Thomas R. Kleyman

This study shows that GRP170 protects podocytes from stress-induced glomerular injury by modulating the UPR, as demonstrated in a podocyte-specific knockout mouse model.

This study shows fructose-induced salt-sensitive hypertension is linked to abnormal MR activation in the ASDN, increasing ENaC expression and Na+ retention.

This study compares Na+ transporter expression and diuretic responses between two mouse strains, finding strain-dependent differences in NHE3, NKCC2, and NCC expression and diuretic efficacy.

This study shows that excess dietary sodium partially restores electrolyte imbalance and kidney injury markers in GRP170-deficient mice but not weight or tubule integrity.

This study identifies glucocorticoid receptor (GR) signaling in myeloid cells as a key contributor to salt-sensitive hypertension (SSBP) through SGK1 and IsoLG pathways, distinct from mineralocorticoid receptor (MR) mechanisms.

This study investigates the impact of proteolytic cleavage of the ENaC gamma subunit on Na+ and K+ handling in mice, finding that cleavage is not essential for channel activity in vivo.

The paper identifies new disease-associated ROMK variants using genomic databases and computational tools, revealing distinct molecular defects in protein folding and function.