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IgA Nephropathy Southwest Nephrology Symposium February 24th 2018.

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Presentation on theme: "IgA Nephropathy Southwest Nephrology Symposium February 24th 2018."— Presentation transcript:

1 IgA Nephropathy Southwest Nephrology Symposium February 24th 2018

2 Nephron Functional unit in the kidney
There are about 1 million nephrons in each human kidney Nephrons remove excess water, wastes and other substances from your blood into urine Each nephron is composed of two main structures. The glomerulus and kidney tubule

3 Nephron

4 Renal Corpuscle

5

6 Glomerulus Tiny blood vessel or capillary Looks like a ball of yarn
Actual filtering of blood occurs in the glomerulus Keeps normal protein and cells in your bloodstream Allows wastes, excess fluid and other substances to pass

7 Nephron

8 Glomerulonephritis Acute inflammation of the kidney
Typically caused by an immune response

9 Immunoglobulins Also known as antibodies
Antibodies are substances made by body’s immune system in response to bacteria, viruses, animal dander or cancer cells There are five major types IgA, IgG, IgM, IgE, IgD

10 IgA Nephropathy First described by pathologist Jean Berger and so also called Berger’s Disease

11 IgA Nephropathy Immune complex disease in which IgA deposits in the glomerular mesangium and cause mesangial injury Most common glomerulonephritis in the western world

12 Henoch-Schonlein purpura
Small vessel vasculitis Defined by tissue deposition of IgA Involves the skin, gut and kidneys Difference from IgA nephropathy is that it has extra renal manifestations

13 IgA Immunoglobulin A is an antibody
Plays critical role in immune function in the mucus membranes

14 IgA nephropathy clinical features
Gross hematuria usually following upper respiratory infection 40-50% Microscopic hematuria and mild proteinuria 30-40% Nephrotic syndrome or rapidly progressive glomerulonephritis characterized by edema, hypertension and renal insufficiency as well as hematuria in less than 10% More common in Asians and Caucasians and Native Americans 2:1 Male to female perdominance in Caucasians but not Asians 20-40% develop ESRD 20 years after diagnosis is made

15 Clinical Associations
Cirrhosis Celiac disease ( Gluten enteropathy) HIV infection

16 Urine Analysis Dipstick: Blood and Protein
Microscopic exam: RBC, RBC casts or dysmorphic RBC

17 RBC Cast

18 Dysmorphic RBC

19 Kidney Biopsy

20 Core Biopsy Specimen

21 Clinical predictors of progression
Elevated serum creatinine Hypertension > 140/90 mm Hg or new difficult to control BP Proteinuria more than 1 gram per day

22 Histological predictors of progression
Mesangial hyprecellularity Endocapillary hyprecellularity Segmental glomerulosclerosis Tubular atrophy and interstitial fibrosis Crescents ( Minimum 8 glomeruli needed for a good diagnosis)

23 Treatment Non immunosuppressive
High BP control: ACE-I or ARB Omega-3 fatty acids Statin therapy: Cholesterol lowering medications

24 Treatment Immunosuppressive
Steroids Cytoxan Imuran

25 ESRD due to IgA Nephropathy
Renal replacement therapy: Hemodialysis or Peritoneal Dialysis Kidney Transplantation

26 Transplantation 60 % of transplant patients show recurrence of IgA nephropathy by transplant biopsy but clinical significance is not that high


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