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Posts by Renal Pathology Society (RPS)

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#UrinarySediment patient with lupus nephritis, and AKI #UrineMicroscopy

13 hours ago 2 1 0 0
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Txp biopsy with rare probable cystine crystals in interstitial mononuclear cells in a patient with history of cystinosis. Rarely seen post-txp not clinically significant to my knowledge. #renalpath #pathsky #nephsky

15 hours ago 6 2 1 0
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Fibrillary or amyloid? How about both! Concurrence of ALECT amyloidosis and DNAJB9+ FGN. EM shows admixed but distinct fibril population. Mass spec was required for definitive diagnosis. www.sciencedirect.com/science/arti... #renalpath #nephsky #pathsky

10 hours ago 6 2 0 0
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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

4 hours ago 3 1 0 0
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Proposed algorithm for the application of rituximab in minimal change disease (MCD) and primary focal segmental glomerulosclerosis (FSGS) ca. 2020
#Nephpearls #NephSky

👉 pubmed.ncbi.nlm.nih.gov/32942039/

5 days ago 5 4 0 0
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#BlueSkyArtShow
#Nephsky

4 days ago 10 3 0 0
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Histopathologic Classification of ANCA-Associated Glomerulonephritis ca. 2010
#GlomConEurope 🇪🇺🇵🇹 #Nephpearls #NephSky

👉 pubmed.ncbi.nlm.nih.gov/20616173/

6 days ago 4 2 0 0
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📖 This weekend don't miss our Kidney International #ISNFridaySelection: Nephrotic syndrome genomic discovery in the Mass General Brigham Biobank identifies monoallelic MEFV variants as a risk factor for focal segmental glomerulosclerosis www.kidney-internati...

6 days ago 2 1 0 0
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This month's Creative Cortex features "Firey Filtration," evoking the firey turbulence of glomerulonephritis. Check it out in #ASNKidneyNews: kidney.pub/KN1804-05

5 days ago 5 2 0 0
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Histopathology of MPGN and C3 glomerulopathies ca. 2015 from @natrevneph.nature.com
#GlomConEurope 🇪🇺🇵🇹 #Nephpearls #NephSky

👉 pubmed.ncbi.nlm.nih.gov/25447133/

5 days ago 5 3 0 0
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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

5 days ago 9 4 1 0
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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

5 days ago 5 4 1 0
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

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...

1 week ago 7 3 0 0
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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

1 week ago 5 4 0 0
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Finding the etiology of MPGN Membranoproliferative glomerulonephritis (MPGN) has undergone a change in classification that is focused on the etiology of MPGN. Thus, MPGN is classified into immune-complex (IC)-mediated MPGN and…

Finding the etiology of MPGN (EDITORIAL: SPECIAL REPORT )

1 week ago 3 2 0 0
Banff 2024 Kidney Meeting Report

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

1 week ago 3 2 0 0
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.

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)

2 weeks ago 3 2 0 0
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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

2 weeks ago 5 6 0 0
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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

3 weeks ago 5 5 0 0
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Renal hemosiderosis in paroxysmal nocturnal hemoglobinuria A middle-aged man presented with >10 years of intermittent dark-colored urine. Laboratory tests showed hemoglobin, 112 g/l; serum creatinine, 75.7 μmol/l; and elevated lactate dehydrogenase, 26.88 μka...

Renal hemosiderosis in paroxysmal nocturnal hemoglobinuria - Kidney International www.kidney-international.org/article/S008...

1 month ago 3 3 0 0
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🤔 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

3 weeks ago 4 3 0 0
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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 🌸

3 weeks ago 3 2 1 0
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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

3 weeks ago 7 5 0 0
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Approach to immune checkpoint inhibitor (ICI) nephrotoxicity and rechallenge
#ISNWCN 🇯🇵 #WCN26 🇯🇵 #WCN2026 🇯🇵
#Onconephrology 🦀 #Nephpearls #NephSky

👉 pubmed.ncbi.nlm.nih.gov/32775813/

3 weeks ago 6 4 0 0
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A pediatric case of C3 glomerulonephritis initially misclassified as IgA nephropathy with a favorable response to C3-targeted therapy - Pediatric Nephrology C3 glomerulopathy is an ultra-rare kidney disease driven by dysregulation of the alternative complement pathway fluid phase C3 convertase. We report the case of a previously healthy 13-year-old girl…

A pediatric case of C3 glomerulonephritis initially misclassified as IgA nephropathy with a favorable response to C3-targeted therapy
#nephsky

3 weeks ago 4 3 0 0
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Adenine phosphoribosyltransferase deficiency and 2,8-dihydroxyadeninuria - Pediatric Nephrology Adenine phosphoribosyltransferase (APRT) deficiency is a rare autosomal recessive disorder of purine metabolism causing 2,8-dihydroxyadenine urinary tract stones and crystal nephropathy. Disease…

Review: Adenine phosphoribosyltransferase deficiency and 2,8-dihydroxyadeninuria #openaccess
#nephsky

buff.ly/ifexeeG

4 weeks ago 2 2 0 0
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Severe renovascular hypertension in an infant with a SMAD3 gene variant - Pediatric Nephrology Introduction Renal artery stenosis is one of the severe secondary hypertension (HTN) causes in children and may lead to hypertension-mediated organ damage (HMOD), including left ventricle hypertrophy ...

Severe renovascular hypertension in an infant with a SMAD3 gene variant #nephsky
#hypertension @ped-neph.bsky.social #pedsky
link.springer.com/article/10.1...

4 weeks ago 4 3 0 0
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Clinical feature analysis of pediatric Castleman disease with renal involvement - Pediatric Nephrology Background Pediatric Castleman disease (CD) is a rare lymph node disorder, and renal involvement is uncommon in pediatric CD. This study aimed to investigate the clinical features of pediatric CD…

Clinical feature analysis of pediatric Castleman disease with renal involvement
#nephsky

3 weeks ago 2 2 0 0
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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

3 weeks ago 5 3 0 0
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.

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)

3 weeks ago 13 9 1 0