Influence of sympathetic activity on the progression of chronic kidney disease

There is clear evidence that chronic kidney disease [CKD] is often characterized by the presence of sympathetic hyperactivity. Data accumulating that this sympathetic hyperactivity is indeed important, because it may influence cardiovascular and renal prognosis. The aim of this study was to assess the relationship between glomerular filtration rate [GFR] and the levels of norepinephrine [NE] in serum and urine in the presence of variable degrees of renal functional impairment. A total of 75 CKD patients were divided into 5 groups according to GFR, group 1: 15 CKD patients with GFR>90ml/min/1.73m2 [stage 1CKD]. group 2: 15 CKD patients with GFR 60-89ml/min/1.73m2 [stage 2 CKD]. group 3: 15 CKD patients with GFR 30-59ml/min/1.73m2 [stage 3 CKD]. group 4: 15 CKD patients with GFR 15-29ml/min/1.73m2[stage 4 CKD]. group 5: 15 CKD patients with GFR<15ml/min/1.73m2 [stage 5, endstage renal failure], in addition to 15 healthy controls were studied. GFR was estimated by Cockroft-Gault formula. Norepinephrine was measured by an enzyme-linked immunosorbent assay. In addition, blood urea, serum creatinine, C-reactive protein [C-RP], fasting blood sugar [PBS], serum total cholesterol, triglycerides and 24-h urinary proteins were performed. Compared with controls, CKD patients had higher levels of serum norepinephrine, urinary norepinephrine was significantly lower among CKD patients. When GFR was reduced in CKD patients, serum norepinephrine was elevated and urinary norepinephrine was reduced suggesting greater renal impairment. In multivariate correlation, GFR were negatively correlated with serum norepinephrine and positively correlated with urinary norepinephrine. Serum norepinephrine levels were increased and urinary norepinephrine excretion were decreased in CKD patients, and may be one of the aggrevating factors for deterioration of renal function in those patients

Hepcidin level and its relation to ferrokinetic status in chronic renal failure patients on regular hemodialysis

Hepcidin, a key regulator of body iron homeostasis by blocking its intestinal absorption and its release by the reticuloendothelial system. The aim of the study was to assess serum hepcidin levels and its relation to ferrokinetic parameters in hemodialyzed [HD] patients. Fifty five patients on regular HD] [35 patients treated with erythropoietin and 20 patients without erythropoietin therapy] and 20 healthy controls were studied. Hepcidin and C-reactive protein [C-RP] were measured. Ferrokinetic parameters, complete blood count, kidney function, liver functions and lipid profile were assessed. The weekly erythropoietin dose and the patients demographics were recorded. In comparison to the healthy controls, the HD patients had higher serum ferritin, C-RP and hepcidin levels. Erythrocyte count, hemoglobin [Hb], hematocrit [Hct], serum iron, total iron binding capacity [TIBC], transferrin saturation [TSAT], total protein and albumin were low in HD patients. In univariate analysis, hepcidin levels were positively correlated with total protein, albumin, triglyceride, S. creatinine, ferritin and erythropoietin dose, and negatively correlated with age, erythrocyte count, Hb and Hct values. In multiple regression analysis, hepcidin levels were positively correlated with serum calcium, albumin, leukocyte count, triglyceride, serum iron, C-RP and TSAT and negatively correlated with hemoglobin. In conclusion, high serum levels of hepcidin in HD patients may be due to accumulation in the serum, and low grade inflammation my also be contributed. Elevated serum hepcidin levels in HD patients could be responsible, at least in part, for functional iron deficiency and anemia in these patients

Evaluation of hepcidin level and its relation to iron status, inflammation and liver function in hemodialyzed patients

Hepcidin, a key regulator of iron metabolism by blocking its intestinal absorption and its release by the reticuloendothelial system, and modulated in response to anemia, hypoxia or inflammation. The aim of the study was to assess hepcidin correlations with markers of iron status, erythropoietin therapy, liver function and markers of inflammation in hemodialyzed [HD] patients. Fifty patients on regular HD [30 patients treated with erythropoietin and 20 patients without erythropoietin therapy] and 20 healthy controls were studied. Hepcidin and C-reactive protein [CRP] were measured. Iron status, complete blood count, liver function and lipid profile were assessed. The weekly erythropoietin dose and the patients demographics were recorded. In comparison to the healthy controls, the HD patients had higher serum ferritin, CRP and hepcidin levels. Serum iron, total iron binding capacity [TIBC], transferrin saturation [TSAT], erythrocyte count, hemoglobin [Hb], hematocrit [Hct], platelet count and albumin were low in HD patients. In the patient group, hepcidin level were positively correlated with leukocyte count, triglyceride, albumin, aspartate aminotransferase, ferritin and erythropoietin dose and negatively correlated with erythrocyte count, Hb and HCt values. In multiple regression analysis, triglyceride [beta value was 0.27, p <0.05] and albumin [beta value was - 0.30, p < 0.05] were correlated with hepcidin in HD patients. In conclusion, high serum levels of hepcidin in HD patients may be due to accumulation in the serum, low - grade inflammation, frequently found in HD patients may also contributed. Elevated hepcidin levels in HD patients could be responsible for functional iron deficiency and anemia and may be considered as a sensitive tool for functional iron deficiency in these patients

