Iron Metabolism in Patients with Chronic Renal Failure

1970 ◽  
Vol 39 (1) ◽  
pp. 115-121 ◽  
Author(s):  
K. Boddy ◽  
D. H. Lawson ◽  
A. L. Linton ◽  
G. Will

1. Iron metabolism has been investigated in patients suffering from chronic renal failure, using a whole body monitoring technique. 2. Absorption of labelled inorganic iron was decreased. 3. Radio-iron was lost from the body at a rate comparable to that found in normal subjects. 4. The red cell incorporation of radioactive iron was diminished. 5. The results suggest that anaemia in these patients was due to decreased erythropoiesis and not due to iron deficiency despite the evidence of markedly abnormal iron handling presented.

1973 ◽  
Vol 44 (1) ◽  
pp. 27-32 ◽  
Author(s):  
K. Boddy ◽  
G. Will ◽  
D. H. Lawson ◽  
Priscilla C. King ◽  
A. L. Linton

1. The oral absorption and the rate of loss from the body of radioactive iron were measured by whole-body monitoring in patients with functioning renal homografts. The incorporation of radioactive iron into erythrocytes was also measured. 2. The results were compared with corresponding values in normal subjects and in non-dialysed and dialysed patients with chronic renal failure. 3. The mean oral absorption and incorporation into erythrocytes of radioactive iron was intermediate between that of normal subjects and of both non-dialysed and dialysed patients with chronic renal failure. 4. The mean rate of loss from the body was not significantly different from that in normal subjects and non-dialysed patients with chronic renal failure but it was significantly less than that in dialysed patients.


1971 ◽  
Vol 41 (4) ◽  
pp. 345-351 ◽  
Author(s):  
D. H. Lawson ◽  
K. Boddy ◽  
P. C. King ◽  
A. L. Linton ◽  
G. Will

1. By using a whole-body monitoring technique iron metabolism has been investigated in patients suffering from chronic renal failure who required regular dialysis treatment. 2. Oral absorption of inorganic iron was low. 3. The incorporation of radioactive iron into erythrocytes was diminished. 4. The rate of loss of radioactive iron from the body was significantly greater than in normal control and non-dialysed patients with chronic renal failure. 5. Iron exchange between dialysate and patient was studied. Patients with chronic renal failure are known to have a decreased rate of erythropoiesis and to develop abnormalities in iron metabolism (Kaye, 1958; Logue, Lange & Moore, 1958; Boddy, Lawson, Linton & Will, 1970). However, considerable controversy exists about the effect of haemodialysis on iron metabolism in such patients (Shaldon, 1966; Eschbach, Funk, Adamson, Kuhn, Scribner & Finch, 1967; Eschbach, Cook & Finch, 1970). The use of a whole-body monitor permitted measurement in a single study of the oral absorption of a tracer dose of 59Fe, its incorporation into erythrocytes and the subsequent long-term rate of loss of 59Fe from the body. We have previously reported the results of an investigation of iron metabolism by using this method in patients with chronic renal failure (Boddy et al., 1970). We now report the results of a similar investigation of iron metabolism in patients with chronic renal failure undergoing regular haemodialysis therapy.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2681-2681
Author(s):  
Jianbiao Wang ◽  
Qishi Fan ◽  
Hourong Shi ◽  
Ping Zhu ◽  
Bin Qu

