Transferrin synthesis is increased in nephrotic patients insufficiently to replace urinary losses (original) (raw)
Related papers
Non-iron mediated alteration in hepatic transferrin gene expression in the nephrotic rat
Kidney International, 1995
Non-iron mediated alteration in hepatic transferrin gene expression in the nephrotic rat. Both transferrin and the iron it carries are lost in the urine in the nephrotie syndrome. Patients may develop hypochromie microcytic anemia and synthesis of transferrin, a protein regulated in large part by iron availability, is increased. Transferrin synthesis has also been reported to be increased in liver slices from rats with hereditary analbuminemia, and their plasma transferrin levels are increased, suggesting that transferrin synthesis may be stimulated by processes other than iron depletion in this hypoalbuminemic condition. Transferrin metabolism was studied in rats with Heymann nephritis (RN), in a strain of Sprague-Dawley (SD) rats with hereditary analbuminemia [Nagase analbuminemic rats (NAR)], and in normal SD rats. Plasma transferrin concentration and mass was decreased significantly in RN, but increased in NAR. Transferrin synthesis was increased both in NAR (measured either as the disappearance of [1251] labeled transferrin or as the incorporation of [3H] phenylalanine) and in RN (incorporation of ['R] phenylalanine). The fractional rate of transferrin catabolism was unchanged in NAR. Thus transferrin mass was increased in NAR entirely as a consequence of increased synthesis. Transferrin and albumin synthesis correlated with one another in both RN and SD (P < 0.001). Transferrin mRNA was increased in both RN and NAR and was unaffected by administration of iron to RN. Repatic transferrin and albumin mRNA levels were also correlated positively in RN and SD, suggesting that increased hepatic synthesis of both proteins might be responding to the same stimuli. Transferrin gene transcription was increased in both RN and NAR and was unaffected by administration of iron to HN. Transferrin mRNA was not increased in the testis in either RN or NAR, suggesting that augmentation in transferrin gene expression is driven by a non-iron dependent process and is confined to the liver. Transferrin synthesis is increased in patients with the nephrotic syndrome [1]. Transferrin is the principal iron carrying protein in plasma [2]. Its urinary loss in the nephrotic syndrome is sufficient to reduce plasma transferrin levels [31 and may produce sufficient iron losses to cause microcytic anemia [4-6]. Thus increased synthesis of transferrin in the nephrotic syndrome could well be a normal physiologic response to this well recognized regulatory stimulus. Although transferrin is synthesized in extrahepatic tis
Transferrin changes in haemodialysed patients
International Urology and Nephrology, 2012
Transferrin (Tf) is a glycoprotein responsible for iron transport in the human body. Physiologically in reaction with Concanavalin A, Tf occurs in four distinct variants Tf1, Tf2, Tf3 (apo-Tf) and Tf4. It was reported recently that Tf is changing, particularly during acute phase response, taking place among others in end-stage renal disease. In this study, we wanted to find the answer to three main questions: firstly, how Tf is changing in patients treated with maintenance haemodialysis (mHD), secondly, whether there are any Tf changes in the course of mHD treatment, and thirdly, what factors can affect Tf microheterogeneity in these patients. Studies were performed on 80 haemodialysed patients and 21 healthy volunteers. The Tf concentration was determined by the rocket immunoelectrophoresis, and its microheterogeneity was assessed by the ConA crossed immunoaffinity electrophoresis. During the annual observation of the distribution of the Tf variants, we have found both changes of the percentage contents of all Tf variants in the whole Tf concentration and a significant decrease in Tf2, Tf3 and Tf4 serum concentrations. Moreover, we found that decrease in the renal function, duration of mHD, and inflammation may contribute to these above-mentioned changes, which are probably the factors that should be taken into account when explaining the mechanisms of persistence of anaemia in haemodialysed patients.
Veterinary World, 2023
Background and Aim: Anemia is an important factor in surviving chronic kidney disease (CKD). Anemia in CKD is associated with various factors, such as inadequate production of erythropoietin and the availability of iron and its binding protein. Reduced total iron-binding capacity (TIBC) and iron concentrations may be related to their urinary loss along with proteinuria. This study aimed to determine the urinary loss of iron and transferrin (TF) in relation to the degree of proteinuria. Materials and Methods: The study was performed on 37 dogs with CKD. Dogs were divided according to the severity of proteinuria into two groups based on the mean of urinary protein–creatinine (UPC) ratio into UPC ratio <4 and UPC ratio >4. The hematocrit (HCT), blood chemistries, plasma iron, plasma TF, UPC ratio, urinary iron per creatinine ratio (U-Iron/ CR), and urinary TF per creatinine ratio (U-TF/CR) were evaluated. Results: Anemia was associated with the severity of renal impairment as demonstrated by reduction of HCT when staging of CKD was higher. Dogs with UPC ratio >4 had higher urinary loss of both U-Iron/CR (p < 0.01) and U-TF/CR (p < 0.001) with lower plasma TIBC (p < 0.001). The UPC ratio was positively correlated with both U-Iron/CR (r = 0.710, p < 0.001) and U-TF/CR (r = 0.730, p < 0.001) but negatively with TIBC (r = –0.462, p < 0.01). Conclusion: Proteinuria was associated with urinary loss of both iron and TF which may contribute to anemia in CKD.
