Co-morbidities of end-stage renal disease (permanent kidney failure) are one of the more complicated elements of the disease. One of the first things medical professionals tell kidney failure patients—usually right after telling them that the disease is incurable—is that they’re unlikely to die from kidney failure, but highly likely to die from something else; one of the many co-morbidities. As I’ve said before, Robert Hunter was more correct than he knew when he wrote, “if the thunder don’t get you, then the lightning will.”
Hyperphosphataemia—high levels of phosphorous in the blood chemistry—is one of those co-morbidities. Hyperphosphataemia is a known contributory factor for increased risk of cardiac problems and death in kidney failure patients. Specifically, it’s responsible for vascular calcification, cardiac interstitial fibrosis, and arterial thickening. And yes, they’re as bad as they sound; they all “highly increase the risk of cardiac death.”
Cardiac death is to be avoided if at all possible.
Hyperphosphataemia is also a contributory factor of bone loss.
Because the normal dialysis prescription—four hours, three times a week—is incapable of removing the amount of phosphorous necessary to consume in order to avoid malnutrition, dialysis patients have two options:
- More frequent dialysis treatments (research indicates that short-duration, daily dialysis is the most beneficial treatment modality but Medicare and few private insurers will cover it).
- Treatment with phosphate binders.
As a result, the vast majority—fully 95% of dialysis patients—have to take phosphate binders. I take Renagel to the tune of 10-12 additional pills each day. Common adverse events include “vomiting, nausea, diarrhea, dyspepsia, abdominal pain, and constipation.” And it’s one of the most expensive drugs I have to take.
An acceptable range of phosphorous in the blood chemistry of kidney failure patients is 2.3-4.5 mg/dL. My blood draw this week revealed a phosphorous level of 7.0. Not good. Not explainable either. I’m fairly strict in following my dietary restrictions and pretty much regularly eat the same foods in the same amounts. It’s not the first time this has happened.
Since February 2000, when I was diagnosed with end-stage renal disease and started dialysis my phosphorous has been 7.0 or higher x times: September 2002 (9.0); May 2003 (7.4); February 2004 (7.7); August 2004 (7.2); November 2004 (7.4); January 2005 (7.4); February 2005 (8.1); November 2005 (7.2); December 2005 (8.1); January 2006 (7.1); March 2006 (7.6); and April 2006 (7.1).
In my case, high phosphorous levels seem to be at least somewhat cyclical, so here’s hoping it comes down on its own within the next month or two. Meanwhile, I’ll have to watch my food intake even closer than usual.
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