Plasma erythropoietin in polycythemia

Garle

Journal of Pharmaceutical and Biomedical Analysis

et al. 2013

The primary production site of erythropoietin (EPO) is shifted from the liver to the kidney shortly after birth. Under conditions of lost or reduced kidney production, it is valuable to measure the production capacity of the liver. However, there is a lack of urine or serum based methods that can distinguish endogenous EPO produced in different cell types. Here is presented a method based on chromatographic interaction with the lectin wheat germ agglutinin (WGA) that can distinguish presumably liver-produced EPO, found in anaemic patients receiving epoetin and darbepoetin, from kidney-produced EPO found in healthy individuals.All the tested samples from haemodialysis patients with end-stage renal disease showed a presence of liver EPO. In some samples, the liver-produced EPO made up 90-100% of total EPO at a concentration of 8-10 ng/L in urine, which indicates that the liver has a quite high production capacity, although not adequate for the degree of anaemia.This glycoform analysis has made it possible to affirm that some anaemic patients can increase their liver-production of EPO. The use of such a method can give better insight into the regulation of non-renal endogenous EPO production, a potential source of EPO intended to replace administration of exogenous EPO.

Section: Introductionmentioning

confidence: 99%

Patients with anaemia can shift from kidney to liver production of erythropoietin as shown by glycoform analysis

Garle

Journal of Pharmaceutical and Biomedical Analysis

et al. 2013

The Journal of Veterinary Medical Science

“…Therefore, the anemia is probably caused by the reduced production of hematogenic factors (e.g. erythropoietin) or a low responsiveness of the hematopoietic stem cells to these factors [3]. With regard to genetic animal models, the renal anemia in polycystic kidney disease has been reported to occur in DBA/2FG-pcy mice.…”

Section: Discussionmentioning

confidence: 99%

“…The hemopoietic response to recombinant human erythropoietin has been examined in this mutant mouse [15]. Some studies have been carried out on erythropoietin, concerning its plasma concentration, production in the kidney, liver, and bone marrow, and the hemopoietic response in renal anemia [3,6,12,15,29]. The examination of a hemopoietic factor such as erythropoietin in hpk/hpk rats would produce useful information because of the congenital reduction in renal tissue, which is the major source of erythropoietin, that exists in these rats.…”

Section: Discussionmentioning

confidence: 99%

“…We consider the hpk/hpk rats to be a good analytical tool with which to study the pathogenesis of renal hypoplasia and the mechanism of the progression from renal hypoplasia to renal failure. In general, the considerable loss of nephrons causes progressive chronic renal failure [1,5,14,22] and, secondarily, induces renal anemia [3,6,12,15,29], hyperparathyroidism, and osteodystrophy at the end stage of renal failure [2,6,7,8,10,11,13,16,17,20,21,23]. Although various animal models have been utilized in the study of these conditions [6,12,16,17,20,21,29], genetic animal models that could develop reproducibly chronic renal failure and induce renal secondary disease have been reported only rarely [11,15].…”

Section: Animalsmentioning

confidence: 99%

See 1 more Smart Citation

Rat Hypoplastic Kidney (hpk/hpk) Induces Renal Anemia, Hyperparathyroidism, and Osteodystrophy at the End Stage of Renal Failure.

Suzuki

1998

ABSTRACT. In rats with genetically hypoplastic kidneys (hpk/hpk) and associated hypogonadism (hgn/hgn), their kidneys contain only onequarter the number of nephrons that are found in those of normal rats [26]. Not surprisingly, therefore, renal excretive function has been shown to be depressed in hpk/hpk rats [26]. In the study presented here, we have examined the process of the progression of renal failure and the development of renal secondary disease in hpk/hpk rats. The plasma concentrations of urea-nitrogen and creatinine were significantly higher in adult hpk/hpk rats than in normal rats. These values elevated gradually and the degree of renal histological damage also progressed with advancing age in the hpk/hpk rats. In addition, renal anemia appeared at 140 days of age or later in these rats, and hyperplasia of the parathyroid glands was visible macroscopically at 280 days of age. In the hpk/hpk rats plasma levels of calcium and phosphorus were significantly lower and higher than in normal rats, respectively, at 280 days of age. Pathologically, the left femora of hpk/hpk rats exhibited fibrous osteodystrophy at 280 days of age and the calcium content of the right femora (as a percentage of the dry weight of bone) was significantly lower than in normal rats at both 210 and 280 days of age. These results indicate that the reduced nephrogenesis of the hpk/hpk rats causes progressive renal failure, secondarily inducing anemia, hyperparathyroidism, and osteodystrophy. -KEY WORDS: disease animal model, hyperparathyroidism, osteodystrophy, renal anemia, renal hypoplasia.J. Vet. Med. Sci. 60(10): 1051-1058, 1998 MATERIALS AND METHODS Animals:The animals used in this study were male hpk/ hpk rats and phenotypically normal litter mates (+/hpk or +/+) from the 24th generation of the HGN line maintained in our department [26]. The hpk/hpk males could be identified externally by their hypogonadism [26]. The rats were bred and fed under the same conditions as described in previous reports [24][25][26][27].Hematological examination: Four groups of 4 hpk/hpk and 4 normal animals were used, one group at each of days 70, 140, 210, and 280 after birth. Blood samples were collected from the jugular vein with a plastic syringe moisturized with a small amount of heparin. Red and white blood cells were counted on a hemacytometer with the aid of a light microscope. The counts of reticulocytes and platelets were performed according to the Rees-Ecker method. The hematocrit was determined using a hematocrit tube and the centrifuging method. The concentration of hemoglobin was determined by the methemoglobin method. Plasma samples were obtained by centrifugation and stored at 40°C until they were used to obtain urea-nitrogen, creatinine, calcium, and phosphorus measurements.Histological examination: After collecting blood samples from the rats they were sacrificed by ether overdose. Their kidneys and parathyroid glands with attached tracheas were removed and fixed in 4% neutral formalin, dehydrated in a graded alcohol series, embed...

“…Non-renal anaemias, such as aplastic anaemia, iron de¢ciency anaemia and haemolytic anaemia, result in an exponential increase in EPO concentration that is inversely related to the haemoglobin concentration. 43 EPO concentrations in patients with anaemia of chronic renal failure are usually inappropriately low for the degree of anaemia. The de¢cient production of EPO is likely to be due to an inability of the diseased kidney to produce EPO in these circumstances.…”

Section: Clinical Applicationsmentioning

confidence: 99%

Erythropoietin - measurement and clinical applications

Marsden

2006

Ann Clin Biochem

Erythropoietin (EPO) is an endogenous hormone produced primarily by the kidney which controls the production of erythrocytes. The main stimulus to production is low tissue oxygen (hypoxia) and EPO triggers the formation of red blood cells by binding to a receptor on erythroid progenitor target cells. Alteration in the EPO regulatory system produces a change in circulating EPO in a variety of disease states, such as renal anaemia and polycythaemia. The availability of recombinant EPO in the 1980s transformed the treatment of anaemia, particularly anaemia of end stage renal disease, and led to the development of more sensitive and specific assays for the measurement of EPO. There are more widespread uses for EPO and preliminary studies indicate that EPO may be useful as a neuroprotective agent by reducing inflammation near the site of injury. The use of EPO to boost endurance in athletes has attracted unwanted publicity, although analytical techniques are now available that can differentiate between endogenous and recombinant EPO. Different types of erythropoietic agents have been developed with a longer plasma half-life and the ability to maintain haemoglobin levels for longer periods and reduce the need for frequent dosing with EPO.