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Metabolism and Renal Physiology

Our team studies the mechanisms by which the kidney regulates ionic transport, adapts to its environment, and controls ionic homeostasis; our investigations span all scales, from genes to the entire organism.

Our work focuses on the mechanisms of ion transport (Na, K, Cl- and divalentcations) along the renal tubules, their regulation, and their dysfunction in primary or secondary renal diseases, such as hereditary tubulopathies, hypertension, and disorders of divalent cation homeostasis. We also study the cross-talk between the kidney and other tissues (gut, muscle, bone) in homeostatic regulation. Our studies integrate all scales between genes and the whole organism. The techniques we use are available through our facility for in vivo and ex vivo kidney phenotyping. Our projects have both fundamental goals and clinical objectives (e.g., identification of candidate genes/pathways in hereditary diseases, and development of new drugs). Our connections to clinical departments allow us to perform clinical investigations in patients. Recent findings include:


  • The discovery of a new, thiazide-sensitive pathway for sodium reabsorption in the aldosterone-sensitive distal nephron.
  • The demonstration that basolateral potassium channels are important modulators of renal sodium reabsorption.
  • The identification of proteases as local mediators of sodium and potassium transport.
  • The demonstration that progesterone is a potassium-sparing hormone in both genders.
  • The discovery of GDF15 as a growth factor promoting adaptive proliferation of fully differentiated tubular epithelial cells.
  • The evidence that the renal calcium-sensing receptor may be a target for treating acquired and inherited calcium homeostasis disorders.

The Kir4.1/Kir5.1 protein complex forms the major basolateral K conductance of the native distal nephron and a defect in salt re-uptake by distal convoluted tubule (DCT) cells is observed in humans with KCNJ10 mutations, leading to a loss of function of the Kir4.1 subunit and ultimately to the hypokalaemic metabolic alcalosis encountered in the SeSAMe syndrome. 





Team Leaders : Gilles CRAMBERT (Dr)  / Pascal HOUILLIER (Pr) 

Team Members : Caroline BERTOYE (Dr), Alain DOUCET (Dr), Kamel LAGHMANI (Dr), Stéphane LOURDEL (Dr), Marc PAULAIS (Dr), Gabrielle PLANELLES (Dr), Jacques TEULON (Pr)
Gaëlle BRIDEAU (Eng), Lydie CHEVAL (Eng), Sylvie DEMARETZ (Eng), Clément DOUCET (Tec), Nadia FRACHON (Eng), Camille GRIVEAU (Eng), Christine LAMOUROUX (Eng), Luciana MORLA (Eng).
Naziah BAKOUH (Post-Doc), Imene SAKHI (PhD). 

Administration : Dalila HAKER

Contact details:  33 1 44 27 50 03

Team Web SIte :


Selected Publications

  • Seaayfan E, Defontaine N, Demaretz S, Zaarour N, Laghmani K. OS9 interacts with NKCC2 and targets its immature form for the endoplasmic-reticulum-associated . J Biol Chem. 2015 Dec 31. PMID: 26721884. 
  • Edwards A, Castrop H, Laghmani K, Vallon V, Layton AT. Effects of NKCC2 isoform regulation on NaCl transport in thick ascending limb and macula densa: a modeling study. Am J Physiol Renal Physiol 307: F137-F146, 2014.
  • Tokonami N*, Morla L*, Centevo G, Mordasini D, Ramakrishnan SK, Nikolaeva S, Wagner CA, Bonny O, Houillier P, Doucet A, Firsov D. Alpha-ketoglutarate regulates acid-base balance through an intra-renal paracrine mechanism. J Clin Invest 123: 3166-3171, 2013.
  • Paulais M, Bloch-Faure M, Picard N, Jacques T, Ramakrishnan SK, Keck M, Sohet F, Eladari D, Houillier P, Lourdel S, Teulon J, Tucker SJ. Renal phenotype in mice lacking the Kir5.1 (Kcnj16) K channel subunit contrasts with that observed in SeSAME/EAST syndrome. Proc Natl Acad Sci U S A, 108:10361-10366, 2011.
  • Elabida A*, Edwards A*, Salhi A, Azroyan A, Fodstad H, Meneton P, Doucet A, Bloch-Faure M, Crambert G. Chronic potassium depletion increases adrenal progesterone production which is necessary for efficient renal retention of potassium. Kidney International 80: 256-262, 2011.

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Link to PubMed


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