Most of the patients with chronic renal failure suffer from a decline in the level of the hormone Erythropoietin. Are there cases where the hormone levels rise in patients with renal failure? and whether research supports this opinion?? and why this increase there?
I hope the physiological explanation for this phenomenon
About 80% of the total erythropoietin comes from the kidney and in chronic renal failure, it is therefore inevitable that the level of the hormone must fall. If the level rises, then there may be a comorbid condition like a functional renal Ca. However, i am not sure of documented cases of CKD with a rise in erythropoietin level.
Anemia is a universal complication among patients with ESRD, due mainly to impaired erythropoietin synthesis. However in some cases of ADPK disease , renal cell carcinoma and chronic hepatitis C tends to have higher baseline hemoglobin than other causes. Some degree of endogenous EPO production also comes from the liver
The exact site of EPO production in the liver is not clear. Simple testing for EPO levels would be inaccurate in most patients unless they were not receiving any
exogenous EPO replacement.
there is no simple answer. As CKD progresses, epo levels increase almost as expected (about 2-3 fold) until a eGFR of ~35 to 40 is reached. At this point, Hb on average is ~ 12-13 g/dL and the anemia is mild. With further progression, epo levels fall but even in ESRD average levels are about 50% higher than in normal individuals without anemia and no kidney disease. These levels however are only 1/10 of those which would have been expected in anemic patients with Hb levels of 8 without kidney disease.
so what causes the mild "increase: in epo. probably output from the liver. However epo produced by the liver has a different glycosylation pattern and may be less active at the EpoR .
The issue whether cystic disease of the kidney increases epo levels is controversial. some studies have shown no increase . Similarly in acquired cystic disease of the kidney, epo levels do not differ from those of patients without cysts
I agree with Dr. Besarab it is a complex pathophysiological pattern. In simple terms EPO should increase with hypoxia however this feedback mechanism is lost in later stages of CKD and we see a drop in EPO.
Tipically EPO secretion increases in patients affcted by polycistic disease, principally ADPKD. Another condition is tyhe ischemic kidney (e.g. renal artery stenosis bilateral causing ESRD). In this condition probably EPO is stimulated by the ischemic condition
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