Hi Barb & all,
thanks for the responses, I had the ultrasound done last Fri. will get the results at next visit. I just looked it up again, there are several things about the elevated creatinine from creatine due to CFS/infections. I have only a mildly elevated level, so I do not think kidney disease is at all involved.
It is more likely the CFS/methyl. block/infections/medications. I have taken hydrocodone/acet. for the last 7 yrs due to bone pain/CFS along with other meds. Here are a couple mentions of infections/CFS effecting creatine/creatinine levels. To me this is what it is going on. But with this DD who knows.
Rhabdomyolysis is the medical term to describe the destruction or breakdown of the skeletal muscle; it can cause a high creatinine level in the urine. It can happen from long-distance running, muscle trauma, electrical shock and as a result of some infections - See more at:
http://www.livestrong.com/article/4...reatine-levels-in-urine/#sthash.sePgZVag.dpuf
http://forums.prohealth.com/forums/index.php?threads/creatine-is-amazing.196554/
Some creatine comes in from the diet, and some is also produced in the kidneys, liver, and pancreas. It is synthesized from glycine and arginine, which form guanidinoacetate, followed by methylation by SAMe. The synthesis of creatine is one of the two main demands for methylation in the body, the other being the conversion of ethanolamine to choline. If there is a partial methylation cycle block, one would expect that the synthesis of creatine would be below normal.
Creatine is carried via the blood to the organs where it is needed, primarily the skeletal muscles, the heart muscle, and the brain. In these organs, it serves as a storage molecule for high energy phosphate groups, forming creatine phosphate. When there is a big, sudden demand for ATP, to operate the muscles in vigorous exercise, for example, the rate of production of ATP by the mitochondria is not high enough to meet the demand. In that case, the creatine phosphate supplies phosphate groups to ADP to regenerate ATP, forming creatine again. ATP produced by the mitochondria eventually recharges the creatine to creatine phosphate, forming ADP. So the creatine acts as an energy buffer for the organs in which it is abundant.
Creatine phosphate spontaneously (without the help of an enzyme) degrades to form creatinine and a phosphate group. This occurs at the rate of about 1 to 2% of the total creatine phosphate per day. The creatinine is carried by the blood to the kidneys and is excreted into the urine. The ratio of creatinine in the blood to that in the urine is used as a measure of kidney function. The amount of creatinine produced per unit time is approximately proportional to the amount of skeletal muscle in the body, i.e. the lean body mass. In urine analysis, it is common to divide the concentrations of various species by the concentration of creatinine in order to normalize them and correct for varying amounts of dilution by water in the urine. The assumption behind this practice is that the rate of production of creatinine is not affected by health problems. This does not appear to be true in CFS and autism, because of the partial methylation cycle block.
It is also common practice when doing magnetic resonance spectroscopy studies on the brain to take ratios of the peak heights for the other substances observed to the peak height for creatine, again based on the assumption that the creatine level should be more or less constant. This is done because it is much easier to take ratios than to measure accurate values for absolute amounts of these substances using MRS. Again, this constancy is probably not true in CFS, because of the partial methylation cycle block. We do not have absolute measurements of brain creatine in CFS, but MRS studies in CFS have found abnormal values of the ratio of choline to creatine. Since the syntheses of both choline and creatine require methylation, I think a partial methylation cycle block is the explanation for these observations.
I suspect that supplementing creatine would give some benefit in many people with CFS in terms of storing energy for relatively short-term high demands. However, I think that in a short time, the creatine phosphate will be converted to creatine, and then the problem will be that the mitochondria are not able to regenerate ADP to ATP fast enough, and the person will "run out of energy" to operate their muscles.
As you know, there are many things that block the proper operation of the mitochondria in CFS, including depleted magnesium, toxins, and infections. In my view, these problems begin with glutathione depletion. Glutathione depletion also allows the rise of oxidizing free radicals in the mitochondria, and these block the Krebs cycle and probably also the respiratory chain. In addition, in CFS there are shortages of Coenzyme Q-10, carnitine, and creatine (the latter is not actually in the mitochondria). These require methylation for their synthesis, so I think their shortages can be traced back to the partial methylation cycle block. So, ultimately, the partial methylation cycle block and glutathione depletion can be shown to be responsible for the mitochondrial dysfunction and the shortage of ATP in CFS.
One more thing, just for completeness, though it isn't directly related to the issue we are discussing: The enzyme that catalyzes the reaction between creatine and phosphate is called creatine phosphokinase or just creatine kinase. This enzyme is normally found inside the types of cells where creatine is abundant. As these cells break down, this enzyme is released to the blood stream. There are different types of creatine kinase found in the skeletal muscles, the heart muscle and the brain. These types of creatine kinase are used as a diagnostic to determine whether these various types of cells are dying at a higher than normal rate in these different organs.