Phylogenetic, ontogenetic, and pathological aspects of the urine-concentrating mechanism

Yoshiaki Kondo, Tetsuji Morimoto, Toshiyuki Nishio, Ulviyya Fizuli Aslanova, Minako Nishino, Elnur Ilham Farajov, Noriko Sugawara, Naonori Kumagai, Atsushi Ohsaga, Yoshio Maruyama, Shori Takahashi

Research output: Contribution to journalReview articlepeer-review

13 Citations (Scopus)


The urine-concentrating mechanism is one of the most fundamental functions of avian and mammalian kidneys. This particular function of the kidneys developed as a system to accumulate NaCl in birds and as a system to accumulate NaCl and urea in mammals. Based on phylogenetic evidence, the mammalian urine-concentrating mechanism may have evolved as a modification of the renal medulla's NaCl accumulating system that is observed in birds. This qualitative conversion of the urine-concentrating mechanism in the mammalian inner medulla of the kidneys may occur during the neonatal period. Human kidneys have several suboptimal features caused by the neonatal conversion of the urine-concentrating mechanism. The urine-concentrating mechanism is composed of various functional molecules, including water channels, solute transporters, and vasopressin receptors. Abnormalities in water channels aquaporin (AQP)1 and AQP2, as well as in the vasopressin receptor V2R, are known to cause nephrogenic diabetes insipidus. An analysis of the pathological mechanism involved in nephrogenic diabetes insipidus suggests that molecular chaperones may improve the intracellular trafficking of AQP2 and V2R, and, in the near future, such chaperones may become a new clinical tool for treating nephrogenic diabetes insipidus.

Original languageEnglish
Pages (from-to)165-174
Number of pages10
JournalClinical and Experimental Nephrology
Issue number3
Publication statusPublished - 2006 Sept


  • Free water
  • Neonate
  • Nephrogenic diabetes insipidus
  • Ontogeny
  • Phylogeny
  • Urea
  • Vasopressin
  • Water and electrolyte metabolism


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