Volker Vallon


Affiliation: University of California
Country: USA


  1. Rieg T, Vallon V. Development of SGLT1 and SGLT2 inhibitors. Diabetologia. 2018;61:2079-2086 pubmed publisher
  2. Nespoux J, Vallon V. SGLT2 inhibition and kidney protection. Clin Sci (Lond). 2018;132:1329-1339 pubmed publisher
  3. Vallon V, Hummler E, Rieg T, Pochynyuk O, Bugaj V, Schroth J, et al. Thiazolidinedione-induced fluid retention is independent of collecting duct alphaENaC activity. J Am Soc Nephrol. 2009;20:721-9 pubmed publisher
    ..These data argue against a primary and critical role of ENaC in thiazolidinedione-induced fluid retention. ..
  4. Fattah H, Vallon V. The Potential Role of SGLT2 Inhibitors in the Treatment of Type 1 Diabetes Mellitus. Drugs. 2018;78:717-726 pubmed publisher
    ..More studies are needed with SGLT2 inhibitors in type 1 diabetic patients, including renal and cardiovascular clinical outcome trials, to fully evaluate their therapeutic potential in this specific population. ..
  5. Vallon V. The mechanisms and therapeutic potential of SGLT2 inhibitors in diabetes mellitus. Annu Rev Med. 2015;66:255-70 pubmed publisher
    ..By lowering blood pressure and diabetic glomerular hyperfiltration, SGLT2 inhibitors may induce protective effects on the kidney and cardiovascular system beyond blood glucose control. ..
  6. Vallon V, Miracle C, Thomson S. Adenosine and kidney function: potential implications in patients with heart failure. Eur J Heart Fail. 2008;10:176-87 pubmed publisher
    ..Despite these uncertainties, the available data on A(1)R antagonist therapy in patients with decompensated heart failure are promising and warrant confirmation in further studies. ..
  7. Vallon V, Osswald H. Adenosine receptors and the kidney. Handb Exp Pharmacol. 2009;:443-70 pubmed publisher
  8. Vallon V. The proximal tubule in the pathophysiology of the diabetic kidney. Am J Physiol Regul Integr Comp Physiol. 2011;300:R1009-22 pubmed publisher
    ..Importantly, these early proximal tubular changes can set the stage for oxidative stress, inflammation, hypoxia, and tubulointerstitial fibrosis, and thereby for the progression of diabetic renal disease. ..
  9. Vallon V, Thomson S. Renal function in diabetic disease models: the tubular system in the pathophysiology of the diabetic kidney. Annu Rev Physiol. 2012;74:351-75 pubmed publisher
    ..Although this growth phenotype explains unusual responses like the salt paradox of the early diabetic kidney, the activated molecular pathways may set the stage for tubulointerstitial injury and diabetic nephropathy. ..

