To meet the ultrafiltration requirements of patients on peritoneal dialysis, the peritoneal dialysate is deliberately rendered hyperosmolar relative to plasma, to create an osmotic gradient that favors net movement of water into the peritoneal cavity. In commercially available peritoneal dialysates, glucose serves as the osmotic agent that enhances ultrafiltration. Available concentrations range from 1.5% to 4.25% dextrose. Over time, the osmolality of the dialysate declines as a result of water moving into the peritoneal cavity and of absorption of dialysate glucose.
The absorption of glucose contributes substantially to the calorie intake of patients on continuous peritoneal dialysis. Over time, this carbohydrate load is thought to contribute to progressive obesity, hypertriglyceridemia, and decreased nutrition as a result of loss of appetite and decreased protein intake. In addition, the high glucose concentrations and high osmolality of currently available solutions may have inhibitory effects on the function of leukocytes, peritoneal macrophages, and mesothelial cells. In an attempt to develop a more physiologic solution, various new osmotic agents are now under investigation. Some of these may prove useful as alternatives to the standard glucose solutions.
Those that contain amino acids have received the most attention.
The sodium concentration in the ultrafiltrate during peritoneal dialysis is usually less than that of extracellular fluid, so there is a tendency toward water loss and development of hypernatremia.
Commercially available peritoneal dialysates have a sodium concentration of 132 mEq/L to compensate for this tendency toward dehydration. The effect is more pronounced with increasing frequency of exchanges and with increasing dialysate glucose concentrations. Use of the more hypertonic solutions and frequent cycling can result in significant dehydration and hypernatremia. As a result of stimulated thirst, water intake and weight may increase, resulting in a vicious cycle.
Potassium is cleared by peritoneal dialysis at a rate similar to that of urea. With chronic ambulatory peritoneal dialysis and 10 L of drainage per day, approximately 35 to 46 mEq of potassium is removed per day. Daily potassium intake is usually greater than this, yet significant hyperkalemia is uncommon in these patients. Presumably potassium balance is maintained by increased colonic secretion of potassium and by some residual renal excretion. Given these considerations, potassium is not routinely added to the dialysate.
The buffer present in most commercially available peritoneal dialysate solutions is lactate. In patients with normal hepatic function, lactate is rapidly converted to bicarbonate, so that each mM of lactate absorbed generates one mM of bicarbonate.
Even with the most aggressive peritoneal dialysis there is no appreciable accumulation of circulating lactate. The rapid metabolism of lactate to bicarbonate maintains the high dialysate-plasma lactate gradient necessary for continued absorption. The pH of commercially available peritoneal dialysis solutions is purposely made acidic by adding hydrochloric acid to prevent dextrose from caramelizing during the sterilization procedure. Once instilled, the pH of the solution rises to values greater than 7.0. There is some evidence that the acidic pH of the dialysate, in addition to the high osmolality, may impair the host’s peritoneal defenses.
To avoid negative calcium balance—and possibly to suppress circulating parathyroid hormone—commercially available peritoneal dialysis solutions evolved to have a calcium concentration of 3.5 mEq/L (1.75 mmol/L). This concentration is equal to or slightly greater than the ionized concentration in the serum of
most patients. As a result, there is net calcium absorption in most patients treated with a conventional chronic ambulatory peritoneal dialysis regimen. As the use of calcium-containing phosphate binders has increased, hypercalcemia has become a common problem when utilizing the 3.5 mEq/L calcium dialysate. This complication has been particularly common in patients treated with peritoneal dialysis, since they have a much greater incidence of adynamic bone disease than do hemodialysis patients. In fact, the continual positive calcium balance associated with the 3.5-mEq/L solution has been suggested to be a contributing factor in the development of this lesion. The low bone turnover state typical of this disorder impairs accrual
of administered calcium, contributing to the development of hypercalcemia. As a result, there has been increased interest in using a strategy similar to that employed in hemodialysis, namely, lowering the calcium content of the dialysate. This strategy can allow increased use of calcium-containing phosphate binders and more liberal use of 1,25-dihydroxyvitamin D to effect decreases in the circulating level of parathyroid hormone.
In this way, development of hypercalcemia can be minimized.
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