Peritoneal dialysis was first employed in patients with acute renal failure in the 1940s and since the 1960s for those with end-stage renal disease. Its popularity increased enormously after the introduction of continuous ambulatory peritoneal dialysis in the end of 1970s. This stimulated both clinical and basic research. In an ideal situation, this should lead to cross-fertilization between the two. The present review describes two examples of interactions: one where it worked out very well and another where basic science missed the link with clinical findings. Those on fluid transport are examples of how old physiological findings on absorption of saline and glucose solutions were adopted in peritoneal dialysis by the use of glucose as an osmotic agent. The mechanism behind this in patients was first solved mathematically by the assumption of ultrasmall intracellular pores allowing water transport only. At the same time, basic science discovered the water channel aquaporin-1 (AQP-1), and a few years later, studies in transgenic mice confirmed that AQP-1 was the ultrasmall pore. In clinical medicine, this led to its assessment in patients and the notion of its impairment. Drugs for treatment have been developed. Research on biocompatibility is not a success story. Basic science has focussed on dialysis solutions with a low pH and lactate, and effects of glucose degradation products, although the first is irrelevant in patients and effects of continuous exposure to high glucose concentrations were largely neglected. Industry believed the bench more than the bedside, resulting in ‘biocompatible' dialysis solutions. These solutions have some beneficial effects, but are evidently not the final answer.
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