Chronic Kidney Disease (CKD) affects more than 16.0% of American adults aged 20 years and older, and is even higher among African Americans due, ostensibly to more severe hypertension in Blacks.
CKD presents initially without specific signs or symptoms and only blood tests can detect it by either an increase in serum creatinine or protein in the urine. As the kidney function decreases, creatinine goes up and the kidney spills more and more protein into the urine. In addition, as the disease progresses, blood pressure increases due to fluid overload and production of renin, further increasing hypertension or causing worsening congestive heart failure.
A poison, urea, accumulates, leading to inflammation or infection around the hearth and occasional brain damage. Excessive potassium accumulates in the blood, anemia develops, and bloods vessels calcify. Metabolic acidosis becomes routine. Chronic kidney disease accelerates hardening of the arteries, and infection is common. It is a relentless and unpleasant death.
Researchers from the University of Colorado, led by Dr. Mcihel Chonchol, began their recent paper with their thesis, “To date, experimental and clinical evidence supports a strong link between vitamin D insufficiency and the risk of cardiovascular disease and infection and it is rapidly accumulating.” Unlike some other nephrologists, the scientists understand that activated vitamin D or its analogues (used in CKD for decades) does not replace vitamin D nor treat vitamin D deficiency in CKD.
The authors cite dozens of papers showing that adding vitamin D (cholecalciferol) to activated vitamin D or its analogues is the treatment for choice for CKD, reducing heart disease and strokes as well as infectious disease. The two forms of vitamin D serve two different and distinct purposes. One, activated vitamin D, replaces the lost ability of the kidneys to make this endocrine hormone that supports blood calcium. And two, vitamin D supplies the substrate necessary for multiple other cells to make activated vitamin D inside the cells of the body (autocrine) that fights infection and prevents and fights cardiovascular disease.
I loved their conclusion, “In patients with any stage of CKD, serum 25(OH)D levels should be measured annually, “ and levels kept above 30 ng/ml (although, as the authors point out, higher levels may be more beneficial). They end with an urgent call for clinical trials.
The only aspect of their paper that I found wanting, or may have missed, was that the skin is second only to the kidneys in the amount of activated vitamin D that it sends out into the blood stream. This supports the thesis that more vitamin D may lower the amount of the expensive activated vitamin D analogues that CKD patients need. That aside, I think it was an excellent paper.