Chris Larsen

I learned so much from this podcast. I encourage you to share it with your colleagues who are wanting to improve their renal biopsy technique! open.spotify.com/episode/7GMA9U…

@arkanalabs @shary_tang Sorry for the delay in responding! Nephrotic-range proteinuria is present in 10% to 26% of cases. ncbi.nlm.nih.gov/pmc/articles/P…

@shary_tang Paging @renalpathdoc — we'll hand this question over to you.

#TeachingPoints A 75 year old woman presented for her annual checkup with no complaints. She had a past medical history of hypertension and her blood pressure at this visit was 160/80. Laboratory findings were significant for an elevated serum creatinine at 2.1 mg/dL (baseline 1.0 mg/dL) as well as proteinuria of 855 mg/24 hr. All serologies, including proteinase-3, myeloperoxidase, and anti-nuclear antibodies were negative. A kidney biopsy was performed to evaluate the decreased kidney function and proteinuria. It revealed a total of five glomeruli were present, three of which showed a global endocapillary proliferation of large atypical cells with frequent mitotic figures (Photomicrographs A and B). These atypical cells were isolated to the glomeruli and stained positive for CD20 . The remaining glomeruli did not contain any proliferative changes. Electron microscopy and immunofluorescence were both negative for immune deposits. This is a rare subtype of extranodal diffuse large B cell lymphoma that has been known in the past by several different names and was originally thought to be a proliferation of endothelial cells; however, it is currently classified by the WHO as “intravascular large B-cell lymphoma” (IVBCL). IVLBCL most frequently affects adults over 60 and is typically widely disseminated in the small vessels of many organs at presentation. It most often presents without tumor masses or lymphadenopathy and lymphoma cells are usually not seen in peripheral blood smears. Clinical symptoms are highly variable and usually result from the occlusion of small vessels. The vast majority of cases are diagnosed in the bone marrow, liver, spleen, or skin. However, there are case reports of the diagnosis being made by kidney biopsy. In these cases, it usually manifests with slowly progressive renal failure and proteinuria which is frequently in the nephrotic range. #RenalPath

The amazing @Tiff_Caza educating us on NELL1 membranous!

Great job @MolenOdia and @nephrosharma on the presentation of ‘Machine Learning Classification of Kidney Biopsy Smartphone Images for Adequacy Assessment’. I look forward to seeing where this goes! asn-online.org/education/kidn…

@lochon77 @arkanalabs A patient with clinical nephrotic syndrome and tip variant on biopsy should be considered to have a primary podocytopathy.

@arkanalabs But in tip lesion FSGS, we are not usually supposed to say primary vs secondary right?

Knowing whether a patient has clinical nephrotic syndrome and knowing the degree of podocyte foot process effacement can be helpful diagnostic clues in separating “primary” from “secondary” forms of focal segmental glomerulosclerosis (FSGS). For example, in a patient with the nephrotic syndrome whose biopsy shows FSGS lesions and no significant immune deposits by immunofluorescence, the presence of global effacement of podocyte foot processes by electron microscopy (as seen in Fig 1) provides support for a “primary” FSGS (see reference). #TeachingPoints #RenalPath Sethi S et al. Focal and segmental glomerulosclerosis: clinical and kidney biopsy correlations. Clin Kidney J. 2014 Dec;7(6):531-7.PMID: 25503953.

Quick teaching on the characteristic IgG staining pattern seen in anti-LRP2 nephropathy/ABBA. Enjoy! loom.com/share/401e4c35…

@BJegorovic @arkanalabs @set_fortess Infection was quite rare in these GIN case series. Tb belongs in the differential though. The series below includes 17 pts with M. tuberculosis and renal biopsy. 16/17 had GIN on biopsy with caseating granulomata in only 3/16. 0/17 were pos for AFB. kidney-international.org/article/S0085-…

@arkanalabs @set_fortess What infectious etiologies are causing those cases of granulomatous interstitial nephritis?

Today's #TeachingPoint is a biopsy from a 25 year old African American female with renal failure. The photomicrographs here show renal involvement by non-caseating granulomas eliciting the diagnosis of granulomatous interstitial nephritis. The patient was found to be hypercalcemic and to have hilar lymphadenopathy and reticulonodular infiltrates on chest x-ray and was diagnosed with sarcoidosis. A case series examining 46 cases of granulomatous interstitial nephritis (GIN) by Bijol et al (ref below) found the most common etiology (45%) of this pattern to be a drug-induced reaction. This was followed by sarcoidosis (29% of GIN), other (including infection) at 16% and there were 10% of cases that proved to be idiopathic. It should be pointed out that this case series was composed of cases from the United States and the etiologies from other parts of the world would likely be different.

