scholarly journals Nutrition, anaemia and erythropoietin therapy

1999 ◽  
Vol 3 (2) ◽  
Author(s):  
Iain C. Macdougall

During the last decade, recombinant human erythropoietin has revolutionised the management of renal anaemia. It is highly effective in the vast majority of patients treated, causing enhanced erythropoiesis and a rise in haemoglobin concentration. This has resulted not only in amelioration of uraernic symptoms, but there has also been objective evidence of improved quality-of-life, exercise capacity, and cardiac function [I]. The most striking benefits seen have been progression of left ventricular hypertrophy which is known to account for much of the high cardiovascular morbidity and mortality seen in dialysis patients. and thus the arguments for correcting renal anaemia is now overwhelming. There is also an improvement in nutrition following erythropoietin therapy, over and above the improvement in appetite associated with correction of the anaemia.

2003 ◽  
Vol 3 (4) ◽  
pp. 11-15 ◽  
Author(s):  
Senija Rašić ◽  
Indira Kulenović ◽  
Irfan Zulić ◽  
Azra Haračić ◽  
Mithat Čengić ◽  
...  

Anaemia appears to play an important role in left ventricular (LV) enlargement in chronic kidney disease patients. The objective of this study was to evaluate LV echocardiography changes during anaemia correction with recombinant human erythropoietin(rHu-Epo) in chronic haemodialysis patients (HD pts) with signs of anaemia and LV hypertrophy (LVH). The study included 20 HD pts aged 39,6 +/- 5,3 yrs, with the same condition of HD treatment, anaemia and echocardiographically LVH verified. At the beginning of the rHu-Epo treatment haemoglobin (Hb) level was < 90 g/L and the target Hb level was 110 g/L. Echocardiography was performed at the beginning (baseline) and after six months of rHu-Epo treatment. LVH was defined as LV mass index >100 g/m2 in women and >131 g/m2 in men. We observed significant reduction of LV mass index (LVMI) (mean 26,4%, p=0.008), as well as LV volumen. There was a significant negative correlation between Hb level and LVMI with predictive LVMI reduction of 2,317 g/m2 for each 1g/L rising of mean Hb level. The results of the study confirm the importance of early anaemia correction in haemodialysis patients aimed to improve LV parameters.


2017 ◽  
Vol 68 (2) ◽  
pp. 354-357 ◽  
Author(s):  
Andrei Niculae ◽  
Cristiana David ◽  
Razvan Florin Ion Dragomirescu ◽  
Ileana Peride ◽  
Flavia Liliana Turcu ◽  
...  

Once recombinant human erythropoietin (r-HuEPO) was introduced in daily practice, huge steps were made in combating the adverse effects induced by anemia in chronic kidney disease population. Still, r-HuEPO resistance and the doses ensuring the maximum therapeutic benefit remain matters of debate. The aim of our study was to assess the correlation between the presence and the degree of inflammation and the r-HuEPO requirements in chronic dialysis patients. We conducted a 2 years prospective study on 146 patients undergoing chronic dialysis treated with r-HuEPO. Based on their average CRP (C-reactive protein) levels, obtained from repeated samplings at 3 months interval, 3 groups were formed; we noted in each group the average values of r-HuEPO prescribed to achieve the optimum hemoglobin levels according to the dialysis best practice guidelines and all the adverse effects of the therapy. A direct correlation was observed between CRP levels and r-HuEPO requirements in the first 2 groups of patients (CRP under 6 mg/L and CRP values 6-20 mg/L), with significant increase in r-HuEPO doses between groups (p [ 0.001); the third group, CRP values over 20 mg/dL, showed a minor, insignificant increase in average r-HuEPO doses compared to mild inflammation group (p = 0.199) and more adverse effects of the therapy (p [ 0.05). Inflammation is an important determinant of anemia in chronic dialysis patients and can induce an increase in the doses of r-HuEPO. However, prescribing excessive r-HuEPO doses is not the answer in severe inflammatory status, due to lack of response and possible adverse effects.