Abstract There are two primary concerns in the management of patients with chronic renal failure (CRF) under hemodialysis who are receiving rHEpo for anemia - determine the ideal dose of iron and predict the response to the rHEpo therapy used to treat their anemia. The classic parameters used for monitoring iron therapy in these patients are Transferrin Saturation (TSAT %) and Ferritin (Ferr) concentration. Recently some new red cell parameters have been proposed to support these existing markers as the new research use only (RUO) tests, called Low Hemoglobin Density % (@LHD%®) and Microcytic Anemia Factor (@Maf®), produced by the LH 700 Series hematology analyzers We also have analysed the best hematological parameters to support TSAT % and Ferritin and the best predictors to predict the response to therapy. A total of 30 adult renal dialysis patients receiving EPO for treatment of anemia secondary to end-stage renal disease were enrolled over a six month period from March to August, 2006. The patients were stable with regard to dialysis treatment for at least 3 months prior to entry into the study. Patients had frequent follow up during therapy, consisting of CBC, auto-differential, automated retic %, absolute #, IRF, MRV and RUO parameters. The testing schedule followed the hospital’s existing standard of care with CBC, WBC Differential and Reticulocyte measurements being performed monthly. Iron levels and iron binding capacity were measured before the beginning the study, and then monthly for the duration of the study. These and other chemistry tests were performed on the Beckman Coulter DxC and DxI chemistry and immunoassay instruments and included serum Ferritin, serum iron, TIBC, Transferrin, transferrin saturation, and CRP. A 1 ml aliquot of serum from each sample was frozen for possible additional testing later (soluble transferring receptor (sTfR), etc.). The patients’ anemias were classified using their ferritin and transferrin saturation according to the KDOQI guidelines as Absolute Iron Deficiency (AID), Functional Iron Deficiency (FID) and any iron deficiency: AID or FID (any ID). CRP results were considered in the diagnosis. A response to the rHEpo therapy was defined as an increase in Hemoglobin concentration of 1 g/dL in 2 months, with a minimum increase of 0.3 g/dL per month. The patients’ results were classified as responder or non-responder based on the delta Hgb and delta reticulocyte results from month to month There were 29.3% (41/140) classified as responders. Using a Mann-Whitney test, significant differences (p<0.05) were found for @LHD%, @MAF, MCH comparing patients with TSAT% <20% vs TSAT%>20% and @LHD% for patients with Ferritin <100 ng/mL vs Ferritin> 100 ng/mL) The best RBC parameters for detecting the types of anemias found in these patients were: Detection of IDA was @LHD%® (>4.7%) Detection of FID: MCH (<29.1 g/dL) and @LHD%® (>6.1%) Detection of any ID (AID or FID): @LHD%® (>4.7%) and MCH (<30 g/dL) The best parameter for the prediction of the response to therapy as indicated by an increase in Hgb is @Maf® (<9.2) with a ROC Area under the curve of 0.714. Red Cell parameters can complement the classic parameters used to detect Iron deficiency and predict the response to therapy. The value of these findings to the clinician is that when the classic chemistry parameters are borderline or indeterminate, these new red cell parameters can be use to arrive at a definitive diagnosis and ensure the correct treatment option. @ Research use only parameters


1988 ◽  
Vol 60 (02) ◽  
pp. 205-208 ◽  
Author(s):  
Paul A Kyrle ◽  
Felix Stockenhuber ◽  
Brigitte Brenner ◽  
Heinz Gössinger ◽  
Christian Korninger ◽  
...  

SummaryThe formation of prostacyclin (PGI2) and thromboxane A2 and the release of beta-thromboglobulin (beta-TG) at the site of platelet-vessel wall interaction, i.e. in blood emerging from a standardized injury of the micro vasculature made to determine bleeding time, was studied in patients with end-stage chronic renal failure undergoing regular haemodialysis and in normal subjects. In the uraemic patients, levels of 6-keto-prostaglandin F1α (6-keto-PGF1α) were 1.3-fold to 6.3-fold higher than the corresponding values in the control subjects indicating an increased PGI2 formation in chronic uraemia. Formation of thromboxane B2 (TxB2) at the site of plug formation in vivo and during whole blood clotting in vitro was similar in the uraemic subjects and in the normals excluding a major defect in platelet prostaglandin metabolism in chronic renal failure. Significantly smaller amounts of beta-TG were found in blood obtained from the site of vascular injury as well as after in vitro blood clotting in patients with chronic renal failure indicating an impairment of the a-granule release in chronic uraemia. We therefore conclude that the haemorrhagic diathesis commonly seen in patients with chronic renal failure is - at least partially - due to an acquired defect of the platelet a-granule release and an increased generation of PGI2 in the micro vasculature.


2016 ◽  
Vol 10 (4) ◽  
Author(s):  
Intesaruk Rashid Khan ◽  
Ahmed Imran Siddiqui ◽  
Wafa Aftab

This retrospective study was conducted to find out the expected ages in the patients of hepatic cirrhosis, chronic renal failure and heart failure. This study thus covers most of the patients of out medical wards presenting with chronic illnesses. On comparison of these expected ages it is also found that the expected age in all these three groups is not much different. So, the disease process or the mechanism of the chronic disease in the body may be different, but somehow the final out come is not much different in terms of life span.


1986 ◽  
Vol 251 (2) ◽  
pp. R398-R408 ◽  
Author(s):  
M. E. Wastney ◽  
R. L. Aamodt ◽  
W. F. Rumble ◽  
R. I. Henkin

Zinc metabolism was studied in 32 normal volunteers after oral (n = 25) or intravenous (n = 7) administration of 65Zn. Data were collected from the blood, urine, feces, whole body, and over the liver and thigh regions for 9 mo while the subjects consumed their regular diets (containing 10 mg Zn ion/day) and for an additional 9 mo while the subjects received an exogenous oral supplement of 100 mg Zn ion/day. Data from each subject were fitted by a compartmental model for zinc metabolism that was developed previously for patients with taste and smell dysfunction. These data from normal subjects were used to determine the absorption, distribution, and excretion of zinc and the mass of zinc in erythrocytes, liver, thigh, and whole body. By use of additional data obtained from the present study, the model was refined further such that a large compartment, which was previously determined to contain 90% of the body zinc, was subdivided into two compartments to represent zinc in muscle and bone. When oral zinc intake was increased 11-fold three new sites of regulation of zinc metabolism were identified in addition to the two sites previously defined in patients with taste and smell dysfunction (absorption of zinc from gut and excretion of zinc in urine). The three new sites are exchange of zinc with erythrocytes, release of zinc by muscle, and secretion of zinc into gut. Regulation at these five sites appears to maintain some tissue concentrations of zinc when dietary zinc increases.


