This Week in Nephrology — Sep 9, 2026

Welcome to This Week in Nephrology. This week we're covering 10 notable papers spanning the frontier of transplantation and organ access, risk prediction and diagnostics across chronic kidney disease, and the practical business of drug therapy and shared decision-making. Let's dive in.

We start with the paper that will get the most attention, in The Lancet, where Riella and colleagues report the first-in-human experience of a gene-edited porcine kidney used explicitly as a bridge to human allotransplantation [1]. A patient with end-stage kidney disease, no living donor and a long expected wait received a pig kidney carrying deletions of the major glycan xenoantigens, inactivated porcine endogenous retroviruses, and seven human transgenes, under costimulation blockade with complement inhibition. The graft worked immediately and kept the recipient off dialysis for 271 days. There was T-cell-mediated rejection on the day 14 biopsy that resolved with treatment, and function held for about six months until immunosuppression was reduced during a bacterial infection, after which microvascular inflammation progressed to thrombotic microangiopathy and the graft was removed, despite a persistently negative donor-specific crossmatch. The infiltrate was macrophage and natural-killer-cell predominant, which points to injury mechanisms outside conventional antibody-mediated rejection. Crucially for the field, no porcine pathogen transmission was detected, anti-HLA antibodies did not change, and 82 days after explant the patient received a human kidney with immediate function and no sensitisation over 231 days. This is a single patient, so the durability question is unanswered, but the two fears that most constrained xenotransplantation, zoonosis and allosensitisation, did not materialise here.

Staying with access to transplantation, the American Journal of Transplantation published an analysis by McMichael and colleagues of more than 53,000 patients starting kidney replacement therapy in Australia and New Zealand across two decades, mapped to 21 transplant referral networks [9]. After adjusting for case mix, the ratio of observed to expected living donor transplants within twelve months ranged roughly sixfold across networks, from about a third of expected to more than double, and four networks performed below expectation. Starting treatment at a centre directly affiliated with a transplant unit, living outside a metropolitan area, and timely nephrology referral were all associated with more living donor transplantation. The message for practising nephrologists is that where a patient enters the system, and how promptly you refer, materially shapes whether they ever get a living donor kidney.

The second theme is risk prediction and diagnostics, and here three papers pull in interesting directions. In the Clinical Journal of the American Society of Nephrology, Malijan and colleagues used the EMPA-KIDNEY trial population of just over 5,000 participants to ask whether nine urine tubular biomarkers add anything to the kidney failure risk equation [4]. Over a median of three and a half years, the risk equation already discriminated treated kidney failure very well and progression only moderately. Adding the three most informative markers, monocyte chemoattractant protein-1, kidney injury molecule-1 and epidermal growth factor, produced a small improvement for kidney failure and a modest one for progression, and going from three markers to all nine added almost nothing. So tubular biomarkers are real but incremental, and creatinine plus albuminuria remain the workhorses.

Which makes the Kidney360 paper from Mi and colleagues the more immediately actionable of the two [7]. In a community cardiovascular high-risk cohort in Changzhou, China, nearly 2,000 participants with a mean age of 67 had first-morning urine albumin-to-creatinine ratios measured alongside conventional dipstick and eGFR screening. Elevated albuminuria was present in just over a third of participants, and dipstick sensitivity was only about 34 percent, meaning two thirds of albuminuric participants were dipstick-negative. Among those not flagged by conventional screening at all, roughly 28 percent were reclassified into the A2 or A3 albuminuria categories and about 2 percent into KDIGO high risk. Single abnormal values need confirmation, and this is a cross-sectional screening analysis rather than an outcome study, but the practical implication is clear: if you are screening a cardiovascular high-risk population and relying on dipstick, you are missing most of the albuminuria.

Also on the diagnostic front, the Journal of the American Society of Nephrology reports a quantum dot-based lateral flow strip for anti-nephrin autoantibodies in childhood idiopathic nephrotic syndrome from Lai and colleagues [10]. Across 191 paediatric serum samples the strip gave a result in ten minutes with sensitivity around 93 percent and specificity around 92 percent, and overall agreement with immunoprecipitation-Western blotting of about 92 percent. Antibody-positive children had heavier proteinuria and lower serum albumin. Notably, all twelve samples positive by strip but negative by Western blot lost signal on nephrin inhibition testing, suggesting the strip may be catching true positives the reference method misses. This is a bench-to-clinic assay development study, not a trial of management, but a ten-minute bedside anti-nephrin result would change how quickly podocytopathies are phenotyped.

