Plasmin and sodium retention in nephrotic syndrome.

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

Who cites it

5 citing papers in PubMed, 8 citations in OpenAlex.

1. Mechanistic insights into the primary and secondary alterations of renal ion and water transport in the distal nephron.Journal of internal medicine · 2023
   Review
2. Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome.Acta physiologica (Oxford, England) · 2021
   Article
3. Increased urinary sodium excretion is associated with systolic blood pressure in first degree relatives of hypertensive patients in Ibadan, Southwestern Nigeria.The Pan African medical journal · 2018
   Article
4. Plasmin and chymotrypsin have distinct preferences for channel activating cleavage sites in the γ subunit of the human epithelial sodium channel.The Journal of general physiology · 2012
   Article
5. Tissue kallikrein activation of the epithelial Na channel.American journal of physiology. Renal physiology · 2012
   Article

Corrections and comments

• Comment on
  Plasmin in nephrotic urine activates the epithelial sodium channel.2009

Authors and funding

2 authors.

Funding

Abstract

PubMed holds no abstract for this paper.

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