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Ridgeview and the Ridgeview Continuing Medical Education Program are proud to present the Ridgeview Podcast: CME Series; a quality, portable and on-demand continuing medical education, that features a variety of exceptional physicians, providers and other staff from Ridgeview and it's affiliates. Hosts of the program are Fred DeMeuse, PA-C, Jason Hicks, PA-C, and Leah Radde, RN. Thanks for tuning-in, downloading and listening! 

 

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The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview & Ridgeview Clinics.  Any re-reproduction of any of the materials presented would be infringement of copyright laws. 

It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented.

Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event.

Mar 25, 2022

In this podcast, Dr. Kim Thielen, a nephrologist/kidney specialist with Minnesota Kidney Specialists joins us today to continue part 2 of our discussion on acute kidney injury, as we wade further "into the weeds" 
discuss intrinsic renal disease. This episode will break down hallmark urinary findings and
further subdivide intrinsic concerns into bland, nephrotic and nephritic, various causes, and
treatment.

Enjoy the podcast!

Objectives:
  Upon completion of this podcast, participants should be able to:

  • State the 3 types of urinary analysis findings related to instrinic acute kidney injury.
  • Describe etiology of presentation of each type of intrinsic acute kidney injury.

CME credit is only offered to Ridgeview Providers & Allied Health Staff for this podcast activity. Complete and submit the online evaluation form, after viewing the activity.  Upon successful completion of the evaluation, you will be e-mailed a certificate of completion within approximately 2 weeks. You may contact the accredited provider with questions regarding this program at  rmccredentialing@ridgeviewmedical.org.

To receive continuing education credit for this activity - click the link below, to complete the activity's evaluation.

CME Evaluation

(**If you are listening to the podcasts through iTunes on your laptop or desktop, it is not possible to link directly with the CME Evaluation for unclear reasons. We are trying to remedy this. You can, however, link to the survey through the Podcasts app on your Apple and other smart devices, as well as through Spotify, Stitcher and other podcast directory apps and on your computer browser at these websites. We apologize for the inconvenience.) 

DISCLOSURE ANNOUNCEMENT 

The information provided through this and all Ridgeview podcasts as well as any and all accompanying files, images, videos and documents is/are for CME/CE and other institutional learning and communication purposes only and is/are not meant to substitute for the independent medical judgment of a physician, healthcare provider or other healthcare personnel relative to diagnostic and treatment options of a specific patient's medical condition; and are property/rights of Ridgeview Medical Center & Clinics.  Any re-reproduction of any of the materials presented would be infringement of copyright laws. 

It is Ridgeview's intent that any potential conflict should be identified openly so that the listeners may form their own judgments about the presentation with the full disclosure of the facts. It is not assumed any potential conflicts will have an adverse impact on these presentations. It remains for the audience to determine whether the speaker’s outside interest may reflect a possible bias, either the exposition or the conclusions presented.

Ridgeview's CME planning committee members and presenter(s) have disclosed they have no significant financial relationship with a pharmaceutical company and have disclosed that no conflict of interest exists with the presentation/educational event.

Thank-you for listening to the podcast.

SHOW NOTES: 
*See the attachment for additional show information.
  
Intrinsic Kidney Injuries: Urinary analysis findings
- Bland Urine: no protein
- Nephrotic: protein
- Nephritic: protein and blood

Hallmark Urinary Findings: Casts
- Tamm Horsfall Protein : Mucoprotein made by tubular epithelial cells that precipitate out and congeal
   to form casts on whatever is in the cells at the time.  (i.e. RBCs, WBCs, tubular debris)

