high-dose folic acid, and red cells had become normocytic. The removal of folic acid supplementation resulted in re-occurrence of macrocytosis and in a significantly lower response to rHu-EPO. In contrast, high-dose folic acid supplementation had no effect on response to rHu-EPO in patients with normocytic anaemia. CONCLUSIONS: Folic acid deficiency may occur in elderly haemodialysis patients with poor dietary folate intake without regular oral supplementation and may cause hyporesponsiveness to rHu-EPO. Macrocytosis is a simple and cheap indicator for folate deficiency in end-stage renal disease patients on maintenance dialysis.     

Correlation of dietary intakes and biochemical determinates of nutrition in hemodialysis patients

OBJECTIVE: The purpose of this study was to determine the effect of dietary intakes on nutritional indicators of patients on hemodialysis. METHOD: This study was carried out at the hemodialysis unit at the Ministry of Health, Ankara Hospital, from 2003-2004. Sixty-seven patients on regular hemodialysis were enrolled in the study. Nutritional status was assessed by biochemical parameters (urea, uric acid, creatinine, Na, K, Cl, Ca, P, alkaline phosphatase, SGOT, SGPT, cholesterol, total protein, albumin, hemoglobin, hematocrit) and anthropometric measurements (height, dry weight, body mass index), and dietary intakes were calculated. RESULTS: In this study, the mean age of the patients was 45.3 +/- 13.49, and the duration of hemodialysis was 4.9 +/- 3.64 year. Dialysis time was 12.4 +/- 2.7 h/week. The ratio of individuals with BMI of 20 kg/m2 or below this value was 19.4%. Blood hemoglobin and hematocrit levels were below than the recommended level. Mean serum urea (148.0 +/- 27.76 mg/dL) and creatinine (8.8 +/- 2.13 mg/dL) were found to be high, while a significant negative correlation was found between blood urea level and dietary fat (p < 0.01, r = -0.31). A significant positive correlation was found between vitamin B1, vitamin B6, folate, potassium, iron, and magnesium; between uric acid and vitamin D; between blood creatinine level and dietary vitamin B1, vitamin B6, folate, vitamin C, potassium, iron, magnesium; between blood potassium level and dietary vitamin C only; and between blood cholesterol level and dietary vitamin D only (p < 0.01).     

Prevalence of Iron, Folate, and Vitamin B12 Deficiency Anemia After Laparoscopic Roux-en-Y Gastric Bypass

Background One of the most common bariatric operations is the laparoscopic Roux-en-Y gastric bypass (LRYGBP) in which the gastric capacity is restricted and the absorption by the small intestine is reduced. The objective of this study was to evaluate the incidence of iron, folate, and vitamin B12 deficiency anemia in patients undergoing LRYGBP. Patients and methods Clinical records of 30 patients who underwent LRYGBP between July 2003 and January 2005 and had a minimum follow up of 24 months at our outpatient clinic were included. Multivitamin supplementation was prescribed to all patients. The complete blood cell count, plasma iron, total iron-binding capacity, transferrin saturation, serum folate, and cobalamin levels before surgery, 6 months, 1, 2, and 3 years after the surgery were analyzed. Results There were 25 women (83.4%) and five men (16.6%) with ages from 21 to 56 years. Before surgery, two patients (6.6%) presented ferropenic anemia. Iron deficiency was seen in 40 and 54.5% 2 and 3 years after surgery, respectively. Cobalamin deficiency was observed in 33.3% at 2 years and in 27.2% at 3 years. At 2-year follow-up, 46.6% of the patients had already developed anemia and 63.6% at 3 years. Folate deficiency was not observed in any patient. Conclusion Our routine scheme of vitamin supplementation is not sufficient to prevent iron and vitamin B12 deficiencies in most patients.     

