IgA Glomerulopathy

by Carlo Raj, MD

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    00:01 Now, the first primary nephritic type of glomerular disease that we’ll take a look at is IgA glomerulopathy or IgA nephropathy. All the same thing, aka Berger. What I wish to bring to attention is there is another condition in pathology that we call Wegener’s disease. Wegener’s disease is going to be associated with small vessel disease or vasculitis. Completely different discussion. That’s point number one.

    00:29 Many students tend to get that confused between Berger’s and Buerger’s. They are two different conditions. One has nothing to do with the other. Berger has to, has to, be dealing with IgA.

    00:42 This IgA is then going to deposit, I’ll tell you in a second but before I get there this IgA could also be found in another important disease. That is an important differential that could also be associated with the kidney. Do you remember which one? What if I told you there’s IgA deposition in the kidney, or in the glomeruli and there’s also palpable purpura in a young child in the lower extremities or perhaps the buttocks. That’s called Henoch-Schonlein Purpura and a better name now clinically, and has been for quite some time called IgA vasculopathy. Are we clear? Be careful.

    01:19 This is only nephropathy. Berger, most common nephropathy worldwide. Meaning to say majority of nephritic and also take a look, nephrotic 5% of the time. So worldwide, this is the one that you definitely want to know. Next, it affects children and adults. Next, increased mucosal synthesis and decrease clearance of IgA. Thus you’ll find 50% of your population in which the IgA levels are elevated in the serum. Next, there is focal proliferative glomerulopathy. And this IgA is then going to deposit on your mesangium. May I ask you something? So therefore, which one of the biopsy patterns would most come in handy here, do you think? It will be the immunofluorescence in which in the mesangium you find green pools. Meaning to say immunoglobulin is accumulating in the mesangium resulting in green pool type of deposition. So mesangium IgA is what you're paying attention to. This immune complex that deposit to the granular immunofluorescence it ends up being in the mesangium. You're going to activate the complement pathway.

    02:27 Complement, the alternative. Overlapping features with Henoch-Schonlein purpura may occur.

    02:34 But the difference is with IgA here and Henoch-Schonlein, you pay attention to purpura in HSP.

    02:40 Henoch-Schonlein, the purpura representing involvement of your blood vessel.

    02:44 In Berger, that is not the case. But in HSP, could you involve the blood vessel and the kidney? Yes, you can. What’s the immunoglobulin? AAA. Episodic bouts of hematuria. I need you to pay attention to the description, episodic. That is big in medicine. You can have episodic type of events with hypertension. That’s pheochromocytoma. You could have episodic events of jaundice, that’s Gilbert or Gilbert’s syndrome. You have episodic bouts of hematuria. Higher on the differential, you should be thinking about IgA nephropathy. Usually following a upper respiratory tract infection.

    03:24 Highlight that in your head. Hyper or upper respiratory tract type of infection, you don’t have this latent period. For example, say that you had sore throat or pharyngitis. Two to four weeks later, that would not be Berger. Two to four weeks later, would be PSGN, with hematuria. If we’re talking days after a sore throat or pharyngitis, that would be Berger IgA nephropathy. Did you hear what I just said? And how important it is based on that history to come up with two differentials and which one will be a more likely differential if you had what's known as synpharyngitic.

    04:06 Synpharyngitic basically means the days after a pharyngitic episode, upper respiratory tract infection, your patient now has developed hematuria. Slow progression to chronic renal failure.

    04:20 Only 40, 50% at a time but it’s slow progression. Many times you can have kidney damage not necessarily going into chronic renal failure. Corticosteroids, decrease proteinuria.

    04:30 Treat the hypertension which you must do. Remember especially for the child, these are things that you want to keep in mind.

    About the Lecture

    The lecture IgA Glomerulopathy by Carlo Raj, MD is from the course Glomerulonephritis.

    Included Quiz Questions

    1. IgA nephropathy
    2. Buerger's disease
    3. Henoch-Schonlein purpura
    4. Post-streptococcal glomerulonephritis
    5. IgA vasculitis
    1. Episodic bouts of hematuria
    2. Episodic bouts of periorbital puffiness
    3. Episodic bouts of hypertension
    4. Episodic bouts of proteinuria
    5. Episodic bouts of vasculitis
    1. Increased hydrostatic pressure due to salt retention
    2. Decreased oncotic pressure due to proteinemia
    3. Decreased hydrostatic pressure due to salt retention
    4. Increased oncotic pressure due to proteinuria
    5. Decreased hydrostatic pressure due to proteinuria
    1. Proteinuria greater than 3.5 g/day
    2. RBC casts are a key finding indicating glomerular damage.
    3. Proteinuria greater than 150 mg/day but less than 3500 mg/day
    4. The tubular function is intact in acute disease.
    5. GFR is decreased due to glomerular inflammation.
    1. Mesangium
    2. Subendothelium
    3. Subepithelium
    4. Epithelium
    5. Vascular
    1. Length of time between infection and clinical manifestation
    2. Vasculitis
    3. Immune complex deposition
    4. Amount of hematuria
    5. Amount of proteinuria
    1. Vasculopathy
    2. Immune complexes
    3. Neuropathy
    4. Proteinuria
    5. Hematuria
    1. Proteinuria > 3.5 g/day
    2. Increased serum IgA
    3. Granular pattern on immunofluorescence
    4. Decreased clearance of IgA
    5. Increased mucosal synthesis of IgA

    Author of lecture IgA Glomerulopathy

     Carlo Raj, MD

    Carlo Raj, MD

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