Huge fan of spiro, but wouldn’t use it first-line if I didn’t suspect hyperaldosteronism. No CVD outcome data and the side effects for men are not trivial. Don’t feel that the modest effect on BP in primary HTN justifies its use over A/C/D.
Posts by Iain Bressendorff, MD PhD
& I will go one step further
The A-C-D combo as first line is based on ALLHAT where Spiro was not on the table
arguably Spiro could even be first line in primary hypertension if we did ALLHAT 2.0
Sodium (yes I am saying that) is so important that Spiro/HCTZ combo makes a great first line drug
I’m seeing more and more ptt referred for resistant HTN and not meeting criteria for PA, once starting spiro gradually come off almost all other drugs. Even after >1 year BP keeps dropping. Assume it is sodium offloading, why else the gradual effect over such a long period?
@hswapnil.medsky.social
Since atrasentan is bound to be approved for use in IgAN, does anyone know whether it will be revived for DKD?
SONAR did in fact show that it was effective, but the premature termination and upstaging by CREDENCE sort of left atrasentan for dead…
#askrenal
Don’t buy that. It’s a relentlessly progressive disease that has shown progression…
but still >3 ml/min loss over 2 years 😳 slowing but not halting disease
Agree to both points. Stop the cause of the disease, not the downstream consequences.
If price were different, would consider complement inhibition as part of “induction” on top of BAFF/APRIL inhibition and stop after weeks/months. But this will not happen…
Figure 2 Survival at 24-month from randomization free of (A) renal flares, (B) extra-renal flares and (C) overall clinical flares in lupus nephritis patients presenting with asymptomatic serological reactivation and randomized to receive pre-emptive treatment (PT Group) or observant management (Control Group).
Interesting trial in @kidneyint@bsky.social
www.kidney-international.org/article/S008...
SLE with remission. No symptoms. When dsDNA becomes positive (or doubles) do you preemptively increase immunosuppression?
#NephSky #RheumSky
"Over 80% of participants with obesity-related hypertension exhibited reproducible pathologic phenotypes of aldosteronism and/or hypercortisolism"
www.jacc.org/doi/10.1016/...
Figure one showing more divers with high dose furosemide
Research letter, pilot trial from Mayo ($locked)
pubmed.ncbi.nlm.nih.gov/41802270/
Diuretic resistance is mostly inadequate furosemide dose. Torsemide not needed™️
(Incidence of deafness 🧏🏽♂️ not reported)
thanks 😃
There’s talk of targeting immunological remission (normal dsDNA and normal C3/C4) instead of just lowering proteinuria. Do you specifically treat or escalate treatment to target this?
My patient still has high dsDNA despite clinical remission.
Thanks. How often do you dose in maintenance? Seems B-cell depletion last up to a year with obi.
Is anyone using obinutuzumab for maintenance in SLE (I know there is no data)?
Have young pt with LN III/IV, MMF + prednisone induction. Doing well, but persistently high dsDNA, C3/C4 normal.
@kidneydoc101.bsky.social @juancarlosqvelez.bsky.social @kronbichlerlab.bsky.social @grahamabra.bsky.social
indeed, similar effect size to the NefIgArd trial. I’m convinced…
We report it for outpatients
We don’t report it for inpatients - it’s easy to calculate if you want to
Don’t check until next follow-up and don’t hold based an any arbitrary increase in creatinine, go by symptoms.
Don’t hold diuretics either.
No problems so far, knock on wood…
Very cool paper from Hamburg! Urinary CD4+ T cells identify Sjögren's patients with nephritis and help monitor treatment response! Awesome work!
pubmed.ncbi.nlm.nih.gov/41673408/
#NephSky
SGLT2i increases urinary EGF, unknown mechanism
likely related to increased urinary epithelial growth factor (EGF), which stimulates expression of TRPM6 in the DCT through the EGF receptor leading to increased tubular reabsorption of Mg
Glomerular basement membrane (GBM) structural integrity dictates trans-tissu... www.sciencedirect.com/science/arti... Really proud of this Cell Reports paper showing that the potentially pathogenic laminin alpha2 in the Alport GBM comes not from glomerular cells, but from the bloodstream.
Yeah, the science is intriguing and I want to be using it for that reason, but so far we’re sticking with ESA for CKD at my department.
In Denmark, HIFs are priced the same as ESA, so the only argument is convenience and needles, not cost.
Not worried about safety, just doesn’t seem that much of a hassle to use ESA.
Maybe I’m being reactionary, but we have a lot of experience with ESA and don’t see a big need for HIF-PHI.
But then again, I’m not the one getting the injections… 😜
In which situation would you use it?
PD? CKD?
Despite the cool science, I have to agree with @kidneyboy.bsky.social on this…
#NephJC
The things that have changed or most influenced my approach to anemia are:
Daniel Coyne
DRIVE 2
PIVOTAL
CHOIR/CREATE/TREAT
(No KDOQI or KDIGO guideline)
#NephJC
Or seeing a lot of young patients with positive cross-matches and with no other cause of allo-/isoimmunization. If not the principal cause of their symptoms/ death-treatening, I always think twice if it's worth it #nephjc
Completely agree. Same for PLA2R-negative membranous. Recently saw a patient with longstanding disease and gradual remission, then increasing proteinuria. Almost restarted rituximab, but bx showed no deposits, only chronic FSGS lesions.
Proteinuria now in remission after tight BP control.
fair amount of chat on hypertension and AKI/critical care. Not much GN and transplantation.
fun review if anyone is interested www.ahajournals.org/doi/10.1161/...
Vaughan Pendred was a house surgeon at Guy's hospital when he reported deaf-mutism with goitre www.sciencedirect.com/science/arti... in @thelancet.com - and went on to become a ....(not nephrologist) a general practitioner
@dialysisbloke.bsky.social
Applied the VIPAR protocol to a patient with cAMR, first time in our centre.
Fingers crossed for positive results 🤞🏻
Just wanted to let you know that it’s being used out there 🤓