Scribd Logo
Upload

Welcome to Scribd!

  • 3 views

    GlomerulonephritisTips and New Pathts UCMI

    Uploaded by

    Afonso Henriques Nunes

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd

    GlomerulonephritisTips and New Pathts UCMI

    Uploaded by

    Afonso Henriques Nunes
    3 views30 pages

    Original Title

    GlomerulonephritisTips and New Pathts UCMI (1)

    Copyright

    © © All Rights Reserved

    Available Formats

    PDF, TXT or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    3 views30 pages

    GlomerulonephritisTips and New Pathts UCMI

    Uploaded by

    Afonso Henriques Nunes

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    of 30

    Glomerulonephritis

    Tips and new paths

    Anabela Rodrigues , MD,PhD


    CHUdSA/ICBAS/ University of Porto/
    Portugal
    Learning objectives
    • Evaluation algorithm and diagnosis of patients with proteinuria,
    hematuria, nephrotic syndrome and acute glomerulonephritis
    • Serological assessment of glomerulonephritis
    • Indications and complications of renal biopsy
    • Treatment of nephrotic syndrome and acute glomerulonephritis,
    primary and secondary to systemic diseases
    Foot prints of glomerular disease
    • Glomerular hematuria
    • the presence of urinary RBC casts (of any number) or hematuria in which more than
    5% of RBCs are acanthocytes or dysmorphic

    • Proteinuria
    • is typically defined as a 24-hour urine protein excretion of ≥150 mg

    • Albuminuria
    • is the major component in glomerular disease, and is the protein that is detected by
    the urine dipstick) is typically defined as a 24-hour urine albumin excretion of ≥30 mg
    (or a corresponding value using the spot urine albumin, spot urine creatinine, and
    the albumin excretion rate equation)
    Copyrights apply
    Copyrights apply
    Copyrights apply
    Urine Sediment as a critical tool of GN evaluation
    DOI:https://doi.org/10.1053/j.ajkd.2018.07.012
    Critical tools of GN Non-invasive evaluation :

    Serology and Immunologic study


    Kidney biopsy
    Indications Contraindications and relative CI

    ● Small hyperechoic kidneys


    Nephrotic Nephritic ●Solitary native kidney
    ●Multiple, bilateral cysts or a kidney tumor
    syndrome syndrome ●Uncorrectable bleeding diathesis
    ●Severe hypertension
    ●Hydronephrosis
    ●Active renal or perirenal infection
    ●Anatomic abnormalities of the kidney
    Unexplained ●Skin infection over the biopsy site
    AKI ●An uncooperative patient
    ●When a skilled operator is not available
    Immune mechanisms of glomerular injury

    Environmental

    Infections Drugs

    Genetics
    Toxins Cancer
    Chek for systemic disorder

    - if there is an infection (particularly with Staphylococcus, Streptococcus,


    hepatitis virus, or HIV).
    - or inflammation of other organ systems, such as
    - the skin (eg, purpura, rash)
    - joints (eg, arthritis)
    - eye (eg, retinitis, uveitis)
    - nose (eg, epistaxis)
    - mouth (eg, ulcers)
    - lungs (eg, hemoptysis, infiltrates)
    - nervous system (eg, seizures, neuropathy)
    - extremities (eg, digital ischemia or infarction)
    - abdomen (eg, enteritis, colitis)
    Immune mechanisms of glomerular injury

    Inflammatory Noninflammatory
    • Glomerular hypercellularity • Usually involve the glomerular
    • hematuria podocyte
    • often dysmorphic appearance, • proteinuria
    with or without red blood cell
    casts
    • little or no hematuria and no red
    blood cell casts
    • varying degrees of proteinuria
    • active urine sediment (nephritic • nephrotic syndrome
    syndrome)
    Site of glomerular injury
    Inflammatory injury (Proliferative GN) Non Inflammatory (Non Proliferative
    GN)
    • endothelial and mesangial cells • epithelial cells (visceral and
    • contact with circulating factors or parietal)
    inflammatory cells • separated from the circulation by
    • Cellular recruitment and the GBM
    complement activation • podocyte lesion is commonly
    associated with little or no
    activation of circulating
    inflammatory cells
    • subepithelial immune deposits
    seldom produce glomerular
    inflammation
    Immune mechanisms of glomerular injury

    Humoral immunity Cellular immunity


    • Immune complexes that contain • particularly lymphocytes and
    immunoglobulins and complement macrophages
    • antigen(s) localized predominantly
    in the glomerulus
    • passive trapping
    • interaction with negatively charged
    sites on the glomerular capillary
    wall
    • receptors located in the
    mesangium
    Bacterial Infection–Related
    Glomerulonephritis
    • Unlike acute poststreptococcal GN in children, the prognosis of
    bacterial infection–related GN in adults is often poor
    • Up to one half of patients will develop persistent kidney
    impairment, and one third will progress to kidney failure
    • Overlap between bacterial infection–related GN, autoimmune
    disease, and complement system dysregulation
    • Universal glomerular C3 deposition and frequent
    hypocomplementemia

    CJASN August 2021, 16 (8) 1149-1151; DOI: https://doi.org/10.2215/CJN.07910621


    IgA GN
    • Presence of circulating and glomerular immune complexes composed
    of galactose-deficient IgA1
    • The presence of aberrant glycosylated IgA1 is an inherited trait
    (common phenotype: asymptomatic hematuria and progressive CKD
    • Clinical-Pathological Correlation: Mesangial hypercellularity (M),
    endocapillary hypercellularity (E), segmental glomerulosclerosis (S),
    tubular atrophy (T), MEST and Crescents
    • In addition to pathological findings, factors associated with poor
    prognosis include hypertension, proteinuria, and decreased eGFR at
    diagnosis.
    Dietary antigens and mucosal infections may drive
    the generation of pathogenic IgA

    Clin J Am Soc Nephrol 12: ccc–ccc, 2017. doi: 10.2215/CJN.07420716


    GN and age of presentation

    Clin J Am Soc Nephrol 12: 1680–1691, 2017. doi: https://doi.org/10.2215/CJN.02500317


    ANCA vasculitis
    • Autoimmune response
    • Pauci-immune necrotizing and crescentic GN
    • ANCA specific for myeloperoxidase (MPO-ANCA) or proteinase 3 (PR3-
    ANCA)
    • Clinicopathologic variant : microscopic polyangiitis, granulomatosis
    with polyangiitis (Wegener), eosinophilic granulomatosis with
    polyangