Nodular diabetic GS can have double contours..But not this much
This case has superimposed chronic TMA related to VEGF inhibitor
🔸Some can have PAS-positive pseudothrombi (also described with TKI inhibitors)
pubmed.ncbi.nlm.nih.gov/30014486/
pmc.ncbi.nlm.nih.gov/articles/PMC...
#renalpath #pathsky
Yes, it was quite pronounced!
It's not always just diabetic GS
Case of diabetic GS with chronic TMA 2/2 tyrosine kinase inhibitor (TKI)
🔸Anti-VEGF effects
🔸Most within weeks to months after starting TKI
🔸TMA +/- PAS+ pseudothrombi
pmc.ncbi.nlm.nih.gov/articles/PMC...
pubmed.ncbi.nlm.nih.gov/19054798/
#renalpath #pathsky
MPO+ANCA GN with concurrent low grade membranous nephropathy. MPO positivity in the MN deposits helps support a unifying etiology is such cases. pubmed.ncbi.nlm.nih.gov/40485711/ #renalpath #nephsky #pathsky
Renal biopsy demonstrated glomerulonephritis with focal immune deposits that stained exclusively for C3 (A and B), consistent with rapidly progressive glomerulonephritis (RPGN) due to C3 glomerulopathy
A 64 y/o woman was admitted for acute kidney injury w/ nephrotic range proteinuria. Prior, she had 3 months of duskiness of distal fingertips w/ mottling. Renal biopsy showed glomerulonephritis w/ focal immune deposits that stained exclusively for C3
Clinical images in ACROR
doi.org/10.1002/acr2...
Autopsy case with incidental ALECT2 amyloidosis with lung involvement. Essentially invisible by light microscopy. Wonder how often this is overlooked. 94% of cases had alveolar involvement in this study (PMID: 26912093). #pathksy #renalpath
COM025’s disease course and eculizumab dosing. Treatment with eculizumab was started 1 day after presentation. Hemolysis resolved within 14 days, proteinuria decreased, and a partial kidney response was achieved 2 days after delivery (A). During treatment, persistent thrombocytopenia and classical pathway functional activity (CPFA) >10% suggested suboptimal complement blockade and thus, free eculizumab levels were measured, which confirmed subtherapeutic drug levels (B). The CPFA has been measured using a commercially available ELISA (Svar Life Sciences, Malmo, Sweden), according to the manufacturer’s instructions. Eculizumab trough levels should be between 50 and 100 μg/mL. CPFA, classical pathway functional activity. Ecu, eculizumab. iHD, intermittent hemodialysis. LDH, lactate dehydrogenase. UPCR, urinary protein-to-creatinine ratio.
Thrombotic Microangiopathy During Pregnancy: Role of Soluble Fms-like Tyrosine Kinase-1–Placental Growth Factor Ratios
bit.ly/3KMpv8m (OPEN ACCESS)
Banff 2024 Kidney Meeting Report
🔓 Open Access
"The Banff 2024 Kidney Meeting Report: Rejection as a spectrum of phenotypes and focus on differential diagnostic reasoning," Naesens et al.
www.amjtransplant.org/article/S160...
#Transplantation #KidneyTransplant #Banff #TransplantPathology #DifferentialDiagnosis #OpenAccess
Transplant bx for renal dysfunction in a patient with shortness of breath. Granulomatous tubulointerstitial nephritis. AFB stain +. Sputum + for TB. Good sample key for making the diagnosis. 2 rounds of AFB stain to find the organism. #renalpath #pathksy #nephsky
Bx for AKI in a pt on checkpoint inhibitor: neutrophil rich tubulointerstitial nephritis. We would usually think pyelonephritis, high risk neutrophil rich variants of CKI inhibitor AIN have been characterized. pubmed.ncbi.nlm.nih.gov/41727781/ #renalpath #pathsky #nephsky
A pediatric case of C3 glomerulonephritis initially misclassified as IgA nephropathy with a favorable response to C3-targeted therapy
#nephsky
Approach to immune checkpoint inhibitor (ICI) nephrotoxicity and rechallenge
#ISNWCN 🇯🇵 #WCN26 🇯🇵 #WCN2026 🇯🇵
#Onconephrology 🦀 #Nephpearls #NephSky
👉 pubmed.ncbi.nlm.nih.gov/32775813/
🤔 What makes IgA pathogenic in IgAN❓
👉🏻 A subgroup of GdIgA1with strong affinity for the glomerulus 🫘
💡 IgA type anti-MEsangial Cell Antibodies (Ig-MESCA) are GdIgA1-Ab.