Prevalence and Management of Anemia in Renal Transplant Recipients: A European Survey

The TRansplant European Survey on Anemia Management (TRESAM) documented the prevalence and management of anemia in kidney transplant recipients. Data from 72 transplant centers in 16 countries were screened, involving 4263 patients who had received transplants 6 months, 1, 3 or 5 years earlier. The mean age of transplant recipients was 45.5 years at transplantation. The most common etiology was chronic glomerulonephritis. The most common comorbidities were coronary artery disease, hepatitis B/C, and type 2 diabetes. The mean hemoglobin levels before transplantation were significantly higher in the more recently transplanted recipients. At enrollment, 38.6% of patients were found to be anemic. Of the 8.5% of patients who were considered severely anemic, only 17.8% were treated with epoetin. There was a strong association between hemoglobin and graft function; of the 904 patients with serum creatinine > 2 mg/dL, 60.1% were anemic, vs. 29.0% of those with serum creatinine 相似文献   

Influence of anticalcineurinic therapy in plasma homocysteine levels of renal transplant recipients: a prospective study

Hyperhomocysteinemia is an independent factor for cardiovascular disease. Renal function and folate level are important determinants of total plasma homocysteine levels. The influence of anticalcineurin drugs on homocysteine levels is controversial. The aims of the study were: (1) to analyze changes in homocysteine levels after the first year of 73 renal transplants and (2) to determine the influence of immunosuppressive anticalcineurin drug therapy on fasting homocysteine concentrations. We examined homocysteine, serum creatinine, folate, and vitamin B12 concentrations immediately after transplant, at 6 months, and after 12 months from renal transplant. Also, MTHFRC677T polymorphism was investigated. Tacrolimus was administered in 28 patients and cyclosporine in 45. Homocysteine levels decreased from 28.41+/-13.71 micromol/L to 18.59+/-8.31 micromol/L after 6 months and to 17.13+/-7.06 micromol/L after 1 year. No relationship was found between homocysteine and folate levels. When anticalcineurin drugs were considered, the homocysteine levels in patients treated with tacrolimus was lower than that in patients treated with cyclosporine at month 6 after transplant (16+/-7.4 micromol/L vs 20.1+/-8.5 micromol/L, P=.03) and after 1 year (15+/-7.6 micromol/L vs 18.4+/-6.4 micromol/L, P=.04). Serum creatinine levels followed the same evolution: they were lower in patients treated with tacrolimus at 6 months (1.35+/-0.36 mg/dL vs 1.57+/-0.45 mg/dL, P=.03) and to a lesser extent at 1 year after renal transplant (1.38+/-0.35 mg/dL vs 1.54+/-0.45 mg/dL, P=.09). The homocysteine value closely related with serum creatinine in both groups. In conclusion, 1 year posttransplant, the homocysteine level was lower among patients treated with tacrolimus, the cohort that also showed the lower serum creatinine concentrations.     

Vitamin B12 deficiency in spinal cord injury: a retrospective study

BACKGROUND/OBJECTIVE: Vitamin B12 (or cobalamin) deficiency is well known in geriatric patients, but not in those with spinal cord injury (SCI). This retrospective study describes vitamin B12 deficiency in SCI. METHODS: This study utilized a retrospective chart review of patients with SCI who had received serum vitamin B12 testing over the last 10 years. RESULTS: Probable vitamin B12 deficiency was noted in 16 patients with SCI. Twelve patients had subnormal serum vitamin B12 levels (< 220 pg/mL), whereas 4 patients had low-normal vitamin B12 levels (< 300 pg/mL) with neurologic and/or psychiatric symptoms that improved following vitamin B12 replacement. Classic findings of paresthesias and numbness often were not evident; such findings likely were masked by the pre-existing sensory impairment caused by SCI. Of the 16 SCI patients, 7 were ambulatory; 4 of the 7 presented with deterioration of gait. In addition, 3 of the 16 SCI patients presented with depression and fatigue, 2 had worsening pain, 2 had worsening upper limb weakness, and 2 had memory decline. Of the 12 patients with subnormal serum vitamin B12 levels, 6 were asymptomatic. Classic laboratory findings of low serum vitamin B12, macrocytic red blood cell indices, and megaloblastic anemia were not always present. Anemia was identified in 7 of the 16 patients and macrocytic red blood cells were found in 3 of the 16 patients. Only 1 of the 16 SCI patients had a clear pathophysiologic mechanism to explain the vitamin B12 deficiency (ie, partial gastrectomy); none of the patients were vegetarian. Twelve of the SCI patients appeared to experience clinical benefits from cyanocobalamin replacement (some patients experienced more than 1 benefit), including reversal of anemia (5 patients), improved gait (4 patients), improved mood (3 patients), improved memory (2 patients), reduced pain (2 patients), strength gain (1 patient), and reduced numbness (1 patient). CONCLUSION: It is recommended that physicians consider vitamin B12 deficiency in their patients with SCI, particularly in those with neurologic and/or psychiatric symptoms. These symptoms often are reversible if treatment is initiated early.     

