Why is hypoalbuminemia common in patients with PD, what are the causes, and how should it be addressed?
Hypoalbuminemia is a frequent finding in patients treated with either peritoneal and HD and is associated with increased overall morbidity and mortality. Serum albumin levels in patients with PD are a function of synthesis, catabolism, volume of distribution, and loss, usually in urine or the peritoneal effluent. Albumin is also a negative acute phase reactant, so inflammation will decrease levels. As such, all these factors should be considered in evaluation and targeted for correction in patients with hypoalbuminemia.
PD patients typically lose about 6 to 8 g/day of albumin in the effluent, more during peritonitis episodes. This process probably contributes to generally lower serum albumin levels in PD compared to HD patients. However, for every specific level of serum albumin, the risk of all-cause and cardiovascular mortality is lower in PD patients than in patients treated with HD. This suggests that the decrease in serum albumin level related to peritoneal protein losses does not result in a higher risk of adverse events. It is also important to note that treatment with HD increases loss of amino acids compared to that seen with PD.
As changes in serum albumin over time impact mortality, therapeutic interventions to improve nutritional status should be undertaken. When nutritional intake is deemed inadequate, attempts should be made to increase intake of protein. Depression and medications should always be considered in the differential of poor dietary intake and should be addressed.
An expanded intravascular volume due to failure to achieve dry weight can cause decreased albumin levels. Therefore, in evaluating hypoalbuminemia, the clinician should look for and treat volume overload.
As albumin is a negative acute-phase reactant, patients should be evaluated for any source of inflammation and treatment should be initiated for this as appropriate.