Late-onset downregulation of NaPi-2 in experimental Fanconi syndrome

Yosef S. Haviv, Hanna Wald, Moshe Levi, Michal Dranitzki-Elhalel, Mordecai M. Popovtzer*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


The pathogenesis of renal phosphate (Pi) leak in Fanconi syndrome is unknown. Disorders of apical membrane transporters, leaky apical membrane, depleted cellular Pi and ATP, and impaired sodium (Na) pumps have been proposed as underlying defects. The present study examined the role of type II Na-Pi cotransport system (NaPi-2) in experimental Fanconi syndrome in rats. Following a single injection of maleic acid (MA), 75 mg/kg body weight IP, rats were sacrificed after 90 min, 4 h, and 24 h. Renal cortical expression of NaPi-2 mRNA was determined by Northern blotting, and brush border membrane (BBM) NaPi-2 protein by Western blotting. Increased urinary excretion of phosphate was demonstrated as soon as 90 min after MA injection, and was sustained at 4 and 24 h. NaPi-2 mRNA expression and NaPi-2 protein were not decreased after 90 min. NaPi-2 mRNA decreased after 4 h, while NaPi-2 protein decreased only at 24 h. Hence, the immediate phosphaturia in experimental Fanconi syndrome may be independent of NaPi-2 downregulation, possibly resulting from energy depletion or membrane dysfunction. The decrease in NaPi-2 mRNA expression and the subsequent NaPi-2 protein decrease may account for the second-phase phosphaturia.

Original languageAmerican English
Pages (from-to)412-416
Number of pages5
JournalPediatric Nephrology
Issue number5
StatePublished - May 2001
Externally publishedYes


  • Brush borders
  • Fanconi syndrome
  • NaPi-2 mRNA
  • NaPi-2 protein
  • Phosphate transport
  • Proximal tubule


Dive into the research topics of 'Late-onset downregulation of NaPi-2 in experimental Fanconi syndrome'. Together they form a unique fingerprint.

Cite this