By Chuck Blazer, MS, RD Vitamins are necessary to defend our bodies against illness and for building and maintaining our organs and tissues. There are four reasons people with end-stage renal disease (ESRD) have extra vitamin needs. First, dialysis cleans blood by removing waste and excess fluid. Along with removing waste, the process of dialyzing the blood also removes important vitamins. Second, people with ESRD need extra protection against heart disease, hemodialysis access damage, and anemia. Third, the meal plan for people with ESRD includes foods that limit important vitamins. Fourth, when wastes build up in the blood, a condition called uremia occurs. Uremia changes the way our body uses vitamins. Vitamins can be classified into two groups, “water soluble” and “fat soluble.” Dialysis patients are less likely to have ideal amounts of water soluble vitamins. The water soluble vitamins are the B vitamins and vitamin C. Improved technology has made dialysis more efficient. But, with better dialysis and more efficient treatment, there is a greater loss of important vitamins, namely folic acid, vitamin B6 and vitamin B12. Homocysteine Homocysteine is formed when protein is broken down to be used by the body. People with chronic kidney disease (CKD) and ESRD have dangerously high levels of homocysteine in their blood. This is important because the kidneys play a role in ridding the body of excess homocysteine. When kidney function begins to decrease, homocysteine levels begin to climb. High levels of homocysteine in your blood can damage your vessels and increase the risk for heart attack and stroke. Lowering Homocysteine Dialysis patients have two to four times higher homocysteine levels than the general population. Patients with ESRD have homocysteine levels of 20-30 micromoles per liter. The Nutrition Committee of the American Heart Association (AHA) states that anyone at risk for cardiovascular disease should have a homocysteine level of less than 10 micromoles per liter. Achieving homocysteine levels of less than 10 micromoles seems very unlikely in the ESRD population. However, high doses of folic acid, and vitamins B6 and B12 are very effective at reducing homocysteine levels in dialysis patients to lower levels. Additional studies are necessary to look at the benefit of lowering homocysteine in the dialysis patient. Homocysteine & Cardiovascular Disease A high level of homocysteine in the blood has been connected to an increased risk of heart disease. It is the number one cause of death in ESRD. According to the United States Renal Data System, Annual Data Report, nearly 50 percent of dialysis patients have atherosclerotic heart disease. Homocysteine is the most common heart disease risk factor in dialysis patients. Is it possible that lowering homocysteine in the dialysis patient may reduce the risk of cardiovascular disease? Scientists are conducting research to find out if lowering homocysteine will protect dialysis patients against heart disease. Because, nearly half of all dialysis patients have cardiovascular events, it is especially important for individuals with ESRD to have adequate levels of the three vitamins that lower homocysteine. Homocysteine & Vascular Access Health An important part of dialysis is having a healthy, working “access.” The vascular access has been called the patient’s “lifeline” because it is where blood is removed from the body for cleansing and returned to the body. A blockage caused by excess clotting of the blood can occur in dialysis patients at their access site. This is known as access thrombosis. High levels of homocysteine have been shown to increase the risk of access thrombosis. This condition can interfere partially or totally with dialysis and result in costly hospitalizations. In fact, access problems are the number one cause of hospitalizations in ESRD. Problems with access sites are estimated to cost Medicare and Medicaid a total of 1.2 billion dollars every year. Homocysteine is a risk factor in clot formation. Addressing homocysteine with high doses of folic acid, vitamin B6 and B12 will lower homocysteine. However, we need scientific studies to investigate whether lowering homocysteine with high dose B vitamins improves the rate vascular access thrombosis. Several ongoing trials are looking at this. B Vitamins and Red Blood Cells The kidneys play a key role in the production of red blood cells. The kidneys make a hormone that signals the bone marrow to make more red blood cells. As kidney function declines over time, the kidneys make less of this hormone, and therefore, our bodies make fewer red blood cells. Low levels of red blood cells is known as anemia. The anemia of kidney failure can usually be successfully treated with erythropoietin therapy (EPO). Interestingly, the same three vitamins that are needed to lower homocysteine are also required to make red blood cells. For EPO to effectively produce red blood cells, we must have enough folic acid, vitamin B6 and vitamin B12, among other factors. Many studies have shown that adequate amounts of folic acid levels are necessary for EPO to work effectively. Conclusion Vitamins are essential for individuals with ESRD. Vitamins may play an important role in protecting dialysis patients against cardiovascular disease and access thrombosis. Getting enough folic acid, vitamin B6 and vitamin B12 may enhance anemia management. A renal vitamin that features high doses of folic acid and vitamins B6 and B12 may be helpful. Renal multivitamins should be taken daily. On dialysis days, wait until after dialysis to take your vitamin. Chuck Balzer, MS, RD, is a Pharmaceutical Consultant and Adjunct Faculty Member at Brookdale College, Lincroft , NJ. The information contained herein is intended for educational purposes only. It is not intended and should not be construed as the delivery of medical care. Persons requiring diagnosis or treatment, or those with specific questions, are urged to contact their local healthcare provider for appropriate care. This article originally appeared in the January 2004 issue of aakpRENALIFE, Vol. 19, No. 4.
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