AN ARTIFICIAL kidney these days still means a refrigerator-sized dialysis machine. Such devices mimic the way real kidneys cleanse blood and eject impurities and surplus water as urine. But they are nothing like as efficient, and can cause bleeding, clotting and infection—not to mention inconvenience for patients, who typically need to be hooked up to one three times a week for hours at a time. Still, for 2m people around the world who suffer from chronic kidney failure dialysis is the best option, unless they are fortunate enough to qualify for one of the 76,000 or so kidney transplants performed each year. Even those lucky few endure a lifetime on immunosuppressant drugs, to stop their bodies rejecting the foreign tissue.

A world in which new kidneys are grown using a patient’s own cells, the desideratum of transplantology, remains some way off—though it did get a little closer with a report in Nature Medicine, by Harald Ott of Massachusetts General Hospital and his colleagues, of a successful graft of just such an organ. The patient in question was a rat and the kidney, much smaller than a human’s, produced urine much less well than a natural one does. But Dr Ott’s work is a clear indication that this technology, in which a donor organ is stripped of living cells using detergent and the organ’s collagen scaffolding is replanted with the right kinds of cell, is maturing.

Before it does, and then secures regulatory approval for clinical use, however, human patients are likely to be offered miniature versions of the dialysis machine. None is available yet, but last year America’s Food and Drug Administration (FDA) picked a couple of candidates to participate in a new fast-track process called Innovation Pathway 2.0, which aims to bring promising medical technologies to market more promptly.

The first is the Wearable Artificial Kidney (WAK), which was designed by Victor Gura of the Cedar Sinai Medical Centre, in Los Angeles, and is being developed by a firm called Blood Purification Technologies. Dr Gura’s device squeezes the old dialysis machine’s clunky warren of tubes and filters into something that weighs about 5kg and can be worn on a belt around the waist.

The WAK works by sucking blood from a patient’s vein and pumping it through a membrane that consists of hollow, semi-permeable fibres a few microns across. As the blood flows through the insides of these fibres, a waste-absorbing fluid, called a dialysate, flows the other way past their outsides. Since the concentration of metabolic waste is higher in the blood than in the dialysate, molecules smaller than the fibres’ pores diffuse from the blood and into the dialysate.

Manipulating the pressure of the blood and the dialysate allows molecules of different sizes to be extracted from the blood. These are then removed from the dialysate by running it through a substance called a sorbent, which soaks up the waste and is binned once a day. Thus cleansed, the dialysate can be recycled, so the WAK needs less than half a litre of it, rather than the 120 litres used—and flushed down the drain—in old-fashioned dialysis.

A few years ago an early version of the WAK was tested on eight patients in London for up to eight hours at a time. Later this year a small trial at the University of Washington, in Seattle, will attempt to extend this to 24 hours, before proceeding to larger trials in hospitals, and ultimately unsupervised ones in patients’ homes.

The WAK does, though, suffer from a problem that is inherent in the process of dialysis, however large or small the machine. Along with the bad substances it removes from the blood, some good stuff vanishes too. The FDA’s second pick, the implantable Renal Assist Device (iRAD), attempts to get round this by harnessing natural kidney cells’ ability to distinguish between wanted and unwanted molecules.

The iRAD, which is the size of a coffee cup, consists of two parts: a filter and a bioreactor, where the cells are stored. Though its layout is different from that of a natural kidney, it works in basically the same way.

In a real kidney, part of the aqueous fraction of blood is squeezed out of it in filters called glomeruli, leaving blood corpuscles, platelets and dissolved proteins behind to be returned to the bloodstream. This aqueous liquid then passes through tubes whose cells absorb valuable chemicals, such as salt and glucose, and also some of the water. These, too, are returned to the bloodstream. What remains drains into the bladder as urine.

In the iRAD, a silicon filter stands in for the glomeruli. The silicon is organised into layers, into each of which millions of slit-shaped pores have been etched using techniques similar to those employed to fabricate computer chips. The pores’ clever engineering and tiny size (just a few billionths of a metre across) allowed the iRAD’s designers—William Fissell of Vanderbilt University, in Nashville, Shuvo Roy of the University of California, San Francisco, and H. David Humes of the University of Michigan—to dispense with an internal pump. Instead, the iRAD relies on natural blood pressure supplied by the heart. The lack of a pump reduces damage to corpuscles.

Once they have been separated, both fluid and filtrate are passed through the bioreactor. This consists of a series of silicon plates similar to those in the filter. In its case, though, some of the plates’ surfaces are covered with kidney cells (taken from human kidneys deemed unsuitable for transplant) of the type that line the urine-generating tubes.

Alternate spaces between the silicon plates carry fluid and filtrate. The cells, which line the spaces carrying the fluid but not those carrying the filtrate, extract glucose, salts and other desirables from the fluid and transfer them through the pores to the filtrate along with some of the water, just as would happen in a real kidney. What emerges, in different streams, is cleansed blood and urine.

Nor does the resemblance to a real kidney end there. The cells in the iRAD produce vitamin D, just as they would in a real kidney, and also help to control blood pressure by regulating the amount of water in the blood. And because the kidney cells inside the device are considerably bigger than the pores in the silicon plates atop which they sit, they do not come into contact—and conflict—with the patient’s cells present in the filtrate flowing on the other side of the plate. Immune cells and antibodies in that filtrate cannot therefore attack them and cause an immune reaction.

Tests in both the laboratory and in pigs suggest the iRAD should work, but it is further away from clinical reality than WAK is. If another $13m-15m-worth of investment materialises, Dr Fissell reckons, human trials might begin in 2017. Moreover, if either WAK or iRAD does eventually arrive, such a device is likely to be costly to buy. But it should be cheap to run. And it will offer hope to the 95% of patients who die while awaiting a transplant.