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Post-Streptococcal Glomerulonephritis

by Carlo Raj, MD
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    00:01 Continuing our discussion of glomerulonephritis.

    00:04 We are still within the realm of nephritic disorders and with nephritic disorders, at this point, you should be pretty good with what the overall signs of the patients are including your hypertension and hematuria.

    00:19 With hematurias, RBC casts, dysmorphic RBCs, oliguria and as far as protein loss is concerned, less than 3.5 grams of protein per day may result in periorbital puffiness.

    00:33 Continuing our discussion of nephritic with post-streptococcal glomerulonephritis.

    00:39 Now, earlier when our discussion began with the overview, I gave you the most common glomerulonephritis or nephritic disorder overall and that was your IgA nephropathy.

    00:51 Now, we take a look at PSGN.

    00:53 And this is the most common type of post infectious glomerulonephritis.

    00:57 Is that clear? In a little bit, I’ll give you some non-infectious glomerulonephritis.

    01:01 Now, with post infectious, this will be most commonly following weeks after exposure to an organism, bacteria known as group A streptococci and here, of course, we’re referring to streptococci pyogenes.

    01:16 Now, before I give you pharyngitis which many of you, most of you are familiar with, I have to point out to you skin, skin, skin.

    01:26 And by skin, maybe perhaps you have a skin infection by the same organism, so, that’s not going to differ.

    01:32 It will be still group A streptococci.

    01:35 However, with the skin manifestation maybe in the form of as an example, scarlet fever, impetigo.

    01:42 Then weeks later, we have issues with the kidney in which there's hematuria, your most likely situation, diagnosis, PSGN, poststreptococcal glomerulonephritis.

    01:54 Now, what you will have to memorize is the fact that it’s subepithelial immune-complex deposition.

    02:01 To make your life a little bit easier, P as in post, P as in subepi.

    02:06 What does that mean to you? Are you on the side of the urine or are you on the side of the blood? You’re on the side of the urine, is that clear? Where? Between the podocyte and the glomerular basement membrane.

    02:20 On immunofluorescence, what are you going to call this? Granular upon immunofluorescence.

    02:26 What about this immune-complex pathway? It is then going to activate complement pathway, so therefore, look for a patient that has hypocomplementemia.

    02:36 Now, on light microscopy, you’re going to find diffused proliferation of that glomerulus.

    02:43 So in your mind, you should be think as to what a light microscopy normally looks like of a glomerulus, and then, here with PSGN, we have diffused proliferation with neutrophilic infiltration.

    02:55 Remember, with nephritic, quite a bit with neutrophilic and oftentimes, with immune-complex involvement.

    03:01 With post-streptococcal glomerulonephritis, we have one to three weeks after infection with the group A streptococcal.

    03:10 This would be something like your streptococcus pyogenes that we talked about just now.

    03:15 What becomes important is the next statement.

    03:17 Every one of these statements here are extremely, extremely common and quite important for you to know clinically.

    03:22 That nephritogenic strain might then give rise to your PSGN, poststreptococcal glomerulonephritis, but however, it will never, never reduce acute rheumatic fever.

    03:33 Rheumatic fever, what is this that I’m doing? I thought Doctor Raj dances. No, that’s called Sydenham chorea.

    03:41 Is that part of rheumatic fever? That it is.

    03:44 Number two, there’s arthritis maybe in the elbow, maybe move down to the knee, it’s called migratory polyarthritis.

    03:52 And so that's also part of rheumatic fever.

    03:54 Number three, there might be issues with the heart, endocarditis, myocarditis, pericarditis, collectively, pancarditis, is that part of rheumatic fever? That it is.

    04:08 There’s skin involvement that you might find.

    04:10 It’s known as erythema marginatum, also part of rheumatic fever.

    04:16 Now, what I’ve given you there is the major Jones criteria for rheumatic fever.

    04:22 Now, with post-streptococcal here with a nephritogenic strain, nephritogenic will never cause heart-genic or cardiogenic, it will then cause strictly your PSGN.

    04:35 Now, the rest of this is following suit with nephritic disorder which means that you might lose protein, and you will, up until 3.5 grams of protein and here, the edema periorbital puffiness of what we talked about, sodium retention.

    04:47 It can be occasionally more extensive and usually not due to hypoalbuminemia but the fact that you’re retaining your sodium.

    04:58 Now, hypertension here is transient but at times, could be severe and it’s something that you wanna keep in mind especially in a child, in a child that was inadequately treated for a sore throat or pharyngitis if the child goes on to develop hematuria.

    05:11 Well, luckily, even the Sydenham chorea that you find, that we’ll talk about that later.