@VrushaliPatho @arkanalabs I have always found the approach of Nasr, et al helpful.... "a ratio of calcium oxalate deposits per glomerulus was calculated. The mean and median number of calcium oxalate deposits per glomerulus was 3.5 and 3.1 (range 1.5 to 7.9)." ncbi.nlm.nih.gov/pmc/articles/P…

@arkanalabs Great case. Is there any objective criterion/number of crystals seen on a biopsy to define oxalate nephropathy? As these crystals are seen many times as non-specific finding in acute tubular injury. Thank you.

For today's #TeachingPoint, we'll review a 51 year old female with a history of SLE who was found to have acute renal failure. There was no evidence of glomerular proliferation by light microscopy but the biopsy did show (A) focal tubules with intraluminal and intracytoplasmic refractile crystals (arrows) (hematoxylin and eosin; original magnification × 100). (B) There are numerous intra-tubular birefringent crystals visible under polarized light (hematoxylin and eosin; original magnification × 50). These findings are consistent with kidney injury due to oxalate nephropathy. Known causes of oxalate nephropathy include primary hyperoxaluria, ethylene glycol intoxication, enteric hyperoxaluria (e.g. due to gastric bypass, chronic pancreatitis, small bowel resection, or malabsorption), exposure to the anesthetic agent methoxyflurane, vitamin B6 deficiency, and excessive ingestion of vitamin C or dietary substances rich in oxalic acid such as parsley, nuts, teas, and star fruit. The patient in the case shown here was found to be taking large daily doses of vitamin C.

@jesperkers 🤔 not sure. I suspect it is negative since these are composed of light chains but I did not check.

The morphologic spectrum of light chain proximal tubulopathy (LCPT). loom.com/share/f3c656d9…

Quick case-based teaching on the active lesions of ANCA including medullary angiitis and necrobiotic granulomas. loom.com/share/0991adb3…

I have an interesting transplant biopsy with a great teaching point. Enjoy! loom.com/share/f88e9712…

Continuing with the theme of genetic tubulointerstitial diseases that can be seen on biopsy. Enjoy! loom.com/share/062427f5…

@BajinderR @arkanalabs No, I have not seen anything specific at all. I'll try to cover that in a future episode!

@renalpathdoc @arkanalabs Dr Larsen Any specific biopsy findings in muci1 related tubointerstial disesease ie deposits

Trying out something new here... Here is a quick teaching point from @arkanalabs to you! loom.com/share/765722c0…

@BajinderR @arkanalabs A pathogenic variant was identified.

@renalpathdoc @arkanalabs any genetic studies

Ever wonder what to look for in uromodulin storage disease? Find out in this quick teaching point from @arkanalabs! loom.com/share/7cde3781…

@DrGeetikaSingh1 @NephBean @MPAlexanderMD @SethiRenalPath @Richard @nephrosharma I usually only count as a percentage of intact glomeruli too. I think of this as a measure of activity and a globally sclerotic glomerulus cannot have an active crescent. As such, it does not make sense to me to use it in the denominator.

@NephBean @MPAlexanderMD @SethiRenalPath @renalpathdoc @Richard My understanding is : Calculate percentage crescents from the non- globally sclerosed glomeruli. This will give the clinician an idea of the extent of severe glomerular injury in salvageable kidney and help plan Rx accordingly @nephrosharma - I remember asking the same Q

In a kidney biopsy with crescents, is the percentage of crescents calculated from total number of sampled glomeruli or just the non-globally sclerosed glomeruli? @MPAlexanderMD @SethiRenalPath @DrGeetikaSingh1 @renalpathdoc @richard

Love this! twitter.com/arkanalabs/sta…

@OpeyemiOlabisi8 @arkanalabs @VertexPharma Thank you! We are very excited and hope this moves the needle on increasing awareness of APOL1-mediated kidney disease.

@arkanalabs @VertexPharma What an excellent development! I am glad to see @arkanalabs and @VertexPharma join the effort to make free APOL1 genotyping wisely available.

Introducing the No Cost to Patient APOL1 Genotyping Program for eligible patients sponsored by @VertexPharma. See if your patients are eligible or learn more about APOL1 high-risk variants. arkanalabs.com/services/apol1…