Homocysteine,folate, vitamin B<Subscript>12</Subscript> levels,and<Emphasis Type="Italic"> C677T</Emphasis> MTHFR mutation in children with renal failure

Hyperhomocysteinemia is well documented in chronic renal failure (CRF) and premature and progressive occlusive vascular disease is common in CRF. The combined effects of renal failure, folate and vitamin B(12) levels, and a common mutation (C677T) in the methylenetetrahydrofolate reductase (MTHFR) gene that leads to total plasma homocysteine (tHcy) elevation in CRF children were investigated. Forty-two children (15 females) with CRF, mean age 10.3+/-4.7 years, were included. The mean glomerular filtration rate (GFR) was 37.3+/-16.9 ml/min per 1.73 m(2). The control group comprised 33 children (18 females) with a mean age of 8.6+/-3.4 years. There were 40% of CRF patients with hyperhomocysteinemia. Folate and vitamin B(12) deficiencies were identified in 14% (n=6) and 5% (n=2), respectively, of all patients. On univariate analysis, the tHcy serum concentration was negatively correlated with the plasma folate concentration (P<0.05) in controls, and with GFR (P<0.05) in patients. On multiple regression analysis for the predictors of tHcy serum concentrations, folic and vitamin B(12 )were significant in controls, whereas only GFR was significant in CRF children. In our patients no effect of the MTHFR polymorphism on tHcy levels was seen This result, in addition to the limited number of patients, may partially be explained by the low prevalence of folate deficiency in our patients.     

Effects of erythropoietin on left ventricular hypertrophy in adults with severe chronic renal failure and hemoglobin <10 g/dL

BACKGROUND: Left ventricular hypertrophy (LVH) frequently complicates chronic renal insufficiency. Anemia is also common in these patients and may contribute to LVH. METHODS: We conducted an open-label interventional trial to evaluate the effect of recombinant erythropoietin (rhEPO) on left ventricular mass index (LVMI) in anemic patients with renal insufficiency. Adults with creatinine clearance 10 to 30 mL/min (nondiabetics) or 20 to 40 mL/min (diabetics) were recruited, and rhEPO was given to those with anemia (hemoglobin level <10 g/dL). Baseline and 6-month LVMI and LVH (LVMI >130 g/m(2) in men and >100 g/m(2) in women), hemoglobin levels, creatinine clearance, blood pressure, medications, and medical history were obtained. Forty anemic and 61 nonanemic control subjects were enrolled. RESULTS: Overall, the prevalence of LVH was 68.3% (95% CI 58.3-77.2), and entry hemoglobin level was the only significant predictor of baseline LVH (adjusted OR 0.69 per g/dL increase in hemoglobin, 95% CI 0.50-0.94). After 6 months, LVMI decreased in anemic patients receiving rhEPO (142 +/- 56 vs. 157 +/- 56 g/m(2)) (P= 0.007), with an increase in hemoglobin (11.3 +/- 1.9 vs. 9.1 +/- 0.7 g/dL) (P= 0.001). There were no changes in LVMI or hemoglobin level among controls. After adjusting for confounders and change in hemoglobin, receipt of rhEPO was associated with a significant reduction in LVMI (P= 0.01). CONCLUSION: Treatment with rhEPO was not independently associated with significant changes in blood pressure or renal function. LVH is a common finding in chronic renal insufficiency and is associated with lower hemoglobin levels. Treatment with rhEPO may decrease LVH in patients with severe renal insufficiency and anemia.     

