People with IgA Nephropathy commonly have high blood pressure.
Doctors prescribe blood pressure lowering medications like ACE inhibitors.
A new paper has revealed that tracking blood pressure co-factors is predictive for progression of IgAN.
What I have learned reading this paper is to be reminded about how important maintaining lower blood pressure is for my weakened IgAN kidneys.
This new paper is a technical one that focuses on the development of diagnostic paths for tracking the progression of IgAN in patients. It focuses on Copeptin, you can read the paper here. In my reading of the paper it reminded me about my study of the mechanisms at work in my IgAN afflicted body and the fact that it gave me high blood pressure.
There are lots of factors that tell us how poorly (or well) our afflicted kidneys are, blood pressure is one.
Many have already learned that they can do this themselves by being observant of their own apparent symptoms. Many of us keep track of our own blood pressure which turns out to be a very good indicator of our kidney health. Since our kidneys are filtering our blood and keeping us healthy they have a lot of power over our circulation. At any given time about 1/3 of your blood is circulating through your kidneys to keep it filtered of metabolic toxins and to keep your salt levels in balance. Our kidneys are not merely filtering they are very well tuned internal blood laboratories that monitor and respond to our blood chemistry.
Our kidneys able to call for more or less blood flow as they sense the levels of the toxins they are filtering. They call for more blood to flow and be filtered by turning up our blood pressure. For people who don’t have kidney disease this up and down blood pressure commanded by the kidneys is a simple healthy means to do more or less filtering.
For those with impaired kidney function higher blood pressure is a bad thing!
One might think that since our kidneys are filters that the more blood that flows through them the better and that might mean higher blood pressure which equals more blood flow is better. The opposite is in fact the truth. Our kidneys which are bundles of incredibly tiny blood vessels are filled with very delicate membranes that do the filtering. When our IgAN condition reduces the ability of our kidney to filter metabolic wastes the levels of the metabolic wastes such as creatinine rise. IgAN is an inflammatory disease that irritates and scars delicate kidney membranes that are part of our endothelial systems. Many auto-immune conditions such as my Type2 Diabetes is an auto-immune attack on my endothelial cells. In IgAN the response to a rise in metabolic waste content in our blood is our kidneys turn up our blood pressure. They do this by signalling for arterial vessels to tighten up and the heart to beat faster. That ‘tightening’ (or loosening) is accomplished by the arginine and related biochemical systems in our body.
This new paper speaks to how the arginine system works and how to measure and monitor it. I suspect the researchers are on the hunt for a valuable medical monitoring technology they might add to the lab sheets where our doctors with a tick in a tick box cause money to be spent on our healthcare.
What blood pressure medications like ACE inhibitors such as the lisinopril I have taken for 20+ years does is it keeps my blood vessels ‘relaxed,’ that keeps my blood pressure lower. The lower pressure blood in my delicate kidney filters keeps them less stressed. It helps keep my protein from leaking out of my blood and into my urine where I see it as ‘foam’ in the toilet bowl when I pee. More foamy urine means more leaked protein. Protein is a big molecule so when at higher pressure it is forcing its way out through my delicate kidney membranes it is punching big holes in those membranes and other good things I want to keep in my blood leaks out as well.
Of course the down-side of having impaired kidney function and low blood pressure is that those danged metabolic wastes are not so well filtered as I would like them to be. It’s a balancing act.
I can help balance myself by watching my salt intake as it also boosts my blood pressure. But for me the older I get the more my kidney function is not what I’d like it to be so I have become also reliant on taking diuretics, aka water pills. My recent onset of Type 2 diabetes didn’t help at all. I take my diuretics but not as a regular dose every day but rather on demand when I notice I am retaining water, aka seeing edema in my lower left leg, or the mysterious weight gain of several pounds that happens regularly. The problem with diuretics is that while they empower our kidney membranes to reduce our water retention as they do this they cause us to lose salts, sodium and potassium. For me I get leg and foot cramps when I have been losing too much of my salts, aka electrolytes.
My body talks to me constantly about my state of kidney function. Sometimes I wish it would shut up and not be so chatty but all in all I am better off being well informed and aware about what my body is telling me. Leg and foot cramps tell me to stretch more or find my pickle jar as salty, high in potassium, pickles (or half an ounce of pickle juice) restore my electrolytes and often end the cramps in a minute or few.
Here’s a snippet from the paper that motivated this post.
The investigators noted that in water deprivation tests in IgAN patients performed by the same research group, an impaired urine concentrating capacity was found with elevated AVP (arginine vascular pressure) and copeptin levels. “We hypothesize that in IgAN, when renal disease progresses, urine concentrating capacity declines,” the researchers wrote. “As a response, AVP secretion is stimulated to maintain water homeostasis. Because AVP levels rise and accelerate kidney damage, this may lead to a vicious circle causing progressive renal function loss.”
The researchers concluded that their results “suggest that measurement of copeptin could be of clinical value in this patient group because it may help to stratify patients according to risk and indication for treatment.”
The study is the first to investigate copeptin in IgAN, the researchers stated. Study strengths include a study population consisting of a well-defined group of patients with biopsy-proven disease, a 5-year follow-up and data collection and sample storage according to standardized protocols. Study limitations include a relatively small patient population and patient use of ACE inhibitors and angiotensin receptor blockers during the study, which “may have weakened the correlation between copeptin and proteinuria and possibly the correlation between copeptin and renal outcome during follow-up.”
Read the paper here….