Study of selected cytokines [tumour necrosis factor -alpha and interleukin-18] in patients with diabetic nephropathy

The aim of the present study was to investigate tumour necrosis factor- alpha [TNF-alpha] and interleukin-18 [IL-18] levels, their roles in the pathogenesis of diabetic complications especially diabetic nephropathy. Sixty patients with diabetes mellitus [30 with type 1 insulin dependent diabetes mellitus [IDDM] and 30 with type 2 non -insulin dependent diabetes mellitus [NIDDM] patients and 20 healthy controls were studied. Serum TNF-alpha and IL-18 was measured by enzyme linked immunosorbent assay [ELISA] for all subjects. In addition, fasting blood sugar [FBS], 2 h postprandial blood sugar [2h PPBS], glycosylated hemoglobin [Hb[AIC]], urinary albumin levels, triglyceride, total cholesterol, low density lipoprotein cholesterol [LDL-c], and high density lipoprotein cholesterol [HDL-c] were performed for all subjects. Increased serum levels of TNF-alpha and IL - 18 was evident in both IDDM and NIDDM patients as compared to the control group. Similarly, their levels in patients with diabetic nephropathy increased gradually according to the clinical stage of the disease, being highest in macroalbuminuric stage. Correlation analyses showed that serum TNF-alpha and IL-18 concentration were positively correlated with each other and positively with FBS,2h PPBS, Hb[A1C], triglyceride and urinary albumin excretion levels and negative correlation between TNF-alpha and HDL-c were also found in diabetic subjects. In conclusion, high serum levels of TNF-alpha and IL-18 suggested that they might play a role in the pathogenesis of diabetes mellitus [DM] and in the development of nephropathy in diabetic patients whether of type 1 or 2

Serum adiponectin in type 1 diabetic patients with nephropathy

The aim of the study was to elucidate whether serum adiponectin is associated with renal function, low - grade inflammatory markers, metabolic control and insulin resistance in type 1 diabetic patients with and without nephropathy. A total of 95 type 1 diabetic patients were divided into three groups based on their urinary albumin excretion rate [AER]: patients with normal AER had no antihypertensive medication, while patients with microalbuminuria or macroalbuminuria were all treated with an angiotensin converting enzyme [ACE] inhibitor. Renal function was estimated with the Cockroft-Gault formula. Adiponectin was measured by an immunofluorometric assay. In addition, glycosylated hemoglobin [HB[AIC]], estimated glucose disposal rate [GDR], urinary albumin levels, triglyceride, total cholesterol, high density lipoprotein cholesterol [HDL-c] were performed for all patients. Adiponectin concentrations were higher in women than in men. The levels of adiponectin in type 1 diabetic patients with nephropathy increased gradually according to the clinical stage of the disease, being highest in macro album inuric stage. In a univariate analysis, adiponectin was positively associated with serum creatinine, systolic blood pressure, HB[AIC], total cholesterol, HDL-C and negatively with estimated glomerular filtration rate [GFR] and waist to hip ratio [WHR]. In a multiple linear regression analysis including the above variables, estimated GFR, AER and WHR were independently associated with adiponectin levels. In conclusion, serum adiponectin concentrations were increased in type 1 diabetic patients with nephropathy, and levels were further associated with renal insufficiency

Evaluation of seminal plasma nitric oxide concertration in infertile males with varicocele

The aim of the present study was to measure and compare NO concentrations in the seminal plasma of infertile patients with/without varicocele. The study enrolled 35 patients with oligo- and/or asthenoteratozoospermia [OAT], and were divided into two groups: Group 1 [OAT with varicocele, n=19] and group 2 [OAT without varicocele, n=16]. Ten healthy subjects without varicocele and with normal semen parameters were taken as normal control. Semen analysis, estimation of NO in seminal plasma [SP] and hormonal assay [FSH, LH and testosterone] for all individuals were done. Nitric oxide concentration was significantly higher in SP of group 1 [varicocele] compared to both group 2 and normal control. Plasma FSH and LH concentrations were evaluated in group 1 versus control. In conclusion, the increased seminal plasma NO concentration is specifically related to the varicocele, not to infertility, since NO production in oligo- and/or asthenoteratozoospermic patients without varicocele did not increase. On the other hand, increased NO concentration may be one of the causes of damage to sperm in patients with varicocele. These data support the need for varicocele repair to interrupt NO overproduction