Nephrology is the specialty that learned to slow a decline it once thought unstoppable.
In November 1993, the New England Journal of Medicine published a trial about kidney damage in type 1 diabetes. Kidney function falls year after year in these patients. Blood pressure drugs might slow the fall, but nobody knew whether any drug protected the kidneys themselves. The trial tested a blood pressure drug called captopril. It asked whether captopril protected the kidneys beyond lowering blood pressure. The trial gave 409 patients captopril or a placebo, and it kept blood pressure under control in both groups. The researchers counted the patients whose kidney function fell sharply, measured as a doubling of creatinine in the blood. That happened to 25 patients on captopril. It happened to 43 patients on placebo. Captopril also halved the risk of death, dialysis or a transplant. The benefit did not come from lower blood pressure alone. A blood pressure drug had protected the kidneys themselves.
Nineteen years later, in December 2012, the same journal published a trial about polycystic kidney disease. Polycystic kidney disease is inherited. Cysts grow in the kidneys and often lead to pain, high blood pressure and kidney failure. Laboratory studies suggested that a drug called tolvaptan could slow the cysts. The trial gave 1,445 adults tolvaptan or a placebo for three years. The kidneys grew by 2.8% a year on tolvaptan. They grew by 5.5% a year on placebo. Kidney function also fell more slowly on tolvaptan. But the drug made patients pass large amounts of water, and it caused some liver problems. Early stopping affected 23% of the patients on tolvaptan. It affected 14% of the patients on placebo. A drug had slowed the growth of the cysts, at a price.
Almost eight years later, in October 2020, the same journal published a trial about chronic kidney disease. Dapagliflozin was a drug for type 2 diabetes. The trial asked whether it could protect the kidneys of people with chronic kidney disease, with or without diabetes. It gave 4,304 people dapagliflozin or a placebo. The trial was stopped early, because the drug worked. Kidney failure, a halving of kidney function, or death from kidney or heart causes affected 9.2% of the people on dapagliflozin. It affected 14.5% of the people on placebo. Deaths from any cause fell from 6.8% to 4.7%. The drug worked just as well in people without diabetes. A diabetes drug had become a kidney drug.
These are three of the thousands of studies that shaped modern nephrology. They taught nephrology that a blood pressure drug could protect the kidneys themselves, that a drug could slow the cysts of polycystic kidney disease, and that a diabetes drug could protect kidneys with or without diabetes, and each time the answer was in a paper years before it was in a textbook.
It is still happening. Recently, in September 2026, The Lancet published a report on a pig kidney transplanted into a living patient. There are not enough human kidneys for everyone who needs one. The patient had kidney failure, faced a long wait for a donor kidney, and had no living donor. Surgeons gave the patient a kidney from a gene-edited pig. The pig kidney worked at once. It kept the patient off dialysis for 271 days. It began to fail after the patient’s anti-rejection drugs were reduced during an infection, and surgeons removed it. No pig infection passed to the patient. The patient received a human kidney 82 days later. It worked at once. This was one patient, not a trial. A pig kidney had bridged the wait for a human one. Practice follows the literature as it goes. It is a good culture. It has exactly one cost.
The literature grows faster than anyone can read it.
Across the medical topics a nephrologist needs to stay up to date on, from chronic kidney disease and dialysis to IgA nephropathy and kidney transplants, around 410 full-text papers now arrive every week. That is about 1,800 a month, and more than 20,000 a year. Chronic kidney disease alone is 132 of each week’s 410. Acute kidney injury is 85. These are not press releases or opinion pieces. They are the same kind of paper as the captopril trial and the dapagliflozin trial, and somewhere in each week’s 410 are the handful that will change a prescription.
It is tempting to believe that experience closes the gap, that twenty years of clinic teach what the papers teach. The evidence points the other way. A systematic review of 62 studies found that in most of them, more years in practice went with lower adherence to current standards of care. Experience is not what keeps a nephrologist current. Reading is. And reading is the one thing the week does not have room for.
So we built the tool you need to stay up to date.
We summarise the latest research for you and send it directly to your email inbox, every week, or whenever you choose.
A gene-edited pig kidney kept a patient off dialysis for 271 days, then bridged them to a human transplant
TakeawayIn the first recipient of a planned three-patient study, a gene-edited pig kidney functioned at once and kept the patient dialysis-free for 271 days; after it failed and was removed, a human kidney transplant worked immediately with no sensitisation.
Kidney xenotransplantation could ease the organ shortage, but its durability, infection risk and effect on later human transplantation were open questions. A patient with end-stage kidney disease, a long expected wait and no living donor received a gene-edited pig kidney at Massachusetts General Hospital on January 25, 2025.
- •Dialysis independence on the xenograft: 271 days.
- •Human kidney transplant 82 days after removal: immediate function, no sensitisation over 231 days.