Laboratory of Vivek Bhalla, MD- Stanford

Thank you to @rmh199 @StanfordDeptMed for highlighting our work

Amazing. Remembering Michelle Winn’s work that pointed the way to this moment. pubmed.ncbi.nlm.nih.gov/15879175/

This month marks 10 years of JCI Insight! A special shoutout to authors, editors, reviewers, readers, and all those dedicated to biomedical research, ranging from preclinical to clinical studies. This video highlights selected covers through the years. — Music: Bensound; License code: LDOZSSOUYFKAOLR8; Artist: Theatre Of Delays @Eickelberg_MD

@proychaudhuryMD @ASNKidney Thank you for your leadership and happy new year 🎊

Today is my last day as ASN President @ASNKidney. The best part of my year by far was the opportunity to meet so many of you in the kidney community all over the world. Which is why I know that the future of nephrology is in good hands. Thank you for all your help and support.

Please help us bring hope and light into this Holiday Season. One of our @StanfordNeph @StanfordAbdTxp faculty families is working to save their child’s life from a rare genetic condition. Please read, share and support. rarebreak.org

@Joseph_C_Wu @StanfordDeptMed @StanfordMed @ScienceTM @StanfordCVI @Stanford_ChEMH @stanfordimmuno @CellStanford @GreenstoneBio @brucegoldman Congrats, @Joseph_C_Wu

Congrats @StanfordMed scientists for publishing @ScienceTM showing how mRNA-based COVID vaccines can cause myocarditis via CXCL10-TNFy signaling axis. @StanfordCVI @Stanford_ChEMH @StanfordDeptMed @stanfordimmuno @CellStanford @GreenstoneBio @brucegoldman med.stanford.edu/news/all-news/…

@kidneyomicsamps @WashU Congrats!

Superduper congrats to my daughter Lily for getting in early decision to @WashU.

Thanks to Jordy and Tammy for their leadership on this important statement! @jordy_bc @TammyBradyMD

who sought to sift through these factors to demonstrate that this could indeed work. There is lots to still do, both in lab and in clinic, and there are risks/benefits to calculate, but for those families suffering with a rare disease, this may be possible @StanfordNeph 4/x.

but there are only historical controls and multiple confounding factors in patients who receive tacrolimus (diuretics, PJP prophylaxis, PPIs, RAASi, etc). I'm thankful to Ms. Halee Yue @UCLAHealth and Dr. Martina Cacciapuoti @MartiCacciaNeph 3/x

Dissecting through renal physiology in the context of patient care is difficult but eminently valuable. Inspired by the landmark work of Hoorn et al., nature.com/articles/nm.24… showing the effect of tacrolimus on phosphorylated NCC, we sought to understand if the use of CNIs 1/x.

Please contact us if you are interested ….

We are thrilled to announce that we have generously received funding for a one-year hypertension fellowship, and we are recruiting now for a candidate to start fellowship July 1, 2026 . med.stanford.edu/hypertension/e… -Jehan Zahid Bahrainwala HTN Fellowship Program Director

This might be the most badass brief report I’ve read in a long time. In @NEJM A team just published what feels like a glimpse straight into the future of cellular therapeutics: successful survival and function of transplanted allogeneic, CRISPR-edited beta cells with zero immunosuppression — in a real human with long-standing type 1 diabetes. No anti-rejection meds. No immune flare. Glucose-responsive insulin secretion documented weeks after implantation. A clean safety profile. This is the kind of translational science that makes you think about how close we might be to rewriting what’s possible in autoimmune and metabolic disease. Medicine is moving fast. This is one of those papers that makes you feel it.

Game changer. ASI directed PET imaging informs the pathogenesis, diagnosis, subtyping, and treatment of primary aldosteronism, but more broadly, hypertension in general. nejm.org/doi/full/10.10…

Some useful information about grants that were supposed to be reviewed during the shutdown.

Prevalence of the M1 Modifier p.N264K in APOL1 Among Individuals With Kidney Disease Undergoing Commercial Genetic Testing in the United States bit.ly/48PB2xk (FREE) @BhallaResearch @gchertow @DianneKeenkim @vcharuMD

Another incredible GWAS finding this year: an African ancestry–specific missense variant confers the largest common-variant risk effect reported to date for SLE. Just weeks ago, there was a GWAS paper reporting the discovery of a major genetic risk factor for dilated cardiomyopathy--an African ancestry-specific loss of function variant in CD36--explaining up to 8% of the cases in African populations. (x.com/doctorveera/st…). Now, deCODE Genetics has uncovered a major genetic risk factor for lupus, a missense variant p.Glu502Lys in IKBKB, explaining 10.4% of cutaneous lupus (CLE) and 6.4% of cases of systemic lupus (SLE) in African populations. The variant increases CLE risk by 5.4 fold, uncovered by comparing just 211 cases to 25,360 controls of African ancestry from the Alliance for Genomic Discovery (AGD). It highlights how deeply African ancestries have been underrepresented in lupus GWAS efforts. Lupus is more common (2-3x) and more severe in individuals of African ancestry compared with those of European ancestry. Certain forms, like discoid lupus, are 10 times more common in African populations. Despite that, only one of the past 33 SLE GWASs involved African-ancestry population!! Interestingly, that one study (Langefeld et al. Nat Comm 2017) that involved African ancestry individuals actually captured this IKBKB locus (connecting the signal to a different nearby gene, PLAT), but they seemed to have never identified the right gene and overlooked the importance of the finding. Here is a plot I roughly made to highlight the effect size of this variant. The plot compares the effect sizes vs minor allele frequency of GWAS loci reported the past large SLE studies in European (Bentham et al. Nat Gen 2015) and East Asian ancestries (Yin et al. Ann Rheum Dis 2021). I overlayed the IKBKB missense variant to show the it's effect size for SLE dwarfing even the largest effect sizes reported for HLA variants. The allele frequency of this missense variant in African ancestries is ~1%. Around 2% of the African ancestry individuals are carriers, and among the SLE/CLE cases, more than 10% carry this variant. Amazing! Analyzing related clinical phenotypes, the authors found that the carriers tend to have a more severe phenotype (more CLE, more glomerular involvement, proteinuria and lower blood counts). The gene IKBKB encodes an immune protein that activates the NF-κB signaling, a key immune response pathway. Partial or complete loss of IKBKB cause Mendelian forms of immunodeficiency conditions. The missense variant likely confers a gain of function effect leading to autoimmunity. This discovery highlights the importance of NF-κB signaling in lupus pathogenesis, particularly in individuals of African ancestries. The finding has many translational implications, for example, it suggests a large target population (~10% of African cases) for any NF-κB targeted SLE treatment. Another great work by deCODE scientists! Thorlacius et al. Nat Gen 2025