Gadolinium in dialysis patients.
What's up with that?
#Tweetorial
1/11
Nephrogenic systemic fibrosis (NSF) is an iatrogenic disease that presents with hardening of the skin and other organs. It is often lethal. I treated 5 people with this condition (including one with AKI). Terrible.
2/11
The etiology of NSF was unknown and there were many theories. In 2006, Thomas Grobner published a small case series showing 5 patients developing NSF within weeks of receiving gadolinium contrast for MRI.
3/11pubmed.ncbi.nlm.nih.gov/16431890/
This observation and theory was rapidly replicated and accepted as the cause of NSF. Nephrologists and radiologists stopped giving gadolinium to patients on dialysis and I haven't seen a case since.
4/11
In 2006 the FDA warned physicians and the public about the risk and then in 2007 added black box warnings to gadolinium based contrast agent package labels.
5/11 wayback.archive-it.org/7993/201610222…
But as we looked at the data further it appeared that not all contrast agents had the same toxicity. Gadodiamide (OmniScan) was the agent in 90% of the cases despite having a market share of only 30%.
The American College of Radiology (ACR) breaks down gadolinium based contrast agents (GBCA) into three categories based on the risk of NSF with:
Group 1 being high risk
Group 2 being low risk
Group 3 being unknown
7/11
The obvious recommendation is to choose GBCA from Group 2 and this was backed up by a meta analysis showing that following 4931 administrations of Group 2 GBCA to patients with CKD stage 4, 5 and ESRD, there were ZERO cases of NSF!
8/11 jamanetwork.com/journals/jamai…
For a deep dive into this check out @NephJC's coverage of this meta analysis:
or listen to the @FreelyFiltered podcast on the same manuscript
Gadolinium is removed by dialysis, with approximately 65% removed with a single dialysis session, and the ACR recommends dialyzing people after gad administration but not to initiate dialysis in patients with advanced CKD not on dialysis.
10/11 pubs.rsna.org/doi/full/10.11…
How is gad in ESRD handled at your institution
11/11
Next session started by Rovin to talk about IGAN pathophysiology and the selection of therapeutics
4-hit model 1. formation of IGA galactose deficient 2. formation of autoantibodies against these IgA 3. Formation of circulating IgG-IgA1 immune complexes 4. Deposition of the immune complexes in the kidney
#RKDSummit
1st case
Hematuria on U/A
Gross hematuria after covid vaccine
10 RBC/HPF, no casts
Scar 0.9 mg/dl, 24-hr urine 750 mg of protein
#RKDSummit
A bit “Juicy”
Mesangial expansion (arrows, fig 1)
Mesangial hypercellularity (circle, fig 2)
Biopsy has no chronicity (fig 3)
Lights up with C3 and IgA (fig 4)
When we published our study <> of ODS and hyponatremia we were pummeled for including people at low risk of ODS because we included Na levels between 120 and 130. They said it is well known "that ODS is incredibly rare/non-existent at those levels." 1/4evidence.nejm.org/doi/10.1056/EV…
Of course one of the reasons it was thought to be incredibly rare was that no one looked for CPM in patients with Na from 120-130. We found a fair number (≤5 of 12). 2/4
Our findings are replicated in a study from Australia. The authors took a different approach to investigating ODS. Instead of starting w/ hyponatremia and working forward to ODS, they started with a dx of ODS and worked backwards
3/4ncbi.nlm.nih.gov/pubmed/35717664
I just recently recommended the Renal Physiology book by Bruce Koeppen and Bruce Stanton. I thought it was a good medical student level text book: pbfluids.com/2023/08/ouwb-s…
But I came across this question in Chapter 8 Regulation of Acid Base. It is a straight forward question asking the learner to interpret simple acid-base cases.
But the question falls apart when you look at the answer...