Bland Urine States
- Crystalline Induced Renal Injury: obstruction and infllamatory response
      - Uric Acid Neuropathy (Most common)
             - Cancers, lymphomas, etc.
             - Drugs: acyclovir, methotrexate, protease inhibitors, etc.
             - Toxins: Ethylene glycol
- Bland Urine Disease states: results from injury to tubules, instertim or pre glomerular blodd vessels, not
   the filters of the kidney
      - Interstital Nephritis
             - Hallmark: pyuria and WBC casts
                     - Biopsy: inflammatory infiltrate
             - Causes:  viral, PPIs, Adenover, mizalamin, etc., Checkpoint inhibitors
      - Acute Tubular Necrosis
             - Hallmark: tubular epithelial cell cast
                     - Granular: (course or fine) diagnostic of ATN
             - Biopsy: denuded dilated tubular cells
             - Causes: #1: Ischemia;  toxins, drugs, contrast dye;  pigment injury. myoglobin
             - What about contrast dye?
                     - Categorized under ATN
                     - Per Dr. Thielen, plays a role, but injury is not solely dependent on dye alone.
      - Hepatorenal Syndrome: ischemic injury to the kidney due to unopposed vasocontstriction
              - Ace inhibitors cause unopposed efferent vasoconstriction + nonsteroidals cause
                unposed afferent vasoconstriction = no glomerular perfusion pressure
      - Multiple Myeloma
             - Hallmark: Light chain cast nephropathy or myeloma kidney 
                    - Light chains precipitate  out causing obstruction, inflammatory response and causes
                       tubular damage
             - Presentation: older possibly with anemia, bone pain and elevated creatinine with a bland urine.
             - Protein to creatinine ratio: + for protein (non albumin)
             - Dipstick: (which measures for albumin and not light chains) will be negative for protein aka
                bland urine
      - Hypertensive Nephrosclerosis
             - Small vessel vascular disease
                    - Blood vessels prematurely atherosclerosis causing glomerular drop out and scarring of the
                       interstim
      - Scleroderma
               - Limited cutaneous systemic sclerosis
               - Diffuse cutaneous systemic sclerosis: 60-80% have renal injury from disease state itself
                          - FANA positive
                          - Concern for Scleroderma Renal Crisis = medical emergency
                                  - AKI, moderate to severe HTN and bland urine
                                  - Uncontrolled accumulation of collage, thickens vascular walls, narrowing and renal
                                      ischemia
                         - Occurs in 10-15% of those with Diffuse Cutaneous Systemic sclerosis and happens early
                             in disease
                                    - Left untreated: renal failure in 1-2 months and death in 1 year
                         - Treatment: ACE Inhibitor

Nephrotic Urine States
- Urine protein: albumin excretion greater than 3.5g in 24 hours
- Nephrotic Syndrome:
     - Present with 3 things (nephrotic range protein, hypoalbuminemia, peripheral edema)
      - Hyperlipidemia: due to increased hepatic lipogenesis
               - Increased risk of renal disease and arthroscleratic
      - Venous thrombotic disease:
                - Loose proteins other than albumin and develop a hypercoagulale state
                - Renal and peripheral venous thrombosis
      - Lipiduria (forms fatty casts,  looks like a latese cross under microscope)
 -Pathophysiology or nephrotic syndrome
   - Glomerular capillary wall
          - 3 layers that work as a glomerular filtration and responsible in the filtration between blood and
            urine
                 - Fenestrated Capillary Enothelial cells (fenestrations allow plasma through to the basement
                    membrane)
                - Glomerular Basement Membrane (maintains glomerular filtration barrier; negatively charged,
                    repels albumin)
                - Epithelium: Podocytes (Have highly specialized foot processes that connect and form slit
                    diaphragms; Slit diaphragm important for the efficient flow of small solute and water)
         - Anything that messes with any of these layers: nephrotic proteinuria
- Nephrotic Disease States:
    - Biopsy: anyone with nephrotic proteinuria (besides diabetics)
         1) Light microscopy: high overview
         2) Immunofluorescens: looks for nephritic component and identif immunce complexes
         3) Electron microscopy: (EM) helps look at the ultrastructure and better identify immune deposits
    - Diabetic nephropathy
          - Leading cause of kidney disease in U.S. and western society
          - Responsible for 30-40% of all ESRD causes
          - Hyperglycemia: produces inflammatory responses, oxidative stress, and injures the podocytes and
            deposits that charge and affect the ability of the kidney to filter.
    - Amyoidosis
           - Organize into betapleted sheets and produce spikes of the capillary uniion and poke through the
              GF membrane
           - Easily identified by apple green birefringence on congo red
           - Terminal illness
           - Present with HTN, cardiac effects and elevated creatine
 - Nephrotic Disease states based of histologic appearance
     - Diagnosed by histologic appearance but does not determine the etiology
     - Minimal Change Disease
             - Fairly common
             - Minimal change under light microscope
             - EM: podocytes are abnormal, fused, no unique cell-cell junction
             - Primary: Immune generated circulating facture;  alters the cytoskeleton of the podocytes
      - Secondary
              - Nonsteriodal - most common cause of secondary minimal change disease
              - Gama interferon
              - Hodgkin's lymphoma
              - Allergy: 30% of minimal change have associate allergy (mechanism unknown)
 