The Open Urology & Nephrology Journal
Background: According to the currently applicable KDIGO-2012 and ERBP 2013 guidelines, iron metabolism assessments for patients with Chronic Kidney Disease (CKD) are performed using such parameters as ferritin concentration and Transferrin Saturation (TSAT). Their values are to be treated as a basis on which to decide on providing iron substitution. Patients with Stage 5 CKD on maintenance hemodialysis commonly suffer from malnutrition syndrome and inflammation. One of the markers for malnutrition and inflammation is low transferrin concentration. Our study focused on establishing what percentage of patients this applied to and whether or not the transferrin saturation figure was artificially inflated in such cases. Materials and Methods: The study group included 66 patients with Stage 5 CKD on maintenance hemodialysis. Such data were analyzed as complete blood count, iron and ferritin concentrations, and Transferrin Saturation (TSAT). Other parameters - age, sex, time from their fi...
Bulletin of Egyptian Society for Physiological Sciences
Nephrosis with minimal glomerular changes, minimal change nephrotic syndrome (MCNS) and focal-segmental glomerulosclerosis (FSGS) are by far the predominant causes of idiopathic nephrotic syndrome (INS). Recently there is an increasing interest in the role of iron in the causation of renal injury and deterioration of renal function in adults and children with nephrotic syndrome. Urinary excretion of Nacetyl--D-glucosaminidase (NAG) may be useful as a marker of tubular dysfunction and damage in idiopathic nephrotic syndrome (INS) which often characterizes steroid-resistant children. The present study was carried out to estimate the level of serum and urinary iron and transferrin to evaluate the effect of their excretion in the development of anemia in nephrotic children, also to clarify the prognostic value of urinary iron according to the histopathological type of the disease. The present work was also devoted to assess the role of immune system in the pathogenesis of idiopathic nephrotic syndrome by determination of serum 2-microglobulin and serum and urinary neopterin. The degree of tubular damage in the most common histopathological types of idiopathic nephrotic syndrome was assessed by estimation of urinary N-acetyl--D-glucosaminidase enzyme (NAG). The study was conducted on 45 children who were grouped as control group and nephrotic children group which was subdivided into two subgroups: minimal-change nephrotic syndrome (MCNS) group and segmental glomerulosclerosis (FSGS) group. The study included fifteen in each group with no significant difference in the mean age and sex between the three studied groups. All children in the study were subjected to thorough history taking, complete physical examination and laboratory investigations which included serum and urinary iron excretion per 24 hours, serum and urinary transferrin excretion per 24 hours, serum ferritin, total iron binding capacity, serum and urinary neopterin excretion per 24 hours, serum 2-microglobulin, urinary N-acetyl--Dglucosaminidase enzyme (NAG) excretion per 24 hours, stool analysis for occult blood to exclude gastrointestinal bleeding and finally renal biopsy was done for all nephrotic children enrolled in the study for histopathological examination. The results of our study showed that idiopathic nephrotic syndrome (INS) is associated with normocytic normochromic anemia despite the increased urinary losses of iron and transferrin. Also, the results of this study showed that both serum neopterin and 2-microglobulin were significantly higher in both nephrotic groups than the control subjects. Serum neopterin level was significantly higher in FSGS group than MCNS
Dialysis & Transplantation, 2006
Objective. The aim of this study was to assess the value of the soluble serum transferrin receptor (sTfR) and the transferrin receptor-ferritin index (sTfR/logF) as new markers of iron status in patients with anemia of chronic kidney disease (ACKD) both treated and not treated with recombinant human erythropoietin (rHuEPO) therapy. Materials and Methods. The study included 53 patients and 61 controls. The concentration of sTfR was determined by an immunoturbidimetric assay. Values for the sTfR/logF index were calculated as the ratio of sTfR to logarithm ferritin level. Results. The results showed iron-depleted patients had significantly higher median sTfR and sTfR/logF values (sTfR: 1.75 and 1.40 mg/L; sTfR/logF: 0.99 and 0.77) relative to those of iron-repleted patients (sTfR: 1.07 and 0.73 mg/L; sTfR/logF: 0.39 and 0.26) in ACKD patients-both those treated and those not treated with rHuEPO. Receiver operating characteristic analysis showed a higher diagnostic accuracy of the sTfR/logF index (area under curve [AUC] ¼ 0.970) versus sTfR concentration (AUC ¼ 0.890) in the assessment of the iron status of ACKD patients. The tested parameters showed no significant differences according to C-reactive protein concentration (p ¼ 0.108 and 0.147), in contrast to serum ferritin concentration (p ¼ 0.045).
