4:12 actually the graph shows less than 30% are anemic ( 500 had the highest mortality at 1.38. I just looked up the paper. Only 'iron deficiency' at < 100 ferritin had NO increase in mortality. So mortality clearly increased with the level of iron, in the presenter's paper of choice. In her defense, the paper makes the same claims even though the data is right there. I'm not sure why anyone would pick hospitalization data (for which the p value was not even significant) when you have significant mortality data. 11:08 trial results irrelevant for non-dialysis patients 15:36 find-ckd results: "The increase in hepcidin from baseline was significantly smaller with low ferritin FCM or oral iron vs high ferritin FCM at all time points up to week 52." In other words, giving a lot of iron is counterproductive since it increases hepcidin and locks down all that extra iron (aka iron overload). Hepcidin levels more than doubled even in the 'low' iron arm. That being said, 16:05 shows that Hb does respond to adding more iron alone. The question is was it worth it (not according to mortality data, and guidelines not to try to raise Hb all the way to normal), when instead Hb could have been raised with ESA alone. The trial nad no mortality data. I think the trick with excess iron raising Hb is, the targeted, way too high, ferritin levels lead to spilling of Fe iron from the ferritin into the blood, which bypasses iron release by macrophages with ferroportin, ie bypasses hepcidin regulation. That's basically freeing iron by making the liver spill over. Which over time will also end up locked into other body cells by hepcidin. 17:45 the confirm-hf trial did allow anemic patients (no limit on low Hb). So obviously they would wind up with more blood and thus more oxygen to walk a few meters more. There was no benefit to mortality. 19:28 it is not clear if high fgf23 in late ckd worsens or improves the condition 36:04 storage level of vitamin D also strongly raises HIF in hypoxia ie in anemia. So raising D storage levels should work just as well as preventing breakdown of HIF with the drug Roxadustat (note it's the circulating storage form, not the active form of vit D, that potentiates HIF): Regulation of Hypoxia Inducible Factors HIF-1 and HIF-2 by Calcidiol in Hepatocellular Carcinoma Cells Under Normoxia and Hypoxia, 2022 40:20 first time I hear a nephrologist describe lower saturation and ferritin as an improvement. According to the 'guidelines', this improvement just made the patients iron deficient.
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4:12 actually the graph shows less than 30% are anemic ( 500 had the highest mortality at 1.38. I just looked up the paper. Only 'iron deficiency' at < 100 ferritin had NO increase in mortality. So mortality clearly increased with the level of iron, in the presenter's paper of choice. In her defense, the paper makes the same claims even though the data is right there.
I'm not sure why anyone would pick hospitalization data (for which the p value was not even significant) when you have significant mortality data.
11:08 trial results irrelevant for non-dialysis patients
15:36 find-ckd results: "The increase in hepcidin from baseline was significantly smaller with low ferritin FCM or oral iron vs high ferritin FCM at all time points up to week 52."
In other words, giving a lot of iron is counterproductive since it increases hepcidin and locks down all that extra iron (aka iron overload). Hepcidin levels more than doubled even in the 'low' iron arm.
That being said, 16:05 shows that Hb does respond to adding more iron alone. The question is was it worth it (not according to mortality data, and guidelines not to try to raise Hb all the way to normal), when instead Hb could have been raised with ESA alone. The trial nad no mortality data.
I think the trick with excess iron raising Hb is, the targeted, way too high, ferritin levels lead to spilling of Fe iron from the ferritin into the blood, which bypasses iron release by macrophages with ferroportin, ie bypasses hepcidin regulation.
That's basically freeing iron by making the liver spill over. Which over time will also end up locked into other body cells by hepcidin.
17:45 the confirm-hf trial did allow anemic patients (no limit on low Hb). So obviously they would wind up with more blood and thus more oxygen to walk a few meters more. There was no benefit to mortality.
19:28 it is not clear if high fgf23 in late ckd worsens or improves the condition
36:04 storage level of vitamin D also strongly raises HIF in hypoxia ie in anemia. So raising D storage levels should work just as well as preventing breakdown of HIF with the drug Roxadustat (note it's the circulating storage form, not the active form of vit D, that potentiates HIF):
Regulation of Hypoxia Inducible Factors HIF-1 and HIF-2 by Calcidiol in Hepatocellular Carcinoma Cells Under Normoxia and Hypoxia, 2022
40:20 first time I hear a nephrologist describe lower saturation and ferritin as an improvement. According to the 'guidelines', this improvement just made the patients iron deficient.