Renal Clinical Anatomy

by Carlo Raj, MD

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    Students often have an issue with figuring out the various pathologies because they dive right into the lesions without really understanding renal clinical anatomy. So in this lecture series, initially we will be laying down the foundation as to which you need to take a look at. For example, you have heard of subepithelial, subendothelial deposits, but once again you will perhaps memorize that and at some point of time, you will be asked on electron microscopy how to identify. It is important that we lay down the foundation, in this first set of lectures so that as we move towards into glomerulonephritis and tubular interstitial disease, everything makes a lot more sense. Let us begin. We had seen this picture before and the reason we had was we were referring to secondary hypertension when dealing renal artery stenosis. Well, that was a beautiful discussion at the time. Let us now move into what we need to know here in the glomerular pathology. The glomerulus, I want you to come down the afferent arteriole and then as you do so, you are coming into the tuft of capillaries versus glomerular tuft or we will be spending a lot of time in that area and in fact, we will be blowing it up, amplifying it and then go through various imaging studies that is relevant for your diagnosis of your patient. What are the different things that are taking place in the tuft capillaries is what is relevant and our next logical question. We begin with this slide as being quite important. Filtration barrier is what we'll set up and before you do any of that, I am going to give you steps that you want to take every single time. When you see a picture like this, that is then...

    About the Lecture

    The lecture Renal Clinical Anatomy by Carlo Raj, MD is from the course Renal Clinical Anatomy. It contains the following chapters:

    • Renal Clinical Anatomy
    • Filtration Barrier
    • Structure of the Glomerulus
    • Clinical Anatomy of the Glomerular Apparatus

    Included Quiz Questions

    1. Fenestrated endothelial cells, GBM, slit diaphragms of podocytes
    2. GBM, slit diaphragms of podocytes, fenestrated endothelial cells
    3. Slit diaphragms of podocytes, GBM, fenestrated endothelial cells
    4. Fenestrated endothelial cells, slit diaphragms of podocytes, GBM
    5. Slit diaphragms of podocytes, fenestrated endothelial cells, GBM
    1. Glomerular basement membrane.
    2. Podocytes
    3. Bowmans space
    4. Fenestrated cells
    5. Slit diaphragms
    1. They are present on the endothelial cells of glomerular capillaries.
    2. They represent the only filtration barrier in the glomerulus.
    3. All of the statements are true.
    4. They are located between the glomerular membrane and the podocytes.
    5. They are responsible for repelling albumin.
    1. Fenestrations
    2. Podocytes
    3. Slit diaphragms
    4. Visceral epithelial cells
    5. Foot processes
    1. Heparin sulfate.
    2. Podocytes
    3. Cationic proteins
    4. Inflammatory mediators
    5. Type IV collagen
    1. Type IV collagen
    2. Heparin sulfate
    3. Immune complexes
    4. Albumin
    5. Type II collagen
    1. Parietal epithelial cells
    2. Type IV collagen
    3. Visceral epithelial cells
    4. Glomerular basement membrane
    5. Mesangial cells
    1. Immune complexes that are deposited are produced in mesangial cells.
    2. It is a cause of glomerular basement membrane thickening.
    3. All the statements are correct.
    4. Post-streptococcal glomerulonephritis is a potential etiology.
    5. It is associated with membranous glomerulopathy.
    1. Supporting glomerular capillaries.
    2. Produce the glomerular basement membrane.
    3. None are functions of visceral epithelial cells.
    4. All are functions of visceral epithelial cells.
    5. Serves as a distal barrier preventing protein loss in the urine.
    1. Visceral epithelial cells
    2. Mesangial cells
    3. Endothelial cells
    4. Fenestrated cells
    5. Parietal epithelial cells
    1. Alport disease
    2. Ehlers Danlos
    3. All have defects of type IV collagen.
    4. Osteogenesis imperfect
    5. Marfans
    1. Strongly negatively charged proteins
    2. Water
    3. Proteins < 70000 daltons
    4. Sodium
    5. Urea
    1. They are the lining cells of Bowmans capsule.
    2. They are contractile.
    3. They are responsible for immune complex deposition in IgA glomerulopathies.
    4. They are phagocytic.
    5. They produce the GBM matrix.

    Author of lecture Renal Clinical Anatomy

     Carlo Raj, MD

    Carlo Raj, MD

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