RGD Reference Report - Altered expression of type II sodium/phosphate cotransporter in polycystic kidney disease. - Rat Genome Database

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Altered expression of type II sodium/phosphate cotransporter in polycystic kidney disease.

Authors: Vogel, M  Kranzlin, B  Biber, J  Murer, H  Gretz, N  Bachmann, S 
Citation: Vogel M, etal., J Am Soc Nephrol. 2000 Oct;11(10):1926-32.
RGD ID: 7242933
Pubmed: PMID:11004225   (View Abstract at PubMed)

Renal phosphate (Pi) absorption is mediated via the type II sodium/Pi cotransporter (NaPi-2) in the brush border membrane (BBM) of proximal tubules. Simultaneous detection of NaPi-2 mRNA by in situ hybridization and of NaPi-2 immunoreactivity by immunohistochemistry was performed to investigate the distribution of the cotransporter in healthy control rats and during progression of autosomal dominant polycystic kidney disease (ADPKD). The purpose of the study was to disclose a relation between proximal tubular cell differentiation and NaPi-2 expression. In controls, NaPi-2 expression was present in the entire proximal tubule. In the Han:SPRD (cy/+) model for ADPKD, the proximal nephron is primarily affected by the cystic changes. Epithelial proliferation and impaired epithelial-matrix interaction result in a loss of cell differentiation that eventually leads to cystic enlargement of the nephron. Normal expression of NaPi-2 in this model was found only in tubules with intact BBM. Loss of BBM and cellular interdigitation were paralleled by the loss of NaPi-2 in situ hybridization and immunoreactive signals. These changes were moderate and focal in 2-mo-old rats and generalized all over the cortex after 8 mo. Advanced renal damage in the older PKD group was associated with mild phosphaturia, which suggests functional insufficiency of tubular NaPi-2 reabsorption. These data show how proliferative changes and loss of tubular epithelial differentiation in ADPKD may prevent functional expression of the NaPi-2 system in the proximal tubule in a rapidly progressive manner. NaPi-2 in proximal tubule BBM is suggested to play an important role in impaired tubular absorption of Pi in renal disease.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
autosomal dominant polycystic kidney disease disease_progressionISOSlc34a1 (Rattus norvegicus)7242933; 7242933mRNA and protein:altered expression:renal cortex (rat)RGD 
autosomal dominant polycystic kidney disease disease_progressionIEP 7242933mRNA and protein:altered expression:renal cortex (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Slc34a1  (solute carrier family 34 member 1)

Genes (Mus musculus)
Slc34a1  (solute carrier family 34 (sodium phosphate), member 1)

Genes (Homo sapiens)
SLC34A1  (solute carrier family 34 member 1)


Additional Information