Soluble transferrin receptors and reticulocyte hemoglobin concentration in the assessment of iron deficiency in hemodialysis patients

BACKGROUND: Diagnosing iron deficiency in hemodialysis (HD) patients is crucial for correct anemia management. Hypochromic erythrocytes appear to be the best available marker, but they are often unavailable. Transferrin saturation (TSAT) and ferritin are also indicated as reference markers by guidelines. We evaluated the usefulness of soluble transferrin receptor (s-TfR) and reticulocyte hemoglobin concentration (CHr), which have been recently proposed as more sensitive functional iron deficiency indicators. METHODS: A single-center unselected cohort of 39 chronic HD patients underwent a cross-sectional determination of hemoglobin (Hb), hematocrit (Hct), CHr, transferrin, iron, TSAT, ferritin, folate, vitamin B12 and s-TfR. Twenty-nine patients (74.4%) were treated with subcutaneous erythropoietin (EPO) at a dose of 122 +/- 98 U/kg/week and 24 patients (61.5%) were treated with intravenous (i.v.) iron gluconate, 62.5 mg/week. RESULTS: Hb was 11.1 +/- 1.2 g/dL, Hct 34.4 +/- 3.7%, CHr 32.7 +/- 3.8 pg, transferrin 170 +/- 31 mg/dL, iron 60.2 +/- 25.9 mg/dL, TSAT 30 +/- 18%; ferritin 204 +/- 219 ng/mL, folate 4.2 +/- 1.0 mcg/L, vitamin B12 0.58 +/- 0.15 mcg/L, and s-TfR 1.94 +/- 0.83 mg/L. Both TSAT and s-TfR significantly correlated with CHr, but no relationship could be found between s-TfR and TSAT or between s-TfR and ferritin. Dividing the population into two groups based on iron repletion (ferritin >100 ng/mL and TSAT >20%) we found no differences for CHr levels and significantly lower levels of s-TfR in the replete group (s-TfR 1.71 +/- 0.70 vs. 2.29 +/- 0.90 mg/L; p=0.033). Analysis of 2x2 tables demonstrated that 44% of patients with TSAT >20% had elevated (>1.5 mg/L) s-TfR, indicating a possible functional iron deficiency, but covariance analysis showed that TSAT had a better correlation to CHr. CONCLUSIONS: No clear-cut advantages in the use of CHr content and s-TfR levels as single diagnostic tests could be demonstrated by this cross-sectional study. However, our results suggest that the combined use of TSAT <20% and s-TfR >1.5 mg/L (therefore, including all patients with low TSAT, but also patients with high s-TfR despite normal TSAT) could improve functional iron deficiency detection in dialysis patients suspected of having inflammatory conditions.     

Hyperhomocysteinaemia, folate and vitamin B12 in unsupplemented haemodialysis patients: effect of oral therapy with folic acid and vitamin B12.

