Can hydralazine trigger ANCA vasculitis? — NephJC A large registry cohort was essential to move beyond scattered case reports and finally quantify the true risk of hydralazine‑associated vasculitis. When rare events blur into background noise, only s...

Check out the VA on hydralazine and population vasculitis risk by Dr. Divya Bajpai #NephSky
www.nephjc.com/news/2026/4/hydralazine-anca-va

What considerations should be included in your differential diagnosis given the provided histologic finding?

#DiagnoseThis #nephtwitter #pathtwitter #renal #kidneypath

M1 Variant Lowers APOL1 Kidney Disease Risk Although APOL1 variants are linked to kidney disease risk, the presence of the M1 genetic variant appears to reduce that risk.

M1 Variant Lowers APOL1 Kidney Disease Risk - Medscape - goo.gl/alerts/pcjuwf #GoogleAlerts

Hypoxia inducible factor network reflects kidney disease progression in diabetes and sodium-glucose co-transporters inhibition Diabetic kidney disease (DKD) is a leading cause of kidney failure globally and is associated with high morbidity and mortality.1 Hypoxic stress contributes to the progressive damage seen in the tubular compartments of the kidneys that is characteristic of DKD in type 2 diabetes (T2D).2 The response to hypoxia is transcriptionally regulated by the transcription factor (TF) hypoxia inducible factor-1A (HIF1A).3 In normoxia, HIF1A protein is targeted for degradation by cytosolic prolyl hydroxylases, while in hypoxia, these prolyl hydroxylases are inhibited, allowing HIF1A to translocate to the nucleus, dimerize with HIF1β protein, and the dimer then binds to hypoxia response elements to modulate transcription of target genes, prompting changes in metabolism and angiogenesis to promote survival.3 In murine models, alterations in the HIF-hypoxia response axis contribute to the pathogenesis of progressive DKD.4,5,6,7,8,9 However, confirming the relevance of this mechanism to human kidney disease remains challenging.10,11 This is due to the complex transcriptional cascade of HIF-driven events superimposed on the intricate anatomy and inherent hypoxia-related physiology of the kidney with highly variable oxygen demand and supply along the nephron.12 Moreover, much of the prior knowledge regarding HIF signaling has been generated from malignant tissue. One long-standing hypothesis, the “chronic hypoxia” hypothesis,...

Hypoxia inducible factor network reflects kidney disease progression in diabetes and sodium-glucose co-transporters inhibition
->Nature | More on "Diabetic kidney disease hypoxia research" at BigEarthData.ai | #Disease #Health

➡️ Tiny warriors, big impact: targeted immunotherapy in kidney diseases www.kidney-internati...

Quick question - if I want to give Cefoperazone-Sulbactam for IP antibiotics for Automated PD with 10L exchanges can I use the Cefoperazone data in ISPD guidelines ie 500mg/L loading with 125mg/L for maintainence or is that overkill? #AskRenal

Why-dralazine?! Population risk of drug induced vasculitis — NephJC This week, we will discuss why a large registry cohort was needed to move past decades of scattered case reports and clarify the true risk of hydralazine‑associated vasculitis. When rare events hide i...

Do you prescribe hydralazine?
Or, do you 🛑 it as soon as you see it?
Hydralazine persists despite TID dosing & risks like... vasculitis 🔥
Are you asking Why-dralazine?
✅The blog by @dramiliflores.bsky.social @nephroseeker.medsky.social
#NephSky
www.nephjc.com/news/hydralazine-anca-vasculitis

Following the publication of this study in JASN, there was an interesting correspondence (see Pabla et al JASN 2024 and authors reply Pyne et al JASN 2024). Pabla et al point out that the organic cation transporter 2 (OCT2, encoded by the SLC22A2 gene) is involved in the basolateral tubular uptake and subsequent secretion of creatinine. PPIs may inhibit OCT2 (Nies et al PLoS One 2011). So Pyne et al, in their reply, present some additional analyses that suggest that the effect of pantoprazole compared with placebo on rate of eGFR change was attenuated in patients who discontinued treatment before eGFR reassessment (−0.04 ml/min per 1.73 m2 per year, 95% CI, −0.26 to 0.17) compared with those who remained on treatment (−0.60 ml/min per 1.73 m2 per year, 95% CI, −0.85 to −0.34). This disparity could support a reversible effect of pantoprazole on eGFR, possibly due to inhibition of creatinine secretion, or reflect a dose-response or threshold exposure effect. The case for PPIs causing kidney churn becomes even more weaker. For a longer explanation, see Lonnie Pyne’s rounds here.

