Abnormalities in the urine of people with ME/CFS? A clinician asks for feedback

Yes I sure it is. But I find that extremely irritating because these small signs can be clues.

me too, & these started around the same time as the pee smelling intermittently stronger - when I was 'mild', & have continued over the yrs. I'm not menopausal & was only 30 when the 2 things started. I don't notice sweat smells any worse, but I certainly get BO sooner & stronger since I had ME (developed at 31) though. I assumed that was age.

Yes, actually when you said this I thought that must be the explanation, because all my sensory sensitivities get much worse during PEM, but, they only get more sensitive - ie things smell the same just stronger more noticeable, so that wouldn't account for the difference in smell, in addition it doesn't account for the phenomena starting when I was mildly affected in the beginning, because I had no sensory processing issues then at all.

 

Can't say I've noticed any difference. I've always been very sensitive to smells, so am aware that I've always had arbitrary episodes of funky or otherwise unusual-smelling pee. Definitely nothing consistently associated with PEM, though I am on the milder end of ME, which could matter.

 

My urine had an ammonia smell when I had h pylori infection years ago, so did my breath.

 

I have much more orange urine during PEM and it isn't merely due to dehydration either. Most blood tests have elevated bilirubin suggesting Gilbert's Syndrome. (which is surprisingly common amongst people with CFS or ME)

So my first guess is elevated bilirubin. This suggests elevated breakdown of red blood cells. Alternatively, it could be due to elevated porphyrins.

The typical yellow colour of urine is due to Urobilin which is oxidised urobilinogen which is a byproduct of bilirubin breakdown.

 

Sampled some more, and my urine seems completely normal in every aspect although I don't go around comparing mine to that of others. After a week of low activity, I did a longer walk yesterday (before this idea came up) but that didn't have an effect on urine.

I don't want to make myself crash hard just to find out if anything changes.

 

Hmm, yes, I recognise several of these from the days when I was having to empty a commode for my caree. However, from the little that's been said I also recognise some of them as things I've probably suffered from myself, and I don't have ME. So to what extent they are actually ME-related I wouldn't like to say.

Interesting, though, that various people say they've had a highly developed sense of smell since childhood or so. Given that so many pwME seem to have hyper-sensitive senses in general, it makes me wonder whether there might be an indication of a predisposition there, or alternatively that something might be lying dormant somewhere.

 

Tight fitting heavy spandex clothing will do that.

 

I had an OAT. RBC Fatty acid and Amino Acid test done 2 days after exercise and they were all abnormal. One thing that was normal though was Lactate.

I don't experience pain. I wonder if that could be why my lactate was normal?

 

Unless you did a significant amount of exercise, or you have a genetic mitochondrial disease that severely limits oxidative phosphorylation, lactate should be normal. Lactate itself does not cause pain.

 

@Snow Leopard I did a significant amount of exercise. I ran for 50 minutes 2 days before the test. I was still in PEM, muscle fatigue was quite bad but no pain.

 

Off topic, but I had always thought the burning pain in my legs was due to a lactic acid buildup and one of the byproducts of anaerobic respiration was said to be lactic acid when I was teaching biology.

There have been so many discoveries since that time, I wonder if you could explain about lactate, but only if you are up to it, thanks.

 

To start, we know that lactate infusions don't cause pain in humans (note: when delivered under physiologically neutral pH conditions).

https://physoc.onlinelibrary.wiley....(ISSN)1469-445X(CAT)VirtualIssues(VI)bbep2016
(notably the receptors they single out are the Acid sensing ion channel, transient receptor potential cation channel subfamily V member 1 (a heat receptor) and ATP-gated P2X receptor cation channel family, which detects extracellular ATP which is indicative of cell damage. Note that none of these preferentially bind lactate.

Lactate build up is not the same as acidosis, Lactic acid is less acidic than Puruvic acid, and lactate has a big advantage that it can be shuttled out of the cell as a metabolic buffering mechanism and then later oxidised back into Pyruvate or even back into D-Glucose. Acidosis can be buffered by various mechanisms that are independent of lactate concentration, but it is important to note that acidosis results from glycolysis in producing pyruvate, not lactate. Lactate dehydrogenase catalyses the equilibrium process of converting pyruvate to lactate and back and although this equilibrium favours pyruvate, there will always be some lactate produced even at rest. During activity, an increased amount of pyruvate and consequently lactate will be produced, even if the level of activity is still well below the oxidative capacity (primarily Krebs cycle, oxidative phosphorylation, but also fatty acid oxidation) of the mitochondria. But obviously during sustained exertion at near to maximal levels, the oxidative metabolism will be too slow to deliver enough energy hence a glycolysis will be the predominant metabolic source, leading to both high acidosis and lactate formation.

 

This is all pretty and scientific explanation, but @Snow Leopard if you are an athlete and your legs hurt after 3 hours of racing (running, biking, cross country skiing, you can’t help but say that lactic acid= pain to the legs. In my past life i have tested this over and over.

 

Yes, but the legs can continue to hurt even when lactate levels normalise.

I too have said many things in day to day life that is wrong, including saying the pain during and post exercise is due to lactic acid, but I know better now.

 

As Snow Leopard implies, I don't think we would expect muscle lactate to be any higher after 3 hours of racing than after five minutes. It would depend only on the intensity of contraction in the previous minute or so that generated the lactate. My understanding of lactate build up in muscle is that it occurs in the sort of situation you get in the last 50 metres of an 800 metre race when you push as hard as possible. My experience of that is that if unfit the legs hurt a bit but more obviously just seize up. And that may be more a reflection of there being no ATP available than of lactate build up.

 

Thank you for your explanations. Since in ME we are easily in the situation of sustained exertion at near to maximal levels does this mean we get burning because of increased acidosis from pyruvate? Or is the buffering system overloaded?

Deep burning pain after exertion, even in a fit person, is such a basic fact of ME I feel it is important to try to work out what is happening. It often feels as if even my bones are on fire and makes it impossible to think.

 

I agree – if it helps in explaining it, I find evenly distributed pressure on the painful muscle helps. I had it last night in my thigh muscles and lay face-down for as long as I could, which reduced the pain level significantly whilst my painkillers started to kick in.

ETA 'I agree'.

 

Topical article (not about ME): https://mashable.com/article/smart-toilets-urine-analysis/

 

Is there a high rate of cell destruction and turnover in mecfs,apoptosis I think it’s called