    05:17 But anytime that you have a group A streptococci, for the most part, take care of the bacteria, antibiotic and many a time, you’re going to be looking for treatment of that hypertension and the reason that I just mentioned the Sydenham chorea is those that occur within non-nephritogenic with pharyngitis causing rheumatic fever, it can be reversed and that’s amazing.

    05:41 Many times, especially with children, things are going to become irreversible, that is extremely sad.

    05:46 But group A streptococci tends to be one in which you can treat antibiotically and the manifestations that might be taking place later on either in the heart or in the kidney may be reversed quite dramatically.

    06:00 It usually resolves and chronic renal failure fortunately in a child, uncommon.

    06:06 Ninety-five percent of children who have PSGN will recover.

    06:11 What kind of deposit is this? You have memorized subepithelial deposit.

    06:16 Supportive, look for that hypertension, that’s huge, highlight that first.

    06:21 As far as your organism’s concerned, you have penicillins that are coming in if and when your patient’s positive for streptococci.

    06:29 I say if because here, once again, you could have noninfectious type of glomerulonephritis which I shall go into in a bit and they had dialysis.

    06:39 Meaning to say that if there’s kidney damage and during that time, if you need to clear out the organism and if there’s emergency hemodialysis that’s required, yes, you don’t hesitate, but the antibiotics are a must and you must treat that hypertension when it’s present.

    06:55 Now, with the Streptozyme test, important ones that you wanna keep in mind here.

    06:59 Typically rise, what you’re seeing here in green.

    07:04 ASO, anti-streptolysin O, anti-hyaluronidase, anti-nicotinamide or adenine-dinucleotidase, all part of typically rising in post-streptococcal, postpharyngeal is what we’re looking for, anti-DNAse B antibody.

    07:25 Once again, post pharyngeal cause, are we clear? Of what? Resulting in PSGN.

    07:31 Next, post-skin causes and by skin, it’s still the same organism.

    07:38 What is it? Group A streptococcus pyogenes, maybe perhaps, you’re thinking scarlet fever impetigo.

    07:44 The two that are typically risen under skin would be anti-streptokinase and anti-DNAse B antibody, and these, you’ll have to memorize.

    07:54 Keep this in mind, many a time, the PSGN is going to rise from the strain that is given rise by the skin streptococcal.

    08:02 It’s imperative that you know these streptozyme tests for all clinical purposes.

    08:08 Labs, what are we looking for? Well, we have nephritic, nephritic, nephritic.

    08:13 We talked about hypertension and its importance for management.

    08:16 Next, you do have your hematuria and under hematuria, RBC casts, yes.

    08:21 Could you find RBC’s? Sure.

    08:24 Most likely, what kind of RBC’s? Dysmorphic.

    08:27 Because you’ve activated your complement system, you can expect there to be deposition every complement and thus in your serum, you have hypocomplementemia, specifically, C3.

    08:38 Next, as far as your streptozyme tests are concerned, well, we just went through both of the strains, pharyngeal and skin.

    08:46 Antistreptolysin O, Anti-DNase B, Anti-cationic proteinase.

    08:51 Clinical features, prognosis, children, recovery, 95% and greater.

    08:56 Adults, not so much.

    08:58 Some may progress to RPGN, keep that in mind.

    09:03 When we get into RPGN, I’ll show you the difference.

    09:07 It’s the fact that your kidney, as the name applies, rapidly, and by rapidly, within three months, twelve weeks, that kidney dies.

    09:16 Now, does that occur commonly? Luckily, not, but keep that in mind because if not properly treated, there’s every possibility going to RPGN.


    About the Lecture

    The lecture Post-Streptococcal Glomerulonephritis by Carlo Raj, MD is from the course Glomerulonephritis.


    Included Quiz Questions

    1. Deposits are subepithelial.
    2. Deposits are between the endothelium and the GBM.
    3. Deposits activate T cell cytokines causing glomerular damage.
    4. Deposits may also be found in the heart tissue leading to acute rheumatic fever.
    5. Immune complexes activate the classical complement pathway.
    1. Hypoalbuminemia
    2. Hematuria
    3. RBC casts in the urine
    4. Hypernatremia
    5. Periorbital edema
    1. Anti-DNAse B antibodies
    2. Anti-streptolysin
    3. Anti-Nicotinamide-adenine-dinucleotidase
    4. Anti-streptokinase
    5. Anti-hyaluronidase
    1. Serum C3
    2. RBC casts
    3. Serum albumin
    4. Azotemia
    5. Proteinuria

    Author of lecture Post-Streptococcal Glomerulonephritis

     Carlo Raj, MD

    Carlo Raj, MD


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    Glomerular diseases
    By adrianmola2014@gmail B. on 17. April 2018 for Post-Streptococcal Glomerulonephritis

    It was great because I achieved to understand in detail a very complex topics. Thanks