Carnitine in dialysis patients

Abstract

Carnitine is often prescribed to patients under dialysis therapy, with the expectation of improving aspects such as the cardiac activity, anemia and muscle symptoms in the patients; both cases in which it is effective and not effective are encountered in clinical practice. In relation to improvement of the cardiac activity or muscle symptoms, in the process of transport of fatty acids into the mitochondria, carnitine is involved only until acyl coenzyme A. Therefore, different results are obtained in relation to the subsequent process of ATP production. Water-soluble vitamins which are easily removed by hemodialysis therapy are required for beta-oxidation and the TCA cycle. Thereafter, coenzyme Q10 is also required for the electron transport chain (respiratory chain system), however, coenzyme Q10 generation is inhibited if a statin is used. In relation to anemia improvement, many elements, including carnitine, are involved. It is necessary to adjust all these elements in the hematopoietic process. Muscle contraction is associated with alkalosis. Furthermore, in the case of cramps occurring during the latter half of hemodialysis therapy, there is the additional component of contraction alkalosis. In general, alkalosis induces the binding of calcium ions to serum albumin and consequently, alkalosis produces hypocalcemia. In order to maintain the serum calcium ion concentration, calcium ions are released from the sarcoplasmic reticulum of the muscle cells, resulting in muscle spasms. When the sarcoplasmic reticulum reabsorbs the released calcium ions via ATP, the muscle contractions cease. However, in the case of carnitine deficiency, the muscle spasms persist due to ATP deficiency. We may be able to use carnitine more effectively by knowing precisely what roles carnitine participates in.