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Dr. Ensign, can you help me understand the term subnephrotic proteinuria? Would this mean proteinuria <3.5 g/day as in the case with nephritic syndrome?

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Dr. Ensign, thank you for all your help on this block of renal! We are all going to do great!

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Question submitted through email and reposted here with permission.

I was wondering how thrombosis, infection, and atherosclerosis cause protein loss resulting in nephrotic syndrome?

Also, why does the body increase hepatic lipoprotein synthesis during nephrotic syndrome?

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Question submitted through email and reposted here with permission.

Hello Dr. Ensign,

I have a question regarding GFR and diabetic nephropathy. I understand that a decreased GFR is seen in all renal diseases. However, I was listening to a USMLE review podcast on my way home from the school, the lecturer said that in very early stage of diabetic nephropathy, you can an increased GFR due to atherosclerosis of the efferent arteriole, creating a back pressure on the glomerulus, therefore, hyperfiltration in the beginning, and then GFR goes down like in all other renal disease. I did a quick research on UpToDate, and it seems like hyperfiltration can be present in DM patients. I would like to double check with you to see if that’s accurate, and if we should remember it for exam purposes.

Thanks,

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If it's ok to ask Dr, should we know the levels and ranges of lab values, like knowing when GFR is considered too high or low?

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Dr.Ensign is there a decisive factor that dictates whether IF will lean towards a linear versus a granular appearance?

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Question submitted through email and reposted here with permission.

Greetings Dr. Ensign,

I hope this email finds you well.

I've used resources to help with my confusion, but I could use some help.

A frequent topic of discussion is "Proliferative Pattern" as seen in APSGN. What does that mean? Does that just refer to the presence of endothelial and mesangial cells?

What is the best way to distinguish between cells of the capillaries and the mesangial cells as seen in the picture I am attaching, in H&E staining?

I try to keep this in mind: in the glomerulus we have capillaries with an endothelium, glomerular basement membrane, and an epithelium. Spread throughout those capillaries are the mesangial cells. But once I see the stains everything goes out the window!

Any tips are helpful!

Thank you!

To piggyback off my earlier [question], when it says “mesangial proliferation” does that refer to hypercellularity?

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Would FSGS be an example of causing glomerulonephritis secondarily?

As a refresh, anything involving immune complexes or the our immune system in automatically cause inflammation?

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Dr.Ensign I noticed on the answer key for your nephrotic syndrome we interchange Membranous nephropathy and Membranous glomerulonephropathy, I presume they mean the same. Is there any more diseases that have interchangeable terms, or what is a good way to catch that and know they mean the same?

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I think I got the way a case is presented. The clinical presentation is what the patients present which includes signs, lab tests, imaging like EM, IF, and symptoms. and then the pathology is the disease that are likely to manifest that. And then the pathogenesis is how that disease in the pathology comes to be, and is reflected by the clinical presentation. Am I in the ball park?

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Dr.Ensign I'm probably beating a dead horse by this point, but to summarize the lectures, were basically covering renal diseases, and that will encompass diseases that are glomerulonephropathies which includes glomerulonephritis right? Or were all the lectures we covered revolving back to glomeruolonephropathy or nephritis?

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I had an email notification of a question, but the question does not seem to be here. Not sure if that's a technical glitch or if the submitter figured it out themselves, or what happened. Anyway, since it appears someone had a question, I'll paraphrase the question and answer here:

The concern was about the time frame of nephritic syndrome versus RPGN, since nephritic syndrome (particularly in cases like PSGN) can have an acute onset and RPGN also has an acute time frame. The difference, though is that RPGN has an acute onset of renal failure, while the less aggressive nephritic diseases may have acute onset of nephritic syndrome, but may never progress to renal failure or may do so over a prolonged period. It is the rapid progression to acute renal failure that sets RPGN apart.

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Hi Dr.Ensign, what is the key difference between fibrinoid necrosis and hyalinization?

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Submitted through email and reposted here with permission:

I was curious if you could recommend any resources for histology practice? I will be honest I was really struggling in the beginning but am starting to get the hang of it. I feel like with more practice I will feel confident for the exam. Any tips you have would greatly be appreciated!

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Submitted through email and reposted here with permission.

Hello Dr. Ensign,

I am working through the practice questions relating to the lecture "Overview of Glomerular Diseases" and I am a little confused on the matching with question 2.

I can tell that A is a normal glomerulus. Since Alport Syndrome in the beginning shows no changes in light microscopy, we can assume that A could be early stages of Alport Syndrome?

Is 7 also A because it is relating to Alport Syndrome or TBMN?

Thank you,

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Good afternoon Dr. Ensign,

Do you have any helpful pointers in distinguishing between Lupus (subtype IV) wire loop lesions & frank capillary thickening (ie membranoproliferative)? Or do we just need to use outside clues to distinguish between the two?

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Hi Dr.Ensign, just to see if I am organising this correctly, but in Lecture 2, there's a slide stating how we are going to cover major clinical patterns of glomerulonephritis, and then we get to a slide going over glomerular disease clinical syndromes providing different clinical patterns, with diseases that fall under each clinical pattern. So are those diseases that fall under a clinical pattern, for example, membranous nephropathy being under Nephrotic Syndrome? Are we also saying membranous nephropathy is considered a glomerular disease, more specifically, glomerulonephritis?