Soluble Serum Transferrin Receptor (STFR) Levels in Hemodialysis Patients
Annals of King Edward Medical University, 2016
Objectives: Anemia is a frequent disorder in patients with end-stage renal disease. Erythropoietin is advised in these patients; however, this therapy is not effective in patients who are iron deficient. So, diagnosis of iron deficiency which is traditionally based on ferritin and other iron parameters becomes difficult in these patients, as chronic kidney disease is a chronic inflammatory condition which affects these markers and masks the iron deficiency. In present study, we assessed the reliability of another indicator of body iron supply; serum transferrin receptor, in hemodialysis patients. It is not affected in case of inflammation unlike other markers of iron status.
Background. Iron balance is critical for adequate erythropoiesis, but its optimal therapeutic regimen remains to be defined. Continuous maintenance therapy with iron has been proposed for dialysis patients on recombinant human erythropoietin (rHuEpo) in the hope that the regimen is adequate and safe. Methods. We determined serum ferritin, transferrin, transferrin saturation (TSAT), serum transferrin receptors, albumin and C-reactive protein (CRP) in a 3-year prospective study in 30 chronic haemodialysis patients on dialysis treatment for 132±111 months (18 males, 12 females; mean age 56±14 years). Beginning in the year 2000, they regularly received low-dose maintenance iron supplementation (i.v. iron gluconate 31.25 mg/week) for 12 months (Period 1 or first treatment phase), followed by a 6-month withdrawal (Period 2 or stop phase) and then by continuous maintenance iron therapy (i.v. iron gluconate 31.25 mg/week) for another 9 months (Period 3 or re-challenge phase). Results. A significant increase in serum ferritin and TSAT was observed, with values exceeding 500 ng/ml and 50% in 10/30 (33%) and 7/30 (23%) of subjects, respectively, in Period 1, and in 11 and 5% in Period 3. A significant decrease in serum transferrin was documented during Period 1, followed by an increase in Period 2 and a decrease in Period 3. Serum albumin remained stable. Serum transferrin was always negatively correlated with ferritin (r ¼ À0.41, P<0.001) and weakly correlated with serum transferrin receptors (r ¼ 0.178, P<0.05), but was not correlated with serum albumin or CRP. Regression equations based on pre-treatment serum ferritin values were developed for predicting the value of serum ferritin at any time following the beginning of continuous iron supplementation. They fitted a linear relationship for males (y ¼ 81 þ 21.5 Â time) and for females (y ¼ 65 þ 22 Â time). Percentile charts for quantitative tracking of serum ferritin increases and decreases in patients have also been developed from values measured at different times. These charts show box-plot distributions of expected ferritin against time.
Anemia in nephrotic syndrome: approach to evaluation and treatment
Pediatric nephrology (Berlin, Germany), 2016
Nephrotic syndrome is one of the most common glomerular diseases that affect in children. Complications may occur in nephrotic syndrome as a result of the disease itself as well as its treatment. Most of these complications result from excessive urinary protein losses, and control of proteinuria is the most effective treatment strategy. Anemia is one of the many complications seen in patients with persistent nephrotic syndrome and may occur as a result of excessive urinary losses of iron, transferrin, erythropoietin, transcobalamin and/or metals. This leads to a deficiency of substrates necessary for effective erythropoiesis, requiring supplementation in order to correct the anemia. Supplementation of iron and erythropoietin alone often does not lead to correction of the anemia, suggesting other possible mechanisms which need further investigation. A clear understanding of the pathophysiologic mechanisms of anemia in nephrotic syndrome is necessary to guide appropriate therapy, but ...
Annals of African Medical Research
The magnitude of chronic renal disease is enormous, as the prevalence of kidney failure is rising. Anaemia is a common complication of chronic kidney disease (CKD) that develops early in its course and becomes increasingly severe as the disease progresses. The aim is to evaluate the serum level of iron, Total Iron Binding Capacity (TIBC), transferrin saturation and ferritin in chronic kidney disease population in Zaria and control subjects. This study was conducted at ABUTH Zaria were 125 patients in various stages of CKD who presented at the nephrology clinic and equal number of apparently healthy age and sex matched controls were recruited. The mean (SD) age of patient and controls were 48 (14) years. These were made up of 53.6% males, and 46.4% females. Mean values of serum creatinine significantly higher in the patients (<0.0001). There was no significant difference in the mean values of iron (p=0.32) and TIBC (p=1.29) in both study groups. The patients had a significantly (p...