The third theme is therapy and how we actually talk about it. In Nephrology Dialysis Transplantation, Yeung and colleagues addressed a very common bedside hesitation with a post-hoc analysis of the CREDENCE trial of canagliflozin in type 2 diabetes and chronic kidney disease [3]. Among 4,401 participants, over half were on five to nine medicines and roughly a third were on ten or more. The relative benefit on the composite of doubling of creatinine, kidney failure or cardiovascular or kidney death was consistent across every polypharmacy stratum, with no signal of differential harm, and discontinuation was actually lower on canagliflozin than placebo regardless of pill burden. Because event rates were higher in the heavily medicated groups, the estimated absolute benefit was largest precisely in the patients we are most reluctant to treat. Polypharmacy on its own is not a reason to withhold an SGLT2 inhibitor.

Also in Nephrology Dialysis Transplantation, Kim and colleagues used Korean national claims data covering more than 900,000 new users of acid suppression to compare tegoprazan, a potassium-competitive acid blocker, with proton pump inhibitors [6]. After propensity matching, proton pump inhibitor initiation was associated with roughly a fifth higher risk of newly coded chronic kidney disease, consistent across subgroups and sensitivity analyses. This is observational, the outcome is a coded diagnosis rather than adjudicated kidney disease, and confounding by indication and surveillance is hard to exclude entirely, but it adds comparative safety data for patients who genuinely need prolonged acid suppression.

Rounding out the therapeutic theme, Nature Reviews Nephrology carries a review from Tuttle and colleagues on inflammation as a target in kidney and cardiovascular disease [5], surveying the largely disappointing investigational history from selonsertib and bardoxolone through to interleukin-1 beta and interleukin-6 monoclonals, and noting that our proven drugs, renin-angiotensin blockade, SGLT2 inhibitors, GLP-1 receptor agonists and non-steroidal mineralocorticoid antagonists, all carry anti-inflammatory properties that may partly explain their benefit. And in a provocative review in the same journal, Zand and colleagues argue against routine protocol kidney biopsy in proliferative class III and class IV lupus nephritis [2], contending the evidence base for guiding relapse risk and immunosuppression withdrawal from repeat histology is weak, and that serological markers of immunological and clinical activity, anti-double-stranded DNA and complement levels, are the better guide. That is a genuinely contested position and worth reading critically.

Finally, in the Clinical Journal of the American Society of Nephrology, Wong and colleagues randomised 74 patients aged 75 and over with stage 4 or 5 chronic kidney disease to either usual care or a structured Jumpstart communication tool given to their nephrologist before the visit [8]. Discussion of conservative management rose from about a fifth of visits to about three fifths, and patients in the intervention arm rated their nephrologist's serious illness communication skills significantly higher after the visit, while control ratings did not move. It is a small single-region pilot, but a one-page prompt tripled the odds that an older patient heard about a legitimate treatment option.

If you only have time for one paper this week, make it the CREDENCE polypharmacy analysis [3]. It directly answers a hesitation that plays out in clinic every day and tells you the patients on ten medications are the ones with the most to gain, not the least.

Here are the key takeaways from this week in Nephrology. First, a gene-edited porcine kidney sustained dialysis independence for 271 days and was safely followed by human allotransplantation without detectable sensitisation or zoonotic transmission, though late microvascular injury remains the limiting problem. Second, do not let pill burden talk you out of an SGLT2 inhibitor in diabetic kidney disease, where absolute benefit is greatest in the most heavily medicated. Third, dipstick screening misses most albuminuria in cardiovascular high-risk community populations, so use a quantitative albumin-to-creatinine ratio and confirm abnormal results. Fourth, urine tubular biomarkers add only incremental discrimination on top of the kidney failure risk equation. And fifth, access to living donor transplantation and to an honest conversation about conservative management both depend heavily on system and clinician behaviour, and both are modifiable.

That's your roundup for This Week in Nephrology. The full transcript and references are available on the episode page in your AudioScholar library. This is an AI-curated summary — for clinical decisions, always consult primary sources and current guidelines. See you next week.

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