Review of dialysate calcium concentration in hemodialysis

Abstract

The dialysate calcium (Ca) concentration for hemodialysis (HD) patients can be adjusted to manage more optimally the body's Ca and phosphate balance, and thus improve bone metabolism as well as reduce accelerated arteriosclerosis and cardiovascular mortality. The appropriate dialysate Ca concentration allowing this balance should be prescribed to each individual patient depending on a multitude of variable factors relating to Ca load. A lower dialysate Ca concentration of 1.25 to 1.3 mmol/L will permit the use of vitamin D supplements and Ca-based phosphate binders in clinical practice, with much less risk of Ca loading and resultant hypercalcemia and calcification. Low Ca baths are useful in the setting of adynamic bone disease where an increase in bone turnover is required. However, low Ca levels in the dialysate may also predispose to cardiac arrhythmias and hemodynamically unstable dialysis sessions with intradialytic hypotension. Higher Ca dialysate is useful to sustain normal serum Ca levels where patients are not taking Ca-based binders or if Ca supplements are not able to normalize serum levels. Suppression of hyperparathyroidism is also effective with dialysate Ca of 1.75 mmol/L, but hypercalcemia, metastatic calcification, and oversuppression of parathyroid hormone are risks. Dialysate Ca of 1.5 mmol/L may be a compromise between bone protection and reduction in cardiovascular risk for conventional HD and is a common concentration used throughout the world. The increase in longer, more frequent dialysis such as short-daily and nocturnal HD, however, provides another challenge with regard to optimal dialysate Ca levels and higher levels of 1.75 mmol/L are probably indicated in this setting. Difficulties in determining the ideal dialysate Ca occur because of the complex pathophysiology of bone and mineral metabolism in HD patients and there needs to be a balance between dialysis prescription and other treatment modalities. To optimize management of the abnormal Ca balance, other aspects of this disorder need to be more fully clarified and, with evolving medications for phosphate control and treatment of secondary hyperparathyroidism, as well as the emergence of a multitude of different HD regimes, further studies are required to make definitive recommendations. At present, we need to maintain flexibility with HD treatments and so dialysate Ca needs to be individualized to meet the specific requirements of patients by optimizing management of renal bone disease and simultaneously reducing metastatic calcification and cardiovascular disease.