This Week in Nephrology — Jun 6, 2026

Welcome to This Week in Nephrology. This week we're covering 10 notable papers, with a major focus on the expanding evidence for finerenone in chronic kidney disease, new data in glomerular disease, and important updates on risk management in advanced CKD. Let's dive in.

This week saw a trio of major publications solidifying the role of the non-steroidal mineralocorticoid receptor antagonist, finerenone, moving its benefits firmly beyond just diabetic kidney disease. The landmark paper comes from The New England Journal of Medicine, which published the primary results of the FIND-CKD trial [4]. In this study, over 1500 adults with chronic kidney disease *without* diabetes were randomized to finerenone or placebo. The key finding was that finerenone significantly slowed the rate of eGFR decline over 32 months. The mean annual decline was -3.3 ml per minute with finerenone, compared to -4.0 with placebo. While this may seem like a small difference, it was statistically significant and points to long-term kidney preservation. The trial also showed a lower risk for a composite of kidney or cardiovascular events in the finerenone group. As expected, hyperkalemia was more common with finerenone, occurring in 17% of patients versus 13% with placebo, but it led to treatment discontinuation in only 1.5% of participants. Building on this, a prespecified subgroup analysis of the same FIND-CKD trial, published in JAMA, focused specifically on the 903 participants with glomerular diseases, including IgA nephropathy and FSGS [5]. Here too, the results were positive. Finerenone slowed the annual rate of eGFR decline, reduced albuminuria at 12 months by 42%, and lowered the risk of a composite of kidney failure or a substantial loss of kidney function. Finally, The Lancet wraps this story up with the INFINITY pooled analysis, which combined individual patient data from over 14,000 participants across three major trials: FIDELIO-DKD, FIGARO-DKD, and the new FIND-CKD [2]. This powerful analysis confirms that finerenone consistently reduces the risk of kidney progression by 24% and a major cardiovascular outcome by 20% versus placebo. Crucially, these benefits were consistent regardless of whether patients had diabetes, their baseline eGFR or albuminuria level, or even if they were already on an SGLT2 inhibitor. The authors conclude that these findings support finerenone as a foundational therapy for CKD across a broad range of disease etiologies. Together, these three papers provide a compelling, unified message for expanding the use of this agent.

Staying on the topic of glomerular disease, The Lancet also published the final 2.5-year results from the ALIGN trial, which investigated atrasentan in patients with IgA nephropathy [6]. Atrasentan is a selective endothelin A receptor antagonist. In this trial of 340 patients on optimized renin-angiotensin system inhibition, the change in eGFR from baseline to week 136 was the key secondary endpoint. The results showed a trend toward benefit: patients on atrasentan lost 7.5 ml/min of eGFR, compared to 9.9 ml/min in the placebo group. This 2.4 ml/min difference did not quite reach statistical significance, with a p-value of 0.057. However, other measures, like the total eGFR slope, did show a significant benefit, and the drug was effective at reducing proteinuria. An exploratory analysis of a small subgroup also on SGLT2 inhibitors suggested a particularly strong effect in those patients. Importantly, the drug was well-tolerated, with similar rates of fluid retention between the atrasentan and placebo groups. This provides another potential tool for managing IgA nephropathy, although the primary endpoint's near-miss warrants careful interpretation.

Next, we turn to risk management in advanced kidney disease, where a major trial from JAMA provides a crucial, practice-changing negative result [7]. The TRACK trial randomized nearly 1500 patients with advanced CKD—stage 4, 5, or on dialysis—and high cardiovascular risk to low-dose rivaroxaban or placebo. The question was whether this antithrombotic strategy could reduce cardiovascular events. The answer was a clear no. After a median follow-up of 1.7 years, there was no difference in the primary composite outcome of cardiovascular death, MI, stroke, or peripheral artery events. What did increase, however, was harm. Major bleeding occurred in nearly 9% of patients on rivaroxaban compared to 6% on placebo, a statistically significant increase. The trial was stopped early for lack of efficacy. The take-home message is direct: low-dose rivaroxaban should not be used for cardiovascular protection in this population as it increases bleeding risk without providing benefit. Also this week, the Journal of the American Society of Nephrology provides a comprehensive clinical review on the diagnosis and management of lithium-associated nephrotoxicity [3]. The review covers the pathophysiology, highlighting that lithium can cause both acute and chronic kidney injury, most commonly a tubulointerstitial pattern. It reminds us that arginine vasopressin resistance is the most frequent complication, and that chronic kidney disease typically occurs after more than a decade of use. The authors provide a practical framework for management, emphasizing the use of the lowest effective dose, close monitoring, and the potential role of amiloride to mitigate toxicity by reducing cellular accumulation of lithium. It’s a valuable resource for a common clinical challenge.

Finally, several papers this week take a broader look at how we diagnose CKD and where the field is headed. A large observational study in JAMA used measured GFR via iohexol clearance in over 6,000 adults to validate our current diagnostic and risk-stratification practices [8]. The study confirmed that a measured GFR of 60 ml/min is indeed associated with a significant increase in all-cause mortality and kidney failure compared to a GFR of 90. It also compared our estimation equations to this gold standard. The finding? The 2021 CKD-EPI equation using both creatinine and cystatin C most closely mirrored the mortality risk associated with measured GFR. The creatinine-only equation tended to underestimate risk, while the cystatin C-only equation overestimated it. This provides strong support for incorporating cystatin C into clinical practice for more accurate risk assessment. To round out the week, The Lancet published two extensive reviews as part of a new series on chronic kidney disease. One paper focuses on the explosion of new therapeutics, like SGLT2 inhibitors and non-steroidal MRAs, discussing the challenges of implementing these drugs in complex patients with multimorbidity and polypharmacy [9]. A companion paper reviews advances in diagnosis and detection, from improved GFR estimation with cystatin C to the promise of artificial intelligence and multiomics [10]. And for those interested in how all this new evidence gets synthesized, Kidney International begins a new series on the KDIGO guideline development lifecycle, offering a look behind the curtain at how evidence becomes official recommendations [1].

If you only have time for one paper this week, make it the INFINITY pooled analysis of finerenone in The Lancet [2]. By combining data from over 14,000 patients across three major trials, it provides the strongest evidence to date that finerenone is a foundational therapy for CKD, with consistent kidney and cardiovascular benefits across a wide range of patients, both with and without diabetes.

Here are the key takeaways from this week in Nephrology: First: The evidence now strongly supports using finerenone to reduce kidney and cardiovascular risk across a broad spectrum of chronic kidney disease, including patients without diabetes and those with glomerular diseases. Monitor for hyperkalemia, but it is generally manageable. Second: In patients with IgA nephropathy on optimized RAS inhibition, the endothelin A receptor antagonist atrasentan reduces proteinuria and shows a strong trend toward slowing eGFR decline over the long term, with a favorable safety profile. Third: Do not use low-dose rivaroxaban for cardiovascular prevention in patients with advanced CKD, including those on dialysis. The TRACK trial clearly shows it increases bleeding risk without providing any cardiovascular benefit. Fourth: When assessing risk in your CKD patients, remember that the combined creatinine-cystatin C eGFR equation most closely reflects the true mortality risk associated with measured GFR. The creatinine-only equation may underestimate this risk. Fifth: For patients on lithium, maintain a high index of suspicion for nephrotoxicity. Using the lowest effective dose, monitoring function closely, and considering agents like amiloride are key strategies to mitigate kidney injury.

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.

This is an automated summary generated by artificial intelligence, which can make mistakes. Always review the original source materials.