Treatment of anemia in non-DX (dialysis) CKD (chronic kidney disease) patients.
Treatment of anemia in non-DX (dialysis) CKD (chronic kidney disease) patients.
Anemia is commonly seen among non-DX (CKD) ptns and it is more prevalent with more decline in the GFR (glomerular filtration rate). All ptns should be screened for the presence of anemia when they’re evaluated for the 1st time for CKD and at a regular basis thereafter. The frequency of monitoring should be based upon the presence of anemia on initial evaluation, whether ptns are treated with erythropoiesis-stimulating agents (ESAs), and upon the magnitude of CKD severity. The management of anemia among non-DX ptns with CKD should rely upon individual basis. CKD ptns, can be mostly initiated with ESAs if the haemoglobin (HB) level is less than 10 g/dL, providing that the transferrin saturation (TSAT) is >25 % & serum ferritin >200 ng/mL. An important exception is among ptns with proven active malignancy or recent history of malignancy, particularly ptns in whom cure can be expected, or who have had a stroke since such ptns may be at a increased risk for adverse effects from ESAs.
Ptns who’re selected for ESA therapy, the subcutaneous root rather than IV. ESA administration. The initial dosage of EPO (epoetin) dose is about 50-100 units/kg/wk and that of darbepoetin is 60-200 mcg every 2-4 weeks. Additional titration is usually depending upon HB response. For most ptns with CKD who’re not on DX and are on ESAs, maintaining HB levels between 10.0 & 11.5 g/dL. Some nephrologists would permit an HB level of more than 11.5 g/dL for younger ptns with CKD with few co-morbidities and showing persistently severe Sms of anemia. There are not enough data on the benefits of HB levels between 11.5 & 13.0 g/dL. Among non-DX CKD ptns who are ttt with ESAs, we should not target HB concentration more than13 g/dL. HB targets more than13 g/dL can be complicated with adverse outcome.
Adverse effects of ESAs: A variety of adverse effects have only been reported when ESAs are used to achieve a normal HB including:
1) CVS events, &
2) Higher mortalities,
3) Increased malignancy.
4) Increased risk of vascular access thrombosis.
5) HT that’s independent of HB target. A rapid elevation of BP may cause hypertensive encephalopathy with seizures.
There’s little evidence of higher incidence of seizures in normotensive ptns ttt with ESA. It’s not possible to anticipate which ptn will develop seizures. Prodromal Sms may include persistent headache or visual disturbances in the early weeks of commencing ESA & suggesting that seizures may occur. Presence of other ESA-related reactions or SE (e.g. exacerbated HT or rapid rise in HB) may anticipate seizures occurrence.
REFERENCES
1. http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO-Anemia%20GL.pdf (Accessed on May 12, 2016).
2. Chapter 1: Diagnosis and evaluation of anemia in CKD. Kidney Int Suppl (2011) 2012; 2:288.
3. https://www.nice.org.uk/guidance/ng8/resources/chronic-kidney-disease-managing-anaemia- 51046844101 (Accessed on May 26, 2016).
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