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Researchers looked at nearly 50,000 kidney biopsy records from diabetic patients collected between 2001 and 2024. They wanted to understand how often biopsies find a second kidney disease hiding alongside diabetes, and whether this discovery changes how sick patients become. Nearly 60% of diabetic patients who got a kidney biopsy had a second, non-diabetic kidney disease. About one-third of these patients had a second disease as their only finding, while the other one-third had both the diabetic kidney disease and something else. Patients who were very young (under 30) or older (60+) were more likely to have a second disease. When patients had an acute flare-up or acute inflammation, biopsies found a second disease more often. Diabetic patients who had both diabetes-related and non-diabetic kidney disease were significantly less likely to progress to kidney failure compared to those with diabetes alone. The study shows that kidney biopsies are genuinely useful in diabetic patients because they frequently catch other diseases that change how doctors treat and monitor the patient.

What is this study about? T cell exhaustion is a big reason cancer immunotherapies stop working, but most of what we know comes from looking at RNA. This study looks at what is happening at the protein level as T cells become exhausted, including how proteins are made, how fast they turn over, and how they are tagged with ubiquitin. What did they do? They modeled exhaustion in CD8+ T cells from 6 healthy donors, comparing acute, chronic, and restimulated conditions. The restim control helps separate true exhaustion from the effects of recent activation. They combined RNA-seq, protein abundance, protein turnover (half-lives for 5,880 proteins), and ubiquitin proteomics (over 22,000 ubiquitination sites). They then checked E3 ubiquitin ligases against single-cell data from 48 melanoma tumors and tested RNF166 overexpression in mouse and human CAR T cells and in two mouse tumor models. Why does this matter? Exhausted T cells turn over proteins more slowly (median half-life 13.9 vs 12.2 hours), and RNA only partly predicts what happens to protein (r = 0.60), so transcript data alone misses a lot. RNF166 is lost as T cells exhaust, and adding it back improved T cell persistence, tumor control, and survival in both mouse models. That points to protein turnover and E3 ligases as new targets for improving immunotherapy.

What is this report about? C3G and IC-MPGN are ultrarare kidney diseases driven by overactivation of the alternative complement pathway, and up to 50% of patients progress to kidney failure within 10 years. Two new complement inhibitors, iptacopan and pegcetacoplan, are now approved. This report looks at how to get patients diagnosed sooner and onto these drugs quickly and fairly. What did they do? This is a meeting report, not a cohort study. The SEISMIC summit in July 2025 brought together about 100 people (63 in person, 36 virtual), including clinicians, patients and caregivers, regulators, payers, and industry reps. A pre-meeting survey of 30 physicians and 43 patients and caregivers helped set the agenda, and the group worked through diagnosis, management, and access in three sessions. Why does this matter? Diagnosis is slow. Fewer than 40% of surveyed patients had a diagnostic biopsy within 6 months of symptoms, and for 21% it took more than 5 years. There’s a pathology angle too. The report calls for better communication between nephrologists and pathologists, consistent nomenclature (for example, reporting “C3 dominant glomerulonephritis” instead of “C3 glomerulopathy” on the diagnostic line), and standards for biopsy processing and reporting. A majority also supported using the new drugs first line in active disease, with cost and access named as the big hurdles.

What is this study about? Glomerulopathy with striated deposits (GSD) is a very rare kidney disease defined by deposits with a striated, muscle-like pattern on electron microscopy. Until now it had only been described in a handful of case reports. This study looks at the clinical and pathologic picture and the outcomes in a larger group. What did they do? The team searched the kidney biopsy archives at Mayo Clinic and Columbia from 2011 to 2025 and found 18 confirmed GSD cases. They reviewed the EM, light microscopy, and IF findings, including IF on pronase-digested paraffin tissue to unmask hidden immunoglobulin deposits. They also pulled clinical, hematologic, treatment, and follow-up data, and ran mass spec on 4 cases. Why does this matter? Most patients were older (median age 73) with CKD and proteinuria, and 88% had a hematologic condition, most often MGRS. Over half of the cases had monotypic Ig deposits, and in 6 of those 10 the deposits were masked and only showed up with paraffin IF after pronase digestion. About 40% of patients with follow-up progressed to kidney failure within a median of 11 months, and all 4 patients who got clone-directed therapy had a kidney response. The authors propose adding GSD with monotypic Ig deposits to the list of MGRS lesions.

What is this study about? Kikuchi-Fujimoto Disease (KFD) is a rare, self-limiting condition that mainly affects lymph nodes. It causes a distinctive pattern of necrotizing inflammation with lots of cell death and debris. This pattern has been seen in skin and lymph nodes, but it has almost never been documented in the kidney. Before this study, there were only 4 reported cases, all in abstract form. That includes 3 cases Drs. Ambruzs, Cossey, and Larsen presented back in 2014. What did they do? The team reviewed 20 years of kidney biopsy records from Arkana, OHSU, and Renopath. They found 9 patients with this KF-like inflammation in the kidney. They compared these patients to 8 patients who had confirmed systemic KFD and also had a kidney biopsy. This comparison group is the largest reported series of KFD patients with kidney biopsies. Why does this matter? 8 of the 9 patients with the KF-like kidney pattern had diagnosed or suspected lupus, and none had systemic KFD. Most had little or no glomerular involvement, which is unusual for active lupus. None of the systemic KFD patients showed this pattern in the kidney. The authors describe this as a novel, lupus-associated form of interstitial nephritis. That gives pathologists a new pattern to recognize and adds to the differential when this type of infiltrate shows up on biopsy.