1985 ◽  
Vol 31 (12) ◽  
pp. 1988-1992 ◽  
Author(s):  
M Shaykh ◽  
N Bazilinski ◽  
D S McCaul ◽  
S Ahmed ◽  
A Dubin ◽  
...  

Abstract We measured the fluorescence, at various excitation (Ex) and emission (Em) wavelengths, of serum ultrafiltrates and fractions of serum resolved by chromatography on Sephadex G15, studying both normal subjects and patients in chronic renal failure requiring hemodialysis. We found hitherto undescribed fluorescence at Ex 380 nm/Em 440 nm and Ex 400 nm/Em 460 nm, the intensity being greatly increased in patients with chronic renal failure in comparison with normal subjects (p less than 0.005). This fluorescence persisted unaltered when serum was filtered through membranes having cutoffs ranging from 10 000 to 500 Da. Each serum fraction resolved by gel chromatography demonstrated a characteristic fluorescence, which was generally much more intense in uremics. The most intense fluorescence (Ex 380 nm/Em 440 nm and Ex 400 nm/Em 460 nm) was emitted in the higher-Mr fractions.


1978 ◽  
Vol 24 (3) ◽  
pp. 451-454 ◽  
Author(s):  
F P Di Bella ◽  
J M Kehrwald ◽  
K Laakso ◽  
L Zitzner

Abstract Antisera directed toward the carboxyl-terminal region of human parathyrin (parathyroid hormone), for use in daignostically applicable radioimmunoassays of the hormone in serum, are scarce, largely because of the lack of suitable immunogens of human origin. We produced four antisera in goats and guinea pigs by immunization with recently discovered carboxyl-terminal fragments of human parathyrin extracted from parathyroid tumors. Here, we report results of radioimmunoassays of nearly 200 normal and pathological sera with one of these antisera; we observed almost complete differentiation between concentrations of parathyrin in serum of healthy normal subjects and patients with primary, secondary (due to chronic renal failure), or "ectopic" hyperparathyroidism (due to nonparathyroid cancer). The availability of a new immunogen should now make possible the deliberate production of large quantities of diagnostically applicable parathyrin antisera directed toward the carboxyl-terminal region of human parathyrin. This should, in turn, lead to more widespread availability of this useful radioimmunoassay.


1981 ◽  
Author(s):  
Y Endo ◽  
M Mamiya ◽  
K Takahashi ◽  

We have reported that jS-thromboglobulin (β-TG) and platelet factor 4 (PF4) increased in chronic renal failure. The purpose of the current study is to reveal a correlation between plasma β-TG (Amersham Corp. England) and renal function, a correlation between plasma β-TG and PF. (Abbott Lab., USA) and the effect of hemodialysis on patients with chronic renal failure.Significantly increased levels of plasma β-TG (76.8±25.5 ng/ml, p<0.01) were observed in 24 patients with chronic renal failure (BUN>20mg/dl), compared to normal subjects (13.2±5.6ng/ml). The increase in β-TG was highly correlated with BUN (r=0.651, p<0.01), creatinine (r=0.778, p<0.01) and creatinine clearance (r=-0.723, p<0.01). Although plasma PF4 (normal 5.0±2.0ng/ml) increased also, no statistical significance could be found. Statistical correlation between β-TG and PF4 was not found in these patients. This reason is thought to Be due to the difference of molecular weight (PF. 8000MW, β-TG 36000MW) and half-life (PF4 30min,β-TG 100min) The high levels of β-TG (89.4±3.4ng/ml) showed a further increase (109.4±5.8ng/dl, p<0.01) after dialysis. This is thought to be due to hemoconcentration, because of no adhesion of platelet to cellulose membrane but about 20% elevation in mean of other blood factors such as RBC, WBC, platelet, fibrinogen etc. The PF4 levels (before, 7.7±1.3ng/ml) which increased at 15min (55.2±19.6ng/ml, p<0.01) and 1 hr (23.7±8.4ng/ml, p< 0.01) are thought to be due to the influence of heparin infusion. The change in PF4. was not accompanied by the change in β-TG. During hemodialysis the decrease of other platelet functions such as adhesiveness, aggregation induced by ADP, collagen and PF3remained unchanged.


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