Nephron ◽  
1990 ◽  
Vol 55 (2) ◽  
pp. 114-120 ◽  
Author(s):  
Patrick S. Parfrey ◽  
John D. Harriett ◽  
Sheila M. Griffiths ◽  
Rhoda Taylor ◽  
John D. Harnett ◽  
...  

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Leah Cannon ◽  
Tadeusz Marciniec ◽  
Bryony Mearns ◽  
Robert M Graham ◽  
Diane Fatkin

Left ventricular hypertrophy (LVH) develops as a compensatory response to myocardial dysfunction due to diverse causes, but is nonetheless a major risk factor for premature cardiovascular morbidity and mortality. It is thus unclear if regressing LVH is beneficial or may worsen patient outcome. To evaluate the effects of LVH regression, we developed a transgenic mouse model in which the expression of a familial hypertrophic cardiomyopathy (FHC)-inducing mutation (R403Q alpha-MHC) can be regulated in a temporal and dose-dependent manner. In this model, transgene expression can be shut off by feeding with a tetracycline analogue (doxycycline). Serial echocardiography and histology studies were performed in a cohort of mice expressing the FHC mutant (“gene-on”) and in wildtype (WT) littermates. A second cohort of WT and 403/+ mice was randomised to placebo or doxycycline (“gene off”) from 6 (Dox6) or 20 weeks (Dox20) and evaluated at 40 weeks of age. Compared to WT littermates, “gene on” 403/+ mice showed increased LV mass, LV end-diastolic diameter (LVDD) and left atrial diameter (LAD), and reduced fractional shortening (LVFS), with changes evident from 12 weeks of age. LV sections from 403/+ mice showed typical features of FHC: myofibre disarray and interstitial fibrosis. LV mass, LV function and myocardial histology were unchanged in both male and female placebo- vs Dox6 or Dox20 mice at 40 weeks (Table 1 ). Thus, consistent with the major LV thickening in FHC humans occurring in adolescence, overexpression of R403Q for only 6 weeks is sufficient to trigger the complete LVH phenotypic response. Moreover, switching off the genetic trigger for LVH in 403/+ mice at 6 weeks (prior to overt disease manifestation) or 20 weeks (established disease) does not induce regression of LVH or exacerbate contractile dysfunction. Interventions to induce LVH regression may, therefore, need to be directed at downstream factors in hypertrophic pathways. Table 1. Echo data for male WT and 403/+ mice aged 40 weeks


2008 ◽  
Vol 61 (7-8) ◽  
pp. 369-374 ◽  
Author(s):  
Dejan Petrovic ◽  
Biljana Stojimirovic

Left ventricular hypertrophy is the main risk factor for development of cardiovascular morbidity and mortality in patients on hemodialysis. Left ventricular hypertrophy is found in 75% of the patients treated with hemodialysis. Risk factors for left ventricular hypertrophy in patients on hemodialysis include: blood flow through arterial-venous fistula, anemia, hypertension, increased extracellular fluid volume, oxidative stress, microinflammation, hyperhomocysteinemia, secondary hyperpara- thyroidism, and disturbed calcium and phosphate homeostasis. Left ventricular pressure overload leads to parallel placement of new sarcomeres and development of concentric hypertrophy of left ventricle. Left ventricular hypertrophy advances in two stages. In the stage of adaptation, left ventricular hypertrophy occurs as a response to increased tension stress of the left ventricular wall and its action is protective. When volume and pressure overload the left ventricle chronically and without control, adaptive hypertrophy becomes maladaptive hypertrophy of the left ventricle, where myocytes are lost, systolic function is deranged and heart insufficiency is developed. Left ventricular mass index-LVMi greater than 131 g/m2 in men and greater than 100 g/m2 in women, and relative wall thickness of the left ventricle above 0.45 indicate concentric hypertrophy of the left ventricle. Eccentric hypertrophy of the left ventricle is defined echocardiographically as LVMi above 131 g/m2 in men and greater than 100 g/m2 in women, with RWT ?0.45. Identification of patients with increased risk for development of left ventricular hypertrophy and application of appropriate therapy to attain target values of risk factors lead to regression of left ventricular hypertrophy, reduced cardiovascular morbidity and mortality rates and improved quality of life in patients treated with regular hemodialyses.


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