Glomerular Disease – AKI

00:01 So this marks our next section in the last section of intrinsic renal disease which is our glomerular diseases, probably my favorite thing to talk about.

00:09 And we'll be talking about it fully in our nephrotic and nephritic syndrome lectures.

00:13 However there's a few points that I'd like to talk about.

00:16 Number one is that when we think about the nephritic syndromes, the things that actually result in acute kidney injury are often what we call rapidly progressive glomerular nephritides or RPGNs and these are marked by three different types: Type I is known as antiglomerular basement membrane or anti-GBM disease.

00:37 Type II are immune-complex diseases that manifest with rapid renal deterioration and necrosis and crescents on biopsy.

00:46 And this includes: lupus nephritis, IgA nephropathy, post-infectious glomerulonephritis, and membranoproliferative glomerulonephritis.

00:58 And finally type III, which as a personal favorite of mine, are the ANCA-associated vasculitides also called Pauci-immune glomerulonephritides.

01:07 And again, and all three of these actually are part of a nephritic syndrome however, when they present as a rapidly progressive GN, that means that we are losing renal function quickly.

01:21 There is significant deterioration in renal function and when we biopsy our patients morphologically, what we actually see are necrosis in crescents.

01:31 So again, I'm underscoring that many diseases involve the glomeruli but it's really the RPGNs that present as an emergent acute kidney injury better outlined here.

01:42 So, there are a couple things that are really important when it comes to diagnosing our patient who have RPGNs.

01:48 Laboratory evaluation is critical.

01:51 The urine analysis really is important because it's going to show us that the patients have microscopic hematuria and proteinuria typically less than the nephrotic range and remember, that hematuria often manifests as dysmorphic red cells and red blood cell casts.

02:06 so again, If I'm looking at that urine sediment underneath the microscope then I'm going to see those funny red blood cell shapes.

02:14 Again, they're called dysmorphic red blood cells .

02:16 and they typically look like a red blood cell with a bleb t hat's located on that outer membrane.

02:22 Red blood cell cast and what you can seeion the image over here is that this is a trichrome stain of our patient who actually has an RPGN and you can see all those red blood cells that are actually collecting in the tubules.

02:35 Those are actually on their way to forming a red blood cell cast.

02:39 Those red blood cells will bind with that Tamm-Horsfall protein and then once they're passed into the urine, you see these beautiful exquisite red blood cell cast And sometimes, in some of the very exudative types of RPGN that would be something like post-infectious GN, you might be lucky enough to see a white blood cell cast as well.

02:58 Our patient's urine sodium is oftentimes less than 20 meq/L, that's not because the pre-renal but actually because of something that happens at the principal cell that causes reabsorption of sodium.

03:09 Again, I just want to make a point here.

03:11 That we talked about FENa at the beginning of the lecture, and this is why FENa can only distinguish between pre-renal and ATN.

03:20 If you can see here that our urine sodium is less than 20 (meq/L), that would probably give us a FENa of less than 1%.

03:26 So again we can't use something like FENa in a case like this.

03:31 And then finally if I really want to clinch my diagnosis for an RPGN, I have to do a renal biopsy.

03:37 That's really gonna give me the definitive etiology behind what's going on.

03:44 So in terms of treatment for our glomerular diseases that manifest as RPGN, it's going to depend on the underlying cause.

03:51 So this typically involves high dose parenteral steroids which can be quite difficult for patients to take.

03:58 Cyclophosphamide, which is an alkylating agent or Rituximab which is a monoclonal antibody to CD20.

04:04 And then tapering those steroids over a 6-month period of time to a lower dose.

04:09 Again, we'll talk about this much more in depth when we get to our nephritic syndrome lectures.

04:14 And patients will often have an extended maintenance therapy as well, either with Rituximab or something like Azathioprine which is an anti-metabolite in order to maintain the remission.

04:26 Okay, so that concludes our glomerular diseases.