ArticleThe Journal of physiology2011
Inhibition of K+ secretion in the distal nephron in nephrotic syndrome: possible role of albuminuria.
Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Vonoprazan attenuates proteinuria in diabetic kidney disease through potential direct renal mechanism.Scientific reports · 2025Trial
- Effectiveness and safety of finerenone in membranous nephropathy patients: a retrospective, real‑world study.International urology and nephrology · 2025Article
- Evolution of hypoxia and hypoxia-inducible factor asparaginyl hydroxylase regulation in chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023Article
- The exacerbated hypokalemia in membranous glomerulonephritis due to proximal tubular injury: a neglect issue from a case report and literature review.BMC nephrology · 2023Review
- Mechanistic insights into the primary and secondary alterations of renal ion and water transport in the distal nephron.Journal of internal medicine · 2023Review
- A variant of ASIC2 mediates sodium retention in nephrotic syndrome.JCI insight · 2021Article
- Role of hepcidin in oxidative stress and cell death of cultured mouse renal collecting duct cells: protection against iron and sensitization to cadmium.Archives of toxicology · 2021Article
- Increased colonic KScientific reports · 2021Article
- Inverse Regulation of Lipocalin-2/24p3 Receptor/SLC22A17 and Lipocalin-2 Expression by Tonicity, NFAT5/TonEBP and Arginine Vasopressin in Mouse Cortical Collecting Duct Cells mCCD(cl.1): Implications for Osmotolerance.International journal of molecular sciences · 2019Article
- Urine exosomes from healthy and hypertensive pregnancies display elevated level of α-subunit and cleaved α- and γ-subunits of the epithelial sodium channel-ENaC.Pflugers Archiv : European journal of physiology · 2017Article
- A Renal Olfactory Receptor Aids in Kidney Glucose Handling.Scientific reports · 2016Article
- Biochemical and Structural Characterization of the Interaction between the Siderocalin NGAL/LCN2 (Neutrophil Gelatinase-associated Lipocalin/Lipocalin 2) and the N-terminal Domain of Its Endocytic Receptor SLC22A17.The Journal of biological chemistry · 2016Article
- Urinary serine proteases and activation of ENaC in kidney--implications for physiological renal salt handling and hypertensive disorders with albuminuria.Pflugers Archiv : European journal of physiology · 2015Review
- A link between fertility and K+ homeostasis: role of the renal H,K-ATPase type 2.Pflugers Archiv : European journal of physiology · 2013Article
- Potassium homeostasis during nephrotic syndrome: signalling via filtered protein?The Journal of physiology · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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