🎯 Mesangial cells
🧫 Molecular mimicry with oral bacteria
#ISNWCN
@theisn.org
Amazing! Paola Romagnani #ISGD #ISNWCN with “Podocytopathies: Knowns and Unknowns”
👉🏻Podocyte loss and regeneration
👀Autoimmune, genetic, adaptive, infectious, toxic, monoclonal
🎯Anti-slit autoantibodies-> ⬇️ prognosis
#GlomerularDisease #Yokohama 🌸
Bx for pt with AKI and nephrotic range proteinuria. Hx of IV drug abuse (with skin popping), and chronic staph infections. AA amyloidosis was the unsurprising finding. #renalpath #pathsky #nephsky
Anti-PLA2R1 IgG-mediated podocyte PLA2R1 cleavage drives glomerular subepithelial immune complex deposition in membranous nephropathy
doi.org/10.1016/j.kint.2026.02.021
#NephSky #MedSky #OpenAccess #membranousnephropathy
Review: Adenine phosphoribosyltransferase deficiency and 2,8-dihydroxyadeninuria #openaccess
#nephsky
buff.ly/ifexeeG
![Figure 1 Therapeutic targets and positioning of treatments in IgA nephropathy (IgAN). Reflecting our latest understanding, treatments should target IgAN-specific drivers for nephron loss (Hits 1-3, Hit 4) and generic response to IgAN-induced nephron loss. Drugs targeting the IgAN-specific drivers for nephron loss likely act on different mechanisms of the 4-hit hypothesis. Triangles denote that a drug class most likely exerts its key actions on either Hits 1-3 or Hit 4 but may target all hits to a variable extent as indicated by their lengths of the triangle. Nefecon, APRIL inhibitors, and dual APRIL-BAFF inhibitors are shown as having a predominant effect on the production of pathogenic forms of IgA and IgA containing immune complexes (IgA-ICs) [Hits 1-3] while systemic glucocorticoids and complement inhibitors are shown as having a predominant anti-inflammatory effect on IgA-IC mediated kidney injury [Hit 4]. Interventions to manage the generic response to IgAN-induced nephron loss include lifestyle modifications, RASi or DEARA use with or without SGLT2i, or use of a DEARA or a combination of ERA and RASi. Additional strategies may also include the use of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors in select patients. The drugs listed here do not imply a recommended ranking or delivery sequence. APRIL, a proliferation-inducing ligand; BAFF, B cell–activating factor; DEARA, dual endothelin angiotensin receptor antagonist; ERA, endothelin type A receptor antagonist; RASi, renin-angiotensin system inhibitor; SGLT2i, sodium-glucose cotransporter-2 inhibitor.](https://cdn.bsky.app/img/feed_thumbnail/plain/did:plc:33h4q6nw674jdcwfxaq2m2nl/bafkreidryzyepbhcxh4g7cjglwmmk6tfgyxmujh55el3ey76ki4zp4qa5i)
Figure 1 Therapeutic targets and positioning of treatments in IgA nephropathy (IgAN). Reflecting our latest understanding, treatments should target IgAN-specific drivers for nephron loss (Hits 1-3, Hit 4) and generic response to IgAN-induced nephron loss. Drugs targeting the IgAN-specific drivers for nephron loss likely act on different mechanisms of the 4-hit hypothesis. Triangles denote that a drug class most likely exerts its key actions on either Hits 1-3 or Hit 4 but may target all hits to a variable extent as indicated by their lengths of the triangle. Nefecon, APRIL inhibitors, and dual APRIL-BAFF inhibitors are shown as having a predominant effect on the production of pathogenic forms of IgA and IgA containing immune complexes (IgA-ICs) [Hits 1-3] while systemic glucocorticoids and complement inhibitors are shown as having a predominant anti-inflammatory effect on IgA-IC mediated kidney injury [Hit 4]. Interventions to manage the generic response to IgAN-induced nephron loss include lifestyle modifications, RASi or DEARA use with or without SGLT2i, or use of a DEARA or a combination of ERA and RASi. Additional strategies may also include the use of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors in select patients. The drugs listed here do not imply a recommended ranking or delivery sequence. APRIL, a proliferation-inducing ligand; BAFF, B cell–activating factor; DEARA, dual endothelin angiotensin receptor antagonist; ERA, endothelin type A receptor antagonist; RASi, renin-angiotensin system inhibitor; SGLT2i, sodium-glucose cotransporter-2 inhibitor.
A KDIGO commentary on B Cell and Complement guided therapy in IgAN
www.kidney-international.org/article/S008... in Kidney Int
Perfectly timed for #NephMadness (and this will be the champion)
Clinical feature analysis of pediatric Castleman disease with renal involvement
#nephsky
Severe renovascular hypertension in an infant with a SMAD3 gene variant #nephsky
#hypertension @ped-neph.bsky.social #pedsky
link.springer.com/article/10.1...
Classic powdery electron dense deposits along GBMs, TBMS, and in vascular walls by EM in this case of light chain deposition disease. #renalpath #pathsky #nephsky
Don't confuse these for crystals. Limiting membrane of peroxisomes in proximal tubules. Normal tubular structure. Mimic of light chain proximal tubulopathy. #renalpath #pathsky #nephsky
Renal hemosiderosis in paroxysmal nocturnal hemoglobinuria - Kidney International www.kidney-international.org/article/S008...
Empagliflozin-associated Armanni-Ebstein lesions in IgA nephropathy - Kidney International www.kidney-international.org/article/S008...
Disappearing glomeruli: loss of linear IgG in anti-GBM nephritis - Kidney International www.kidney-international.org/article/S008...
Integrating Tissue Proteomics and Urinary Analyses to Capture Dynamic Podocyte Injury - Kidney International Reports www.kireports.org/article/S246...
Genetic testing and kidney biopsies: complementary to another, not substitutive - Kidney International Reports www.kireports.org/article/S246...
Crystalglobulin-Induced Nephropathy and Cardiac Non-amyloidotic Immunoglobulin Deposition Disease: A Fatal Case Report
#nephsky #nephrology
www.kidneymedicinejournal.org/article/S259...