Do PPIs cause kidney damage?

Read an update at the bottom of our summary www.nephjc.com/news/compass...

#MedSky #NephSky #EMIMCC

A 49-YO♀️kidney #transplantation & immunosuppression: headache, dizziness, & pruritic umbilicated, pink papules with crusting on her face, trunk, arms, & legs.

CSF: encapsulated budding yeast.
🔬of papule: yeastlike organisms with mucinous capsules
½

DOI: 10.1056/NEJMicm2109090
#MedEd #dermatology

B-cell-targeting therapies in podocytopathies
@ped-neph.bsky.social
#nephsky #pedsky
rdcu.be/feb6g

#BlueSkyArtShow
#Nephsky

Comparison of 8.4% Sodium Bicarbonate vs. 3% Sodium Chloride in Severe Hyponatremia: A Retrospective Cohort Study - PubMed This study found that a single 50 mL dose of HTB more often resulted in obtainment of guideline-recommended post-intervention serum sodium goal concentrations than a 100 mL HTS dose. Additional studies...

Cool study - an amp of sodium bicarbonate (50 ml 8.4%) raises sodium similar to a boils of 3% - as expected of course!

pubmed.ncbi.nlm.nih.gov/41937305/

@pulmcrit.bsky.social @kidneyboy.bsky.social

#nephsky #emimcc

Clinical Journey in Translational Medicine is a new Kidney International article type that uses a case report format as a catalyst for discovery. In the nephrology clinic, we regularly face important decisions with incomplete mechanistic or causal information as the science continues to evolve and the access to latest modalities is uneven. Each case advances understanding by tracing a focused "journey" of the clinical presentation, diagnostic pathway, and therapeutic reasoning and then pairing it with the mechanistic insight the case reveals through genetics, cell and molecular biology, pathology, biomarkers, or treatment-response. The goal for this article type is to show how bedside observations prompt targeted investigations and how those findings, in turn, refine diagnosis, prognosis, or therapy. We developed this format because translational progress is increasingly driven by granular phenotyping and precision tools that can be hard to connect to everyday clinical reasoning. "Clinical Journeys in Translational Medicine” makes this connection explicit, providing practical examples for integrating emerging science into patient care across diverse practice settings.

This looks cool

www.kidney-international.org/article/S008...

New journal type in @kidneyint.bsky.social

More details: www.kidney-international.org/content/auth...

JAMA Internal Medicine presents 'Pitfalls to Procalcitonin—Elevation in a Postvaccine Fever' by Virginia H. Sun, MD@1, Esdras O. Rodriguez, MD@1, Clement D. Lee, MD. Published online: April 13, 2026. doi: 10.1001/jamainternmed.2026.0673

📃 This case report describes a patient receiving peritoneal dialysis who presented to the emergency department with a fever and elevated procalcitonin levels the day after receiving a COVID-19 vaccine.

ja.ma/4sU8ucF

Extreme Side Effects Followed Overdose of Unapproved Weight-Loss Drug 'This case report contains a dramatic presentation of unintended consequences,' author notes

Several brandname #GLP-1 #WeightLossDrugs are approved by FDA, but numerous versions that are not approved are being sold and can be dangerous.

A man who injected #retatrutide—a GLP-1 that is NOT FDA-approved—ended up in the ER with severe dehydration and early kidney injury after an overdose.

This renal biopsy illustrates severe chronic kidney injury and its effects on all major compartments of the cortex: most glomeruli are globally sclerotic, the atrophic tubules are widely spaced, the interstitium is fibrotic, and the arterial walls show intimal fibrosis. 

#TeachingPoints #pathology

Successful Treatment With Rituximab for Severe Immune Thrombocytopenic Purpura During Hemodialysis - PubMed Immune thrombocytopenic purpura (ITP), an autoimmune disorder characterized by peripheral platelet destruction, is uncommon in patients undergoing hemodialysis, who have an inherently elevated bleedin...

Successful Treatment With Rituximab for Severe Immune Thrombocytopenic Purpura During Hemodialysis

Therapeutic and mechanistic insights on mitochondrial transplantation in kidney disease
->Nature | More on "Mitochondrial therapy for kidney disease" at BigEarthData.ai | #Health #Disease

1/ Hey #NephSky! 👋
We’re back with a fresh #Skytorial by @nephromommy-akshu.bsky.social
We spend half our lives worrying about how bad creatinine is.. then keep using it anyway.
What if we could measure bedside GFR - no serial blood samples? Let’s talk transdermal GFR (tGFR).
@theisn.org

Targeted-release budesonide dose tapering with reported adverse effects. HbA1c: haemoglobin A1C; WBC: white blood cells; URTI: upper respiratory tract infection.

