Consider enhancements in membranes, quantity of dialysis, anemia and iron control, social services, intradialytic symptom control, and many, many others. Perhaps there is a fundamental underlying cause of morbid and mortal events which the nephrology community now understands more lucidly. The following, simplistically, presents an overview of the problem. Patients with chronic renal insufficiency begin to develop anemia that is more than just erythropoeitin deficiency. It seems to be an anemia, in part, like ones seen in chronic inflammatory states, such as rheumatoid arthritis.
Patients begin to eat less protein.
And the albumin drops. But experts tell us that one almost has to starve in order to decrease protein synthesis just from a dietary protein intake. Why do pre-ESRD patients begin to eat less and why does albumin decrease, disproportionately, along with other visceral protein markers. Then creatinine excretion begins to decrease, suggesting that somatic protein stores are decreasing. And this when dietary protein intake should be sufficient to maintain somatic stores.