RGD Reference Report - Inhibition of K+ secretion in the distal nephron in nephrotic syndrome: possible role of albuminuria. - Rat Genome Database

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Inhibition of K+ secretion in the distal nephron in nephrotic syndrome: possible role of albuminuria.

Authors: Fila, M  Brideau, G  Morla, L  Cheval, L  Deschenes, G  Doucet, A 
Citation: Fila M, etal., J Physiol. 2011 Jul 15;589(Pt 14):3611-21. doi: 10.1113/jphysiol.2011.209692. Epub 2011 May 23.
RGD ID: 7244390
Pubmed: PMID:21606114   (View Abstract at PubMed)
PMCID: PMC3167121   (View Article at PubMed Central)
DOI: DOI:10.1113/jphysiol.2011.209692   (Journal Full-text)

Nephrotic syndrome features massive proteinuria and retention of sodium which promotes ascite formation. In the puromycin aminonucleoside-induced rat model of nephrotic syndrome, sodium retention originates from the collecting duct where it generates a driving force for potassium secretion. However, there is no evidence for urinary potassium loss or hypokalaemia in the nephrotic syndrome. We therefore investigated the mechanism preventing urinary potassium loss in the nephrotic rats and, for comparison, in hypovolaemic rats, another model displaying increased sodium reabsorption in collecting ducts. We found that sodium retention is not associated with urinary loss of potassium in either nephrotic or hypovolaemic rats, but that different mechanisms account for potassium conservation in the two models. Collecting ducts from hypovolaemic rats displayed high expression of the potassium-secreting channel ROMK but no driving force for potassium secretion owing to low luminal sodium availability. In contrast, collecting ducts from nephrotic rats displayed a high driving force for potassium secretion but no ROMK. Down-regulation of ROMK in nephrotic rats probably stems from phosphorylation of ERK arising from the presence of proteins in the luminal fluid. In addition, nephrotic rats displayed a blunted capacity to excrete potassium when fed a potassium-rich diet, and developed hyperkalaemia. As nephrotic patients were found to display plasma potassium levels in the normal to high range, we would recommend not only a low sodium diet but also a controlled potassium diet for patients with nephrotic syndrome.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
KCNJ1Humannephrotic syndrome  ISOKcnj1 (Rattus norvegicus) RGD 
Kcnj1Ratnephrotic syndrome  IEP  RGD 
Kcnj1Mousenephrotic syndrome  ISOKcnj1 (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Kcnj1  (potassium inwardly-rectifying channel, subfamily J, member 1)

Genes (Mus musculus)
Kcnj1  (potassium inwardly-rectifying channel, subfamily J, member 1)

Genes (Homo sapiens)
KCNJ1  (potassium inwardly rectifying channel subfamily J member 1)


Additional Information