Major faculty and Division research contributions

Since the Division’s founding in 1956, our faculty and staff have made some incredible contributions to nephrology research.


  • First successful hemodialysis conducted by division – 1958.
  • Proposed the “Intact nephron Hypothesis” – Bricker, Am J Medicine, 28:77-98, 1960.
  • First kidney transplant performed at Barnes Hospital – 1963.
  • First of a series of manuscripts detailing phosphate handling with reduced nephron mass – Slatopolsky et al, J Clin Invest, 47: 1865-1874, 1968.
  • Evidence for a circulating humoral factor in volume expansion and uremia – “third factor” – Bricker and KlahrNature, 219:1058-1059, 1968.
  • First demonstration of thromboxane A2 production by the injured kidney – Morrison et al, Nature, 267:259-260, 1977.


  • One of two laboratories in the country to first demonstrate arachidonic acid metabolism by the cytochrome P450 system in kidney. Morrison – Proc Natl Acad Sci, 165:508-511, 1980.
  • Demonstration of the relative contribution of hepatic and renal clearance of iPTH in normal and uremic animals – Hruska et al, J Clin Invest, 67:885-892, 1981.
  • The first-ever islet of Langerhans transplant to achieve insulin-independence is carried out at Barnes Hospital –1990.
  • Demonstration of Cl-/HCO3-regulation in the cortical collecting duct – Hamm et al, J Clin Invest, 87:1553-1558, 1991.
  • First demonstration that IGF-1 administered to individuals with ESRD is well tolerated and associated with increased GFR. – Hammerman et al, Kidney International, 46:201-207, 1994.
  • Demonstration of the essential role for laminin beta2 in glomerular permselectivity – Miner et al , Nat Genet, 10:400-406, 1995.
  • Provided conclusive evidence that phosphate restriction prevented parathyroid gland growth and secondary hyperparathyroidism in renal failure – Slatopolsky et al, J Clin Invest, 97:2534-2540, 1996.
  • First demonstration that functioning kidneys that excrete urine via the bladder can be “grown” in situ following transplantation of renal primordia – Hammerman et al, Kidney International, 54: 27-37, 1998.


  • Generated and characterized mouse models of two human glomerular basement membrane diseases (Person’s syndrome and Alport’s syndrome) – Miner et al, J Cell Biol, 135:1403-1413, 1996 and Chen and Miner, J Amer Soc Nephrol, 22: 849-856, 2011.
  • Demonstration that calcineurin is required in urinary tract mesenchyme for the development of the pyeloureteral peristaltic machinery – Feng Chen et alJ Clin Invest, 113:1051-1058, 2004.
  • Demonstration that congenital progressive hydronephrosis(cph) is caused by an S256L mutation in aquaporin-2 that affects phosphorylation and apical membrane accumulation – Feng Chen et al, Proc Natl Acad Sci, 103: 6952-6957, 2006.
  • Proposed what remains today the most effective induction regimen for renal transplantation -– Brennan et al, NEJM, 355: 1967-1977, 2006.
  • Demonstration that claudin-16 and claudin-19 interact to form a cation-selective complex regulating Mg reabsorption in TALH – Hou et al, J Clin Invest, 118: 619-628, 2008.
  • Demonstration that Claudin-4 forms a paracellular chloride channel in the kidney and requires Claudin-8 for tight junction localization – Hou et al, Proc Natl Acad Sci, 107: 18010-18015, 2010.
  • First demonstration of the tight junction’s role in kidney stone pathogenesis – Hou et al, EMBO Journal, 31: 1999-2012, 2012.
  • Demonstration of novel early regulatory mechanisms of early upper and lower urinary tract patterning by RetY1015 docking tyrosine in mice including the importance of MAPK signaling in multiple budding, boundary formation and joining of ureters to bladder – Jain et al, Development, 139: 2405-2415, 2012.
  • Discovery that common rare and novel functional deleterious variants in RET signaling complex account for up to 5% of urinary tract malformations in living US patients – Jain et al, Human Genetics, 131: 1725-1738, 2014.