     - Presentation
              - Sudden onset (days to weeks)
              - Marked edema and hypoablbuminemia
              - 60% have normal blood pressure,    82% have normal creatinine
- Focal Segmental Glomerulosclerosis (FSGS) - primary and secondary 
       - Most common cause idopathic nephrotic syndrome in adults
       - Primary glomerulonephritis in the US that causes ESRD
       - Widespread podocyte injury
    - Primary: circulating factor that messes with regulation of foot process and adhesion to the
        glomerular basement membrane (afffect all podocytes)
         - Present with nephrotic syndrome and rapid progression
         - HTN and elevated creatinine
   - Secondary: the visceral epithelial cells don't replicate
         - Nephron loss or obesity or direct foot process injury
         - Cannot replicate (podocytes), leads to decreased to podo denisty at specific areas (focal injury)
         - 2/3 of all cases FSGS
         - Present: with slowly increasing proteinuria and kidney impairment over time
         - Causes: interferon, bisphosphonates, talc, anabolic steroids
   - Genetics: gene mutations that encode for the slit diaphragms of the podocytes (affect all podocytes)
           - Present in Childhood: full blown nephrotic and progress rapidly to ESRD

Membranous Nephropathy
- Most common cause of nephrotic syndrome in caucasion adults
- 80% present with nephrotic but develops more slowly to ESRD
- Primary: Major antigen identified
     - antibody to trans-membrane receptor that is highly expressed on the glomerular podocyte
- Secondary: Cancers (lung, breast, GI), Lupus, Thyroiditis, Hep B, Syphilis, Nonsteroidals, Monoclonal
   Antibodies

Nephritic Syndrome
- Hematuria and proteinuria
   - Hematuria: blood from kidney or outside the kidney
            - Outside the kidney: look the same
            - Inside the kidney: dysmorphic red cells
   - Present:
            - Renal impairment for days to weeks
            - Edmatous, HTN and look critically ill 
            - Vasculitis, sinusitis, oral ulcers
            - Pulmonary renal syndrome: short of breath or hemoptysis
            - Skin changes: bruising , bleeding, purpura
            - Myalgias and arthritis
    - Urine:
            - Hallmark: red blood cell casts (polymorphic red cells)
            - dipstick + for blood
            - elevated proteinuria
   - Biopsy: nephritic and + urine

Nephritic Disease States (based on immunofluorescence staining)
- Pauci Immune Disease
        - Ankle vasculitis, common
        - A paucity (little amount) of immune complexes
        - See black on imaging
        - Lab work: check on ANCA and peripheral eosinophils
- Anti-GBM Disease
        - Renal limited, or classic pulmonary renal: Good Pasture's
         - linear staining of the glomerular basement with anti IGG (looks like a ribbon on a package)
         - Treat with cytotoxic agents
 - Immune Complex
         - Starry sky pattern
         - Glomerulus looks dotted with stars
               - Stars = immune complex definition
         - Diseases:  Lupus (FANA), Post Infectious GN, Membranous Proliferative GN
 - IGA Nephropathy 
         - Most common cause of glomerulonephritis in the world
         - Presentation:
                - Peak incidence is the 2nd and 3rd decades of life
               - 40-50% gross hematuria with upper respiratory and GI illness
         - Risk Factors for Progression:
               - younger age or hypertension at time of presentation
               - > 1g proteinuria
               - Elevated creatinine at time of presentation

Thanks for listening.