Is targeted release budesonide really free of systemic steroid action?

In the CKJ academic.oup.com/ckj/article/... Adrenal insufficiency after Nefecon withdrawal

Gender Medicine in Nephrology: From Biological Mechanisms to Clinical Inequities
#nephrology #nephsky
www.mdpi.com/2673-8236/6/...

What’s your diagnosis?

#DiagnoseThis #nephtwitter #pathtwitter #renal #kidneypath

Sparsentan approved for FSGS for age 8+! www.streetinsider.com/dr/news.php?...

Pathophysiology, risk factors and clinical management for polymyxin-associated acute kidney injury Abstract. Polymyxins serve as a ‘last-line’ defence against Gram-negative bacterial infections and are frequently used in critically ill patients with mult

Pathophysiology, risk factors and clinical management for polymyxin-associated acute kidney inj - goo.gl/alerts/SNiNfQ #GoogleAlerts

That said phosphate containing colas are not great #StoneCamp

Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of diabetic kidney disease (DKD) Magee C, Grieve DJ, Watson CJ, Brazil DP. Diabetic nephropathy: a tangled web to unweave. Cardiovasc Drugs Ther. 2017;31:579–92. https://doi.org/10.1007/s10557-017-6755-9. KDIGO 2024 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int. 2024;105:S117–314, https://doi.org/10.1016/j.kint.2023.10.018. Pavkov ME, Collins AJ, Coresh J, Nelson RG. Diabetic Kidney Disease. In: Cowie CC et al., editors. Diabetes in America. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases (US); 2018. Cleveland KH, Schnellmann RG. Pharmacological targeting of mitochondria in diabetic kidney disease. Pharmacol Rev. 2023;75:250–62. https://doi.org/10.1124/pharmrev.122.000560. Martinez Leon V, Hilburg R, Susztak K. Mechanisms of diabetic kidney disease and established and emerging treatments. Nat Rev Endocrinol. 2025. https://doi.org/10.1038/s41574-025-01171-3. Oshima M, Shimizu M, Yamanouchi M, Toyama T, Hara A, Furuichi K, et al. Trajectories of kidney function in diabetes: a clinicopathological update. Nat Rev Nephrol. 2021;17:740–50. https://doi.org/10.1038/s41581-021-00462-y. Stanton RC. Clinical challenges in diagnosis and management of diabetic kidney disease. Am J Kidney Dis. 2014;63:S3–21. https://doi.org/10.1053/j.ajkd.2013.10.050. Thrailkill KM, Clay Bunn R, Fowlkes JL. Matrix metalloproteinases: their potential role in the pathogenesis of diabetic nephropathy. Endocrine. 2009;35:1–10. https://doi.org/10.1007/s12020-008-9114-6. Romagnani P, Remuzzi G, Glassock R, Levin A, Jager KJ, Tonelli M, et al. Chronic kidney disease. Nat Rev Dis Primers. 2017;3:17088. https://doi.org/10.1038/nrdp.2017.88. Samsu...

Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of diabetic kidney disease (DKD)
->Nature | More on "Diabetes kidney disease treatment research" at BigEarthData.ai | #Disease #Health

Daily Pearl(s):

Signs of GPA

The combination of an acute kidney injury with a nephritic sediment and any upper respiratory symptoms (sinusitis, otitis, nasal deformity) should immediately raise suspicion for GPA.

“Our findings demonstrate that an injury-induced, sterile immune response regulates kidney regeneration by establishing a nephrogenic niche of Fgf and Wnt signaling that supports tissue-resident kidney stem cell differentiation into functional nephrons.”

New work from Drummond Lab @mdibl.org 🐟

Genetic testing (Next Generation Sequencing)—A Sherlock Holmes in discovering the truth of ADPKD Next-generation sequencing (NGS) is transforming how we diagnose autosomal dominant polycystic kidney disease (ADPKD), particularly in atypical or unclear cases. While most diagnoses rely on imaging and family history, genetic testing offers critical insights into prognosis, mutation type, and family planning. This evolving tool helps unravel diagnostic uncertainty and supports more precise, personalized care in ADPKD.

🧬 Genetic testing #ADPKD isn’t always straightforward.

Dr SaiVani Yellampalli discusses #NGS; diagnose, refine prognosis, & guide family planning—but when should we use it?

🔍 Sherlock Holmes meets #nephrology.

👀
https://ow.ly/BnMr50YHcze

#NephTwitter #NephX #MedEd #FOAMed #Genetics