BACKGROUND: Hyperhomocysteinaemia, a risk factor for atherosclerosis, is common in dialysis patients and particularly in those homozygous for a common polymorphism in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene (C677T transition). B-complex vitamin supplements have been shown to lower plasma total homocysteine (tHcy) concentrations, but the respective effectiveness of folate and oral vitamin B12 is not yet known. Our objectives were: (i) to determine the status of folate and vitamin B12 in a cohort of unsupplemented dialysis patients (ii) to assess the homocysteine-lowering effect of a folate supplement and then of a folate supplement with added vitamin B12. The responses were analysed for the C677T genotypes of MTHFR. METHODS: Plasma tHcy, folate and vitamin B12 were measured in 51 haemodialysis patients genotyped for the C677T MTHFR mutation (homozygotes, TT; heterozygotes, CT; without mutation, CC). All patients were then given daily supplements of 15 mg of folic acid for 2 months. They were given daily supplements of 1 mg of vitamin B12 in addition to the folate supplements for a further 2 months. Plasma tHcy, folate and vitamin B12 were monitored after each intervention. RESULTS: At baseline folate and vitamin B12 deficiencies were found in 10% and 6% of the patients. Initial plasma tHcy concentrations were high in all patients (mean 38.1+/-15 micromol/l). CC patients tended to have a lower tHcy concentration than pooled CT and TT patients. After 2 months of folate therapy, tHcy concentration decreased significantly to 20.2+/-7 micromol/l (P<0.001) and no significant differences were observed between the different genotype subgroups (19.4+/-6 for CC, 21.3+/-8 for CT, 18.5+/-4 for TT). A significant positive relationship was found between the reduction of tHcy and its initial value (rho=0.615, P<0.0001). The impact of the added vitamin B12 was negligible since tHcy concentrations did not change for the patients as a whole (19.8+/-7 micromol/l, NS) or in any subgroup (19.1+/-5 for CC, 20.3+/-9 for CT and 20+/-7 micromol/l for TT). CONCLUSIONS: (i) Folate and vitamin B12 deficiencies were observed in 10% and 6% respectively of our unsupplemented dialysis patients. (ii) After folate therapy, tHcy levels decreased significantly in all patients and were identical between the three C677T MTHFR genotype subgroups. (iii) Vitamin B12 supplements are useful in folate treated patients to prevent cobalamin deficiency and its neurological consequences but they did not lower tHcy plasma levels for the patients as a group or for any of the MTHFR subgroups.     

Vitamin B12 Deficiency In Spinal Cord Injury: A Retrospective Study

Abstract

Background/Objective: Vitamin B12 (or cobalamin) deficiency is well known in geriatric patients, but not in those with spinal cord injury (SCI) . This retrospective study describes vitamin B1 2 deficiency in SCI.

Methods: This study utilized a retrospective chart review of patients with SCI who had received serum vitamin B1 2 testing over the last 1 0 years.

Results: Probable vitamin B1 2 deficiency was noted in 1 6 patients with SCI. Twelve patients had subnormal serum vitamin B12 levels (< 220 pg/ml), whereas 4 patients had low-normal vitamin B12 levels (< 300 pg/ml) with neurologic and/or psychiatric symptoms that improved following vitamin B1 2 replacement. Classic findings of paresthesias and numbness often were not evident; such findings likely were masked by the pre-existing sensory impairment caused by SCI. Of the 1 6 SCI patients, 7 were ambulatory; 4 of the 7 presented with deterioration of gait. In addition, 3 of the 1 6 SCI patients presented with depression and fatigue, 2 had worsening pain , 2 had worsening upper limb weakness, and 2 had memory decline. Of the 1 2 patients with subnormal serum vitamin B12 levels, 6 were asymptomatic. Classic laboratory findings of low serum vitamin B1 2 , macrocytic red blood cell indices, and megaloblastic anemia were not always present. Anem ia was identified in 7 of the 1 6 patients and macrocytic red blood cells were found in 3 of the 1 6 patients. Only 1 of the 1 6 SCI patients had a clear pathophysiologic mechanism to explain the vitamin B12 deficiency (ie, partial gastrectomy); none of the patients were vegetarian. Twelve of the SCI patients appeared to experience clinical benefits from cyanocobalamin replacement (some patients experienced more than 1 benefit), including reversal of anemia (5 patients), improved gait (4 patients), improved mood (3 patients), improved memory (2 patients), reduced pain (2 patients) , strength gain (1 patient), and reduced numbness (1 patient).

Conclusion: It is recommended that physicians consider vitamin B1 2 deficiency in their patients with SCI , particularly in those with neurologic and/ or psychiatric symptoms. These symptoms often are reversible iftreatment is initiated early.     

