Secondary polycythemia, also known as secondary erythrocytosis or secondary erythrocythemia, is a rare condition in which your body produces an excess amount of red blood cells.
This overproduction of red blood cells thickens your blood. This thickened blood can’t pass through your small blood vessels like capillaries easily. This increases your risk of having a stroke
https://www.webmd.com/a-to-z-guides/what-is-secondary-polycythemia
This is my newest diagnosis, that is added to the Chronic Kidney Disease and Hereditary Hemochromatosis with the two H63D genes, on top of primary Progressive Multiple Sclerosis
The Kidney Role is to control the EPO or erythropoiesis
Red blood cells are made by the bone marrow. To get the marrow to make red blood cells, the kidneys make a hormone called erythropoietin, or EPO. When the kidneys are damaged, they may not make enough EPO. Without enough EPO, the bone marrow does not make enough red blood cells, and you have anemia.
Red blood cell productionEdit
Erythropoietin is an essential hormone for red blood cell production. Without it, definitive erythropoiesis does not take place. Under hypoxic conditions, the kidney will produce and secrete erythropoietin to increase the production of red blood cells by targeting CFU-E, proerythroblast and basophilic erythroblast subsets in the differentiation. Erythropoietin has its primary effect on red blood cell progenitors and precursors (which are found in the bone marrow in humans) by promoting their survival through protecting these cells from apoptosis, or cell death.
Erythropoietin is the primary erythropoietic factor that cooperates with various other growth factors (e.g., IL-3, IL-6, glucocorticoids, and SCF) involved in the development of erythroid lineage from multipotent progenitors. The burst-forming unit-erythroid (BFU-E) cells start erythropoietin receptor expression and are sensitive to erythropoietin. Subsequent stage, the colony-forming unit-erythroid (CFU-E), expresses maximal erythropoietin receptor density and is completely dependent on erythropoietin for further differentiation. Precursors of red cells, the proerythroblasts and basophilic erythroblasts also express erythropoietin receptor and are therefore affected by it.
The Kidney specialized Dr told me this EPO pathway was working good, and with me off all Nsaids, diclofenac, that being off, was helping the Chronic Kidney Disease, and I would see him in person in three months.
Gene location
I have the H63D Gene with H63D Gene, both mutated, causing iron overload. 17 phlebotomy were done last quarter of 2018. Then Nothing. I should of bounced back, and needed phlebotomy every three months. But no iron, or ferritin made.
H63D gene from
Instead, the bone marrow, that makes the red blood cells, shown from other blogs, makes lots of hemoglobin and Hematocrit, causing the blood to be thick again. Solution is a phlebotomy, but not in reality, as no iron or ferritin, and would make me Anemic.
Speaking of which, I had been low in iron, or iron deficient, along with ferritin level of 7, I had been complaining about my shortness of breath for two years, since the phlebotomy. This seemed to be getting worse.
I remember telling my partner, 20 minutes of moving twigs, was all I could do. We had started a fire outside during burning season, when we realized our helpers were not coming back. Tree limbs from the falling of many trees had to slowly be added to the pile. It took a lot of work just doing simple tasks. I finally collapsed on the ground and watched the fire being what I thought was out of breath.
My heart would race, my blood pressure increase, and a air pathway seemingly odd at catching breath. This was told to many doctors over the two years
I think I will leave this blog here, as a whole blog has to be about the Diagnosis they have now found. A few more specialized Drs, more Test done, but nerd time to absorb all this new info
Thanks for reading, leave me comments below
JoeY