More Information


  1. Vallon V, Platt K, Cunard R, Schroth J, Whaley J, Thomson S, et al. SGLT2 mediates glucose reabsorption in the early proximal tubule. J Am Soc Nephrol. 2011;22:104-12 pubmed publisher
    ..This mouse model mimics and explains the glucosuric phenotype of individuals carrying SLC5A2 mutations. ..
  2. Vallon V, Thomson S. Targeting renal glucose reabsorption to treat hyperglycaemia: the pleiotropic effects of SGLT2 inhibition. Diabetologia. 2017;60:215-225 pubmed publisher
    ..This review discusses the role of SGLT2 in the physiology and pathophysiology of renal glucose reabsorption and outlines the unexpected logic of inhibiting SGLT2 in the diabetic kidney. ..
  3. Vallon V, Rieg T, Ahn S, Wu W, Eraly S, Nigam S. Overlapping in vitro and in vivo specificities of the organic anion transporters OAT1 and OAT3 for loop and thiazide diuretics. Am J Physiol Renal Physiol. 2008;294:F867-73 pubmed publisher
    ..When searching for polymorphisms involved in human diuretic responsiveness, it may be necessary to consider both OAT1 and OAT3, among other genes. ..
  4. Vallon V, Komers R. Pathophysiology of the diabetic kidney. Compr Physiol. 2011;1:1175-232 pubmed publisher
  5. Vallon V, Rose M, Gerasimova M, Satriano J, Platt K, Koepsell H, et al. Knockout of Na-glucose transporter SGLT2 attenuates hyperglycemia and glomerular hyperfiltration but not kidney growth or injury in diabetes mellitus. Am J Physiol Renal Physiol. 2013;304:F156-67 pubmed publisher
  6. request reprint
    Vallon V, Lang F. New insights into the role of serum- and glucocorticoid-inducible kinase SGK1 in the regulation of renal function and blood pressure. Curr Opin Nephrol Hypertens. 2005;14:59-66 pubmed
    ..SGK1 may affect renal transport mechanisms beyond Na+ reabsorption and K+ secretion in ASDN. Polymorphisms of SGK1 may be relevant to the pathophysiology of hypertension and other diseases. ..
  7. Vallon V, Grahammer F, Volkl H, Sandu C, Richter K, Rexhepaj R, et al. KCNQ1-dependent transport in renal and gastrointestinal epithelia. Proc Natl Acad Sci U S A. 2005;102:17864-9 pubmed
    ..In mice lacking functional KCNQ1, impaired intestinal absorption is associated with reduced serum vitamin B12 concentrations, mild macrocytic anemia, and fecal loss of Na+ and K+, the latter affecting K+ homeostasis. ..
  8. Vallon V, Gerasimova M, Rose M, Masuda T, Satriano J, Mayoux E, et al. SGLT2 inhibitor empagliflozin reduces renal growth and albuminuria in proportion to hyperglycemia and prevents glomerular hyperfiltration in diabetic Akita mice. Am J Physiol Renal Physiol. 2014;306:F194-204 pubmed publisher
  9. Vallon V, Eraly S, Wikoff W, Rieg T, Kaler G, Truong D, et al. Organic anion transporter 3 contributes to the regulation of blood pressure. J Am Soc Nephrol. 2008;19:1732-40 pubmed publisher
    ..Moreover, polymorphisms in human OAT3 might contribute to the genetic variation in susceptibility to hypertension. ..
  10. Vallon V, Schroth J, Satriano J, Blantz R, Thomson S, Rieg T. Adenosine A(1) receptors determine glomerular hyperfiltration and the salt paradox in early streptozotocin diabetes mellitus. Nephron Physiol. 2009;111:p30-8 pubmed publisher
    ..A(1)Rs determine glomerular hyperfiltration and the salt paradox in early diabetes, which is consistent with the tubulocentric principle. ..
  11. Vallon V, Eraly S, Rao S, Gerasimova M, Rose M, Nagle M, et al. A role for the organic anion transporter OAT3 in renal creatinine secretion in mice. Am J Physiol Renal Physiol. 2012;302:F1293-9 pubmed publisher
    ..The results are consistent with a contribution of OAT3 and possibly OAT1 to renal creatinine secretion in mice. ..
  12. Rieg T, Masuda T, Gerasimova M, Mayoux E, Platt K, Powell D, et al. Increase in SGLT1-mediated transport explains renal glucose reabsorption during genetic and pharmacological SGLT2 inhibition in euglycemia. Am J Physiol Renal Physiol. 2014;306:F188-93 pubmed publisher
    ..When SGLT2 is fully inhibited by SGLT2-I, the increase in SGLT1-mediated glucose reabsorption explains why only 50-60% of filtered glucose is excreted. ..
  13. Vallon V, Rieg T. Regulation of renal NaCl and water transport by the ATP/UTP/P2Y2 receptor system. Am J Physiol Renal Physiol. 2011;301:F463-75 pubmed publisher
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    Vallon V, Richter K, Huang D, Rieg T, Schnermann J. Functional consequences at the single-nephron level of the lack of adenosine A1 receptors and tubuloglomerular feedback in mice. Pflugers Arch. 2004;448:214-21 pubmed
  15. Vallon V. Regulation of the Na+-Cl- cotransporter by dietary NaCl: a role for WNKs, SPAK, OSR1, and aldosterone. Kidney Int. 2008;74:1373-5 pubmed publisher
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    Vallon V, Wulff P, Huang D, Loffing J, Volkl H, Kuhl D, et al. Role of Sgk1 in salt and potassium homeostasis. Am J Physiol Regul Integr Comp Physiol. 2005;288:R4-10 pubmed
    ..Further studies are required to elucidate renal and nonrenal aldosterone-induced effects of Sgk1, the role of other Sgk1 activators, as well as the link of Sgk1 polymorphisms to arterial hypertension in humans. ..
  17. Vallon V, Schroth J, Lang F, Kuhl D, Uchida S. Expression and phosphorylation of the Na+-Cl- cotransporter NCC in vivo is regulated by dietary salt, potassium, and SGK1. Am J Physiol Renal Physiol. 2009;297:F704-12 pubmed publisher
    ..The two maneuvers dissociated plasma aldosterone levels from NCC expression and phosphorylation, implicating additional regulators. Regulation of NCC expression and phosphorylation by dietary NaCl restriction appears to involve SGK1. ..