Dr. Vrushali Mahajan Deshpande

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Dr. Vrushali Mahajan Deshpande

Dr. Vrushali Mahajan Deshpande

@VrushaliPatho

Pathologist by heart. Consultant Renal and Transplant Pathology @Institute of Surgical Pathology, Nagpur. PDCC Renal and Tx Pathology, Advanced ISN ANIO CNC.

Nagpur, India เข้าร่วม Mayıs 2021
261 กำลังติดตาม286 ผู้ติดตาม
Dr. Vrushali Mahajan Deshpande รีทวีตแล้ว
Arkana Laboratories
Arkana Laboratories@arkanalabs·
Answer: Focal and Segmental Glomerulosclerosis, Favor Secondary. The biopsy shows sclerosis involving a portion of the glomerular tuft (segmental) of some, but not all, glomeruli (focal). These findings are consistent with focal and segmental glomerulosclerosis, a morphological lesion that reflects not a single disease entity, but can result from multiple etiologies (genetic, viral, drug-induced, hyperfiltration-related, among others). The presence of nephrotic syndrome and diffuse foot process effacement favors a primary FSGS, while the absence of the later favors secondary FSGS. #renalpath #kidneypath #pathology #renal #pathtwitter
Arkana Laboratories@arkanalabs

In a patient with subnephrotic proteinuria, negative immunofluorescence, and segmental foot process effacement, what is your diagnosis? #DiagnoseThis #nephtwitter #pathtwitter #renal #kidneypath