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Hello Dr. Ensign,

In the case of nephritic syndromes, why is it that the basement membrane is destroyed enough or potentially widened enough to allow red blood cells to go through, but GFR is decreased? My initial thought is that if there are holes big enough for red blood cells to go through. Then GFR would increase because more fluid would be able to leak out through those same holes. My other thought is if the proteins and red blood cells are leaking through the glom, maybe that decreases overall capillary oncotic pressure, causing Edema in the rest of the body, which would then potentially decrease GFR. Thanks!

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Submitted through email and reposted here with permission so all can benefit:

I seem to always get lost in the weeds when it comes to determining if something is a symptom, a sign, a syndrome, or a disease, or even something that is a disease secondary to disease. May you have any advice  please on how I can better sort this out?  I thought about this more after seeing the clues slide for the different clinical syndromes. Thank you

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submitted through email and reposted here with permission so all can benefit:

Hello Dr. Ensign,

Could you please help me visualize the "gbm splitting" in MPGN type 1 on electron microscopy? I am not entirely sure how to tell from the slide. I attached it here. Thank you!

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Dr. Ensign,

I am not sure if this is just me or if there is an issue with recordings, but there seems to be a slight delay in the audio versus your drawings for any of the histology drawings. It has been difficult to follow along with your drawings as you are identifying structures.

If possible, could you upload a packet or practice document for us to identify the histology slides?

Format:

Slide A: Blank histology/EM photo with you asking us to identify structures.

Slide B: Answers slide of said structures, and then ask us to clinically correlate.

Slide C: Answer slide for slide B at the very end of the document.

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Hey Dr Ensign, I have noticed that in your lectures you sometimes list your units of measure as "gm", is this unit supposed to denote grams(g) or milligrams(mg)?

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I am having trouble understanding the difference between primary autoantibody to intrinsic antigen and secondary antibody to cationic "planted" subepithelial antigens.

Do the autoantibodies attach to free-floating antigens in the system and then form a complex that attaches to the PLA2 receptor? Or are the antigens already on the receptor and the autoantibodies attach to the antigen there?

My question is similar with secondary planted. Are the antigens already in the subepithelial layer before attaching to an antibody? And are they attaching to something specific in the subepithelial area?

Slide 22 of nephrotic syndrome

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This question came through email and is reposted here with permission so all can benefit:

I am a little confused about RPGN and GFR. On your slide #5 you mentioned it results in increasing eGFR over a short period of time however, on your lecture recording you said the GFR goes down and serum creatinine goes up. Would you be able to clarify if the GFR does up or down with RPGN? Thank you!

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Hi Dr. Ensign,

I had a question about the Clues slide at the end of the nephritic lecture. It says in the clues page that FSGS can have both IgG and IgM involvement, but in the explanation for question 3 in the nephrotic questions it says that the only disease we have covered so far with IgG involvement is membranous glomerulonephropathy. Can you clarify if FSGS is both IgG and IgM, or just IgM? Thank you in advance!

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Hi Dr. Ensign,

I have a question about the Pathogenesis of Glom Inj lecture. With regard to Pattern 3, Nephritic Syndrome, I understand that RBCs are bigger than protein and that with this pattern there is enough damage to the glomerulus that both hematuria and proteinuria occur. Given that, I don't understand how hematuria could occur without proteinuria in other diseases. If there is enough damage for blood to filter through the glom when it isn't supposed to, how would protein, which is smaller, not escape too?

Thanks!

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Nephrotic Syndrome Lecture Clarification

Hi Dr. Ensign,

I had a question about slide 15 on FSGS. The slide says that diabetes is the most common cause of primary nephrotic syndrome in adults.

It was unclear to me if you meant that it was the most common cause of primary nephrotic syndrome generally, or that it was the most common cause of FSGS?

I apologize if this is a basic question, but I'm wasn't sure if diabetic nephrotic syndrome was separate pathological process or if it would qualify as an adaptive secondary cause of FSGS.

Thank you!

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Question # 2 on GN Overview

I noticed that on question 2 #9 that the answer key says TBMN is Autosomal Recessive but that in the PP it says Autosomal Dominant? May I please get some clarification?

Thank You!

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This question came from one of the students through email and is reposted here with permission so all students can benefit:

I had one question about the practice questions for the nephritic syndrome lecture. Question 2 has us matching the pictures with the buzzwords. Buzzword 8 is MRSA and you have it matched to image A in the key, which correlated with PSGN. My understanding is that MRSA is a staphylococcal infection (S. Aureus), not streptococcal. As you mentioned in the lecture, that would make it correlated with nonstreptococcal GN, and therefore 8 would not correlate with any of the images attached.

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Hi, everyone. Please feel free to post your questions about my lecture material here. I will get on at least once a day to respond to your questions. My only rule is that you be respectful of myself and the other students while you are here. I look forward to talking with you as we explore non-neoplastic renal path together.