The Importance Of Nutrition In The Care Of Persons With Spinal Cord Injury

Abstract

Background/Objective: Vitamin B12 (or cobalamin) deficiency is well known in geriatric patients, but not in those with spinal cord injury (SCI) . This retrospective study describes vitamin B1 2 deficiency in SCI.

Methods: This study utilized a retrospective chart review of patients with SCI who had received serum vitamin B1 2 testing over the last 1 0 years.

Results: Probable vitamin B1 2 deficiency was noted in 1 6 patients with SCI. Twelve patients had subnormal serum vitamin B12 levels (< 220 pg/ml), whereas 4 patients had low-normal vitamin B12 levels (< 300 pg/ml) with neurologic and/or psychiatric symptoms that improved following vitamin B1 2 replacement. Classic findings of paresthesias and numbness often were not evident; such findings likely were masked by the pre-existing sensory impairment caused by SCI. Of the 1 6 SCI patients, 7 were ambulatory; 4 of the 7 presented with deterioration of gait. In addition, 3 of the 1 6 SCI patients presented with depression and fatigue, 2 had worsening pain , 2 had worsening upper limb weakness, and 2 had memory decline. Of the 1 2 patients with subnormal serum vitamin B12 levels, 6 were asymptomatic. Classic laboratory findings of low serum vitamin B1 2 , macrocytic red blood cell indices, and megaloblastic anemia were not always present. Anem ia was identified in 7 of the 1 6 patients and macrocytic red blood cells were found in 3 of the 1 6 patients. Only 1 of the 1 6 SCI patients had a clear pathophysiologic mechanism to explain the vitamin B12 deficiency (ie, partial gastrectomy); none of the patients were vegetarian. Twelve of the SCI patients appeared to experience clinical benefits from cyanocobalamin replacement (some patients experienced more than 1 benefit), including reversal of anemia (5 patients), improved gait (4 patients), improved mood (3 patients), improved memory (2 patients), reduced pain (2 patients) , strength gain (1 patient), and reduced numbness (1 patient).

Conclusion: It is recommended that physicians consider vitamin B1 2 deficiency in their patients with SCI , particularly in those with neurologic and/ or psychiatric symptoms. These symptoms often are reversible iftreatment is initiated early.     

Oxidative stress in kidney transplant patients

BACKGROUND: Little information is available about the role of oxidative stress in renal transplant patients. To evaluate the prevalence and severity of oxidative stress in renal transplantation, the authors conducted a cross-sectional study. METHODS: In 112 cadaver or living-donor kidney transplant recipients with a follow-up of at least 6 months and with plasma creatinine less than or equal to 2.5 mg/dL, complete blood count, serum vitamin B12, serum folate (s-F), reactive oxygen species (ROS), thiol groups (-SH), total antioxidant activity (TAOC), serum homocysteine (Hcy), and intraerythrocyte folate (ery-F) were measured. RESULTS: The mean levels of Hcy (21.1 microM vs. <10 microM), ROS (302.7 U. Carr (Carratelli units) vs. 250-300 U. Carr), and TAOC (410.6 micromol/HclO/mL vs. >350 micromol/HclO/mL), were higher than the reference interval, whereas -SH groups, vitamin B12, s-F, and ery-F were within the normal range. In the multivariate model, plasma creatinine (P=0.0062), vitamin B12 (P=0.0121), and TAOC (P=0.0007) were independently associated with oxidative stress. At multiple regression analysis, -SH groups and ROS were directly and inversely related to hematocrit (P=0.0007 and P=0.0073). There was also a negative correlation between -SH groups and blood pressure levels (P=0.0095). CONCLUSIONS: Renal transplant patients have a pattern of increased oxidant stress that is counterbalanced by an enhancement of the antioxidant mechanisms. Besides the well-known risk factors, the authors found that anemia is an independent risk factor for an increase of ROS. Further studies are needed to evaluate whether the correction of anemia might prevent or reduce the oxidative stress in renal transplant patients.