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Dr. Vrushali Mahajan Deshpande รีทวีตแล้ว
Wenyan Zhou
Wenyan Zhou@Zhou1217001·
#renalpath Discarded donor kidney, massive thrombi in glomeruli
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Dr. Vrushali Mahajan Deshpande
Dr. Vrushali Mahajan Deshpande@VrushaliPatho·
@KidneyPath Thank you for sharing Is there an associated nodular glomerulosclerosis? Proteinuria? Recently came across a similar case. The patient had significant proteinuria without nodular glomerulosclerosis and features LCCN with LCDD on IF, lambda chain type
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Kuang-Yu Jen, MD, PhD
Kuang-Yu Jen, MD, PhD@KidneyPath·
Unfortunately, great cases are almost always not good for the patient. This one has light chain cast nephropathy and deposition dz. PAS-weak casts with cellular reaction. Super bright kappa (lambda neg). Powdery electron-dense material along TBM and mostly mesangium #RenalPath
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Dr. Vrushali Mahajan Deshpande รีทวีตแล้ว
Kuang-Yu Jen, MD, PhD
Kuang-Yu Jen, MD, PhD@KidneyPath·
Deceased donor biopsy with prominent ATI, some areas of frank tubular necrosis, and collapsing glomerulopathy likely due to ischemia. #RenalPath
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Dr. Vrushali Mahajan Deshpande รีทวีตแล้ว
Arkana Laboratories
Arkana Laboratories@arkanalabs·
A case of active lupus nephritis in a limited sample. Only renal medulla was present for IF. Two glomeruli total were present for LM and paraffin IF was performed, which demonstrated near "full house" staining. The glomeruli were no longer present on the paraffin C1q stained slide. One glomerulus had endocapillary hypercellularity. In this patient with SLE, a diagnosis of active lupus nephritis was made. However, distinction between class III and class IV and the ISN/RPS activity/chronicity scoring could not be completed.   #GlomGoals #biopsyadequacy #pathtwitter #renaltwitter
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Dr. Vrushali Mahajan Deshpande รีทวีตแล้ว
Dr.Sridatta A.K.A Nephron_Endowment
🧵 Young CKD is REAL and we are missing it. I have not personally seen this patient.this post is quite long Views are based only on the clinical details provided. ESRD & HD management may vary among nephrologists. Young patients can have chronic kidney disease. Yes very commonly. T2DM is now the most common cause. Next most common: IgA nephropathy. Many IgA patients reach ESRD by the 2nd–4th decade. Hence IgAN should always be high on the differential. CKDu is also highly prevalent in our population. ❌ A dangerous misconception: “Long-standing hypertension causes CKD.” Not completely wrong but in young patients, it is very often the wrong assumption. 🚨 A scenario we see every day: 21-year-old with headache. BP ~160 mmHg. Conclusion: “Stress-related hypertension.” No urine routine. No serum creatinine. Started on BP tablets. 3 months later: BP uncontrolled. Patient complains of fatigue. Investigations finally done: Hb 10 g/dL Creatinine 2 mg/dL Conclusion given: by the doctor “BP has damaged your kidneys.” Fast forward 4 months. Creatinine → 10 mg/dL. Patient reaches nephrology late. Ultrasound: bilateral shrunken kidneys. Diagnosis: ESRD. Only option left: hemodialysis. What actually happened? 👉 Kidney disease caused hypertension. Not the other way around. Uncontrolled BP only accelerated the damage further it is a cycle What should have been done? Any young patient diagnosed with HTN must have: ✔ Urine routine (nobody does,if they also they dont know to interpert ) ✔ Serum creatinine Yes an USG Before echo. Before stress theory. If detected early: • Renal biopsy could have been done • Disease identified • Treatment started • Kidney life prolonged Remember: 🧠 Biopsy is possible only when kidneys are normal size. Once shrunken diagnosis is lost forever. Other common causes of young CKD: • Reflux nephropathy • FSGS • C3 glomerulonephritis These can destroy kidneys very rapidly if untreated. Sadly, most remain untreated due to late diagnosis or wrong diagnosis Why IgA nephropathy stays on top: • Very common • Often silent • No definitive cure So prevention and early detection matter most. Asia has the highest burden of IgAN. Some Asian countries screen children with: ✅ Yearly urine routine from school age. Not echo. Not LFT. Only urine routine. Simple. Cheap. Powerful. Final message: When you see hypertension in the young ❌ Don’t chase the consequence. ✅ Chase the cause. Early suspicion saves kidneys. Late referral leaves no options. Coming to this patient’s risks I am not very worried about hemoglobin. These patients are usually chronically compensated. Renal replacement therapy can be performed in various ways to prevent complications. It is the disease that kills the patient, not the dialysis process itself. This patient carries a high risk of dialysis disequilibrium syndrome, which must be anticipated and prevented. Based on symptoms, urine findings, labs, and imaging, we can usually reach a broad diagnosis of CGN vs CIN.
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Dr. Vrushali Mahajan Deshpande
Dr. Vrushali Mahajan Deshpande@VrushaliPatho·
@arkanalabs Collapsing FSGS, possibly COVID related, with prominent protein resorption droplets in the visceral epithelial cells highlighted with albumin.
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Dr. Vrushali Mahajan Deshpande รีทวีตแล้ว
Sanjeev Sethi
Sanjeev Sethi@SethiRenalPath·
Thrombotic microangiopathy (TMA) manifesting as florid mesangiolysis Glomeruli show mesangial expansion by fluffy material + schistocytes -Interstitium well preserved -Arteries not involved Dx: TMA, chemotherapy-associated 50 yr-old woman with ovarian cancer, on chemotherapy
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Dr. Vrushali Mahajan Deshpande รีทวีตแล้ว
Jonathan Zuckerman MD PhD
Jonathan Zuckerman MD PhD@JZRenalPath·
Surprisingly focal case of light chain cast nephropathy seen at autopsy in a patient with multiple myeloma. Good reminder that might be missed or very focal on a biopsy. Bone marrow packed with myeloma cells with exuberant Russel bodies. #renalpath #nephropath #autopsypath
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Vishal Ramteke
Vishal Ramteke@nephrosapien·
Non academic post !!! Elated to have my work featured as a cover page for the January issue of @NDTsocial Journal of @ERAkidney ...
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Jonathan Zuckerman MD PhD
Jonathan Zuckerman MD PhD@JZRenalPath·
@VrushaliPatho Unsure. While the deposits are small they do involve GBMs and injury podocytes segmentally, perhaps allows for a lot of filtration through those areas.
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Jonathan Zuckerman MD PhD
Jonathan Zuckerman MD PhD@JZRenalPath·
One of the more subtle cases of amyloidosis I have seen. Few spicules on silver stain. Minimal congo red positivity. Despite early amyloid deposition, pt had nephrotic syndrome. Likely AL type (pt has LPL); MS pending. #renalpath #pathtwitter #nephrology.
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Dr. Vrushali Mahajan Deshpande
Dr. Vrushali Mahajan Deshpande@VrushaliPatho·
Can we get neutrophilic casts and neutrophilic tubulitis due to involvement by lupus in a biopsy otherwise showing lupus podocytopathy @Tiff_Caza @arkanalabs . There are no clinical signs of infection in the patient.
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Dr. Vrushali Mahajan Deshpande รีทวีตแล้ว
Sourabh Sharma
Sourabh Sharma@iamnephrologist·
💥Is there an entity called “Fatty Kidney Disease” ⁉️ ⚡️Can kidneys too be obese? Yes indeed ‼️ #NephroNotes #NephPearls #FOAMEd #MedEd
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Dr. Vrushali Mahajan Deshpande
Dr. Vrushali Mahajan Deshpande@VrushaliPatho·
@arkanalabs Thank you for the educational post. How does cholesterol emboli in glomeruli or blood vessels cause nephrotic range proteinuria?
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Arkana Laboratories
Arkana Laboratories@arkanalabs·
Cholesterol emboli involving the kidney may manifest clinically as acute kidney injury, hematuria, proteinuria (both non-nephrotic and nephrotic range), and even new onset hypertension. This biopsy illustrates a rare example of glomerular involvement. Most emboli are identified “upstream” within interlobular and/or arcuate arteries. Prior to this biopsy, the patient had recently undergone an arterial catheterization procedure.   #TeachingPoints #kidneypath #renal #pathology #nephx #pathx
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Dr. Vrushali Mahajan Deshpande รีทวีตแล้ว
Hans-Joachim Anders
Hans-Joachim Anders@hjanders_hans·
Now online in @NDTsocial Anti-nephrin antibodies in patients with IgAN and nephrotic syndrome 🧐The majority of MCD-IgAN patients were positive for circulating anti-nephrin antibodies! ▶️academic.oup.com/ndt/article-ab…
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