Obesity may be erythropoietin dose-saving in hemodialysis patients

BACKGROUND: In dialysis patients, the obesity-survival paradox still requires an explanation. Anemia and high doses of erythropoiesis-stimulating agents (ESAs) are associated with worse outcomes in the hemodialysis (HD) population. In the present study, we explored the relation between obesity and anemia control in a sample of maintenance HD patients in Egypt. METHODS: This multicenter observational study included 733 patients on maintenance HD from 9 hemodialysis centers in Egypt. Clinical and laboratory data as well as average doses of ESAs and parenteral iron were recorded. The erythropoietin resistance index (ERI) was calculated. RESULTS: Obesity, defined as a body mass index (BMI) ≥ 30 kg/m2, was present in 22.6% of the studied population. The target hemoglobin level (10.0–11.5 g/dL) was achieved in 27.3% of non-obese and 25.3% of obese patients, with no significant difference. The median serum ferritin and the values of transferrin saturation index did not differ significantly between these two groups. The weekly ESA dose was significantly lower in obese than in non-obese patients (P = 0.0001). A trend toward higher ESA doses and ERI values was observed in patients with lower BMIs (P < 0.0001). Multiple linear regression revealed that the BMI and urea reduction ratio were the strongest predictors of the ERI. CONCLUSION: Our study adds more evidence to obesity-associated advantages in HD patients. BMI may determine ESA response, with better responses observed in patients with higher BMIs.

Aging is an inevitable risk factor for insulin resistance

The present work looks into the different aspects of glucose homeostasis in the elderly patients in comparison to healthy younger subjects and patients with type 2 diabetes mellitus, relying on intravenous glucose tolerance test. A clinicobiochemical study was carried out comprising forty apparently healthy non-diabetic non-obese old individuals [mean age 65 +/- 4.8 years]. Forty type 2 diabetic patients compared to thirty healthy young subjects. The senile group had no family history of diabetes. Cases with renal, hepatic, gastrointestinal, or endocrine abnormalities were excluded from the study. Intravenous glucose tolerance test [ivGTT] was done with sampling at 0, 5, 10, 15, 30, 45, and 60 min after glucose load and the following estimations were undertaken: glucose constant decay [KG], glucose and insulin area under the curve, insulnogenic index, first phase insulin response, insulin resistance index and fractional insulin clearance. The senile and diabetic groups, when compared to the control, had non-significantly different fasting plasma glucose in senile group but it was higher in diabetic patients, while fasting serum insulin was significantly higher in the studied groups than in healthy control group. The senile group showed significant reduction in glucose tolerance [KG 1.36 +/- 0.3%/min], decreased insulin sensitivity index [5.19 +/- 1.4 10[-4] min[-1] /[uIU/ml]] and marked reduction of first phase insulin response [2.45 +/- 0.78 uIU/ml per mg/dl], when compared with the control group. However, the degree of glucose intolerance and insulin insensitivity of the senile group was still significantly less than of type 2 diabetic patients. This study revealed that the insulin resistance seems to be characteristic feature of normal aging process and senility could be considered as an inevitable risk factor for glucose intolerance and metabolic syndrome with its accompanying health hazards. Insulin secretion, insulin clearance and interaction between insulin and target tissues are defective in elderly subjects. These functions are intermediate between healthy controls and type 2 diabetic patients and may predispose the elderly population to the risk of impaired glucose tolerance or diabetes mellitus with its attendant macrovascular and microvascular complications

Effect of intravenous 1-alpha-hydroxy cholecalciferol on serum parathyroid hormone [PTH] level and T-cell subsets in hemodialysis patients with severe secondary hyperparathyroidism

Chronic renal failure and dialysis are commonly associated with increased liability to infection and abnormal immune reactions. However, the exact definition and pathogenetic mechanisms of such immune dysregulation have remained elusive. The present work has been undertaken to examine the effect of lowering serum parathyroid hormone [PTH] level with 1-alpha hydroxy cholecalciferol [alfacalcidol] injections on the disturbance of T cell subpopulations in chronic renal failure patients having severe hyperparathyroidism. Twenty-two chronic renal failure patients maintained on regular hemodialysis therapy completed the 3-month period of the study. All had a starting serum PTH level> 1000 pg/ml. Patients with diabetes mellitus, liver disease, chronic infections, hypercalcemia or marked hyperphosphatemia were excluded. During the study period, alfacalcidol [One-Alpha] 2-4 mcg were injected intravenously at the end of each dialysis session 3 times per week. Routine biochemistry and blood count as well as serum PTH were examined monthly. At the start- and end-points of the study, total lymphocytic count and T cell subpopulations were analyzed utilizing monoclonal antibodies against the surface markers CD3, CD4 and CD8 by double-color flow-cytometry technique. The changes in serum PTH and T cell subsets as well as the other routine biochemical parameters were compared at the start- and end points of the study, and the linear association of their degree of change was tested. Serum PTH dropped sign [p