Morgenstern, Bruce Z.

T he simplicity of performing peritoneal dialysis belies the physiologically complex processes that underlie the removal of solutes and water from the bloodstream. The successful removal of solutes and water during a peritoneal dialysis (PD) exchange represents the multiple interactions of a number of properties of the peritoneal exchange surface (something more than merely a “membrane”; this multi-layered, physiologically active surface is in many senses “alive” and may well respond to the process of an exchange, rendering it quite difficult to measure and characterize) and the steps of the PD exchange, such as the nature of the dialysate, the volume instilled, the times of the cycle, etc. Peritoneal equilibration is defined as the tendency of the concentration of solutes in the blood and the dialysate to come into balance. Other similar concepts have been developed or applied to this process, such as clearance, dialysance, and mass transfer, but these in fact represent very different entities. It is important to understand some of the fundamental aspects of the PD process. Once again, the basic contributing factors to the removal of solute and water seem quite simple: blood must get to the membrane and be spread over an area available for exchange. The membrane must allow for the movement of water and solutes, but some selectivity must exist. The dialysate must contain an osmotic agent to drive fluid removal. The access device must allow for free and rapid flow of dialysate. It should be emphasized that the peritoneal exchange process is the sum of two simultaneous and interrelated transport mechanisms: diffusion and convection. Diffusion refers to the movement of solute down a concentration gradient, while convection refers to the movement of solutes that are more or less trapped in a fluid flux.

To the Editor.— The cases reported by Olson et al1 of pulmonary hemorrhage in children with systemic vasculitis clearly highlight the fact that children are not "immune" to these conditions. We must take issue, however, with the diagnosis of Henoch-Schönlein purpura in the patients described. Because Henoch-Schönlein purpura is a subset of systemic vasculitis, the clinical manifestations may mimic or be mimicked by other vasculitis syndromes such as polyarteritis nodosa, Wegener's granulomatosis, and systemic lupus erythematosus.2