Polycystic kidney disease is the most common monogenic cause of kidney failure and affects over 10 million individuals. We've known most PKD is caused by mutations in PKD1 for over 30 years. But how PKD1 prevents disease has remained mysterious, limiting effective therapy.

What an awesome session on common variant CKD genetics @ASNKidney #KidneyWk @kidneyomicsamps @LoebLab @LimdiNita

Nice talk by @LoebLab at #KidneyWk! -Approved targeted therapies for monogenic kidney disease -Next generation therapies for genetic disease

Incredible session on Genetics in Kidney Disease #KidneyWeek @ASNKidney Outstanding organization & insightful talks by @Vishal_D_Patel #DanielGale #AliGharavi #GabrielLoeb Grateful for the opportunity to present on Genetics of TMA🙏 Thx #ArleneChapman & #EmilieCornecLeGall

Thank you @ASNKidney! Our lab is very grateful to receive the 2025 Carl W. Gottschalk Research Scholar Grant. Read more about the work here: kidneycure.org/pages/qa.aspx….

#Whyscience Day51🧠✨A strong finish to our Renal Grand rounds series by a rising star physician scientists ⁦@LoebLab⁩ ⁦@UCSFNephrology⁩ Pushing the frontiers of kidney genomics and single cell omics. The future of nephrology is bright🔆

Exciting paper by @CanaudLab in @jclinicalinvest--doi.org/10.1172/JCI176402. 1) Somatic mutation as a (presumably) very rare cause of FSGS, 2) Targeting the mutated gene PIK3CA is helpful in multiple mouse FSGS models, 3) Activity of podocyte targeted therapy in mouse FSGS.

We are pleased to announce that the first participant has been dosed in our Phase 1 clinical trial evaluating MZE782. MZE782 is a potentially first-in-class, oral, small molecule targeting the solute transporter, SLC6A19, and has the potential to address chronic #kidneydisease (CKD) patients. Learn more about the MZE782 program here: businesswire.com/news/home/2…

Great paper that dissects the genetics of kidney function by combining GWAS results with data from single cell ATAC sequencing of kidney tissue. The authors make a strong case for the majority of the heritability of polygenic traits come from a small portion of disease-relevant regions in the genome and not from all over the genome. Using LD score heritability enrichment analysis, the authors show that - 63% of the SNP heritability of kidney function comes from cis regulatory elements related to kidney tubular epithelial cells (56%) and podocytes (7%), which together represent mere 5.4% of the genome - 10% come from coding regions containing genes well implicated in kidney function, either through Mendelian diseases or mouse knockout studies, which represent mere 1.4% of the genome - and the rest 27% of SNP heritability come from the remaining 93% of the genome. Loeb et al. Nat Gen nature.com/articles/s41588-0…