Kidney Function

Calcium is the most abundant element in the human body. 95% of your body’s calcium can be found in your bones and teeth. The second most abundant element in the human body is phosphorus. A large percentage of your body’s phosphorus is combined with the calcium in your skeletal structure. A lesser amount of phosphorus lies in the soft tissues and fluids of your body.

Both calcium and phosphorus are required for the proper formation of bones. The body cannot utilize calcium whatsoever unless active Vitamin D is present. Because non-functioning kidneys cannot activate Vitamin D, calcium from food eaten by someone with non-functioning kidneys cannot be absorbed adequately. Subsequently, your body’s blood calcium level can drop dramatically.

Phosphorus is known to build up in the bodies of patients with non-functioning kidneys which can result in a decrease in the level of blood calcium present. When calcium levels drop, the parathyroid glands secrete the parathyroid hormone which causes calcium to be released from the bones and then sent back into the bloodstream. This release of calcium from your bones may cause them to become weak or brittle, and if this process continues for a prolonged period of time, bones may break.

A doctor monitors this delicate relationship between phosphorus and calcium and may prescribe a calcium supplement. Foods high in phosphorus should be avoided altogether. Additionally, phosphate binders (like calcium salts) may be prescribed in order to prevent the phosphorus in your food from being absorbed into your body.

Why Do I Need to Restrict My Phosphorus Intake?
Due to the fact that high levels of phosphorus in your bloodstream can result in your bones being deprived of much needed calcium, it is of the utmost importance that phosphorus be restricted from your diet. Also, high levels of phosphorus may potentially combine with calcium and deposit in the soft tissues such as your blood vessels, skin, and lungs. If this occurs, you may experience joint pains, itching, and/or eye irritation.

Protein-energy wasting (PEW) is highly prevalent in people with stages 4 and 5 chronic kidney disease, particularly in maintenance dialysis patients, and many indicators of PEW correlate strongly with mortality. Consequently, the causes, prevention, and treatment of PEW are active areas of investigation. A major cause of PEW is insufficient intake of nutrients, especially protein and energy (calories). Standard methods for increasing nutritional intake in patients with chronic kidney disease with PEW include dietary counseling and use of food supplements. If nutrient intake does not increase sufficiently, tube feeding and total parenteral nutrition may be considered. For maintenance hemodialysis patients, intradialytic parenteral nutrition (IDPN), an intravenous infusion of essential nutrients during hemodialysis treatments, may be used. Many studies have evaluated the effectiveness and safety of IDPN and show that IDPN has a good safety profile and also may improve protein-energy status. However, most studies have limitations in experimental design, such as small numbers of patients, lack of adequate controls, inclusion of patients without PEW, uncontrolled or unmonitored oral intake, nonrandomized design, or short duration. Additionally, most studies used nutritional or inflammatory indicators, rather than the more important outcomes of morbidity, mortality, or quality of life. Thus, although IDPN may partially satisfy the nutritional needs of maintenance hemodialysis patients who have or are at risk of PEW and who have substantial, but not adequate, protein and/or energy intake, longer term randomized prospective clinical trials with appropriate control groups are necessary to more definitively evaluate the clinical effectiveness and indications for IDPN.

Kidney transplant in patients with atypical hemolytic uremic syndrome (aHUS) is associated with a poor outcome because of recurrent disease, especially in patients known to have a factor H mutation. Long-term prophylactic plasma exchange and combined liver-kidney transplant have prevented graft loss caused by recurrence. However, the mortality associated with liver transplant is not negligible, and prophylactic plasma exchange requires permanent vascular access and regular hospitalization and exposes the patient to potential allergic reactions to plasma. Eculizumab is a high-affinity humanized monoclonal antibody that binds to C5 and thus prevents generation of C5a and the membrane attack complex. We report the case of a 17-year-old girl with aHUS associated with a mutation in the gene for complement factor H (CFH; c.3572C>T, Ser1191Leu) who was highly dependent on plasma exchange. Because of severe allergic reactions to plasma after the third renal graft, eculizumab was introduced in place of plasma exchange without problems. This and other reports suggest that the promise of complement inhibitors in the management of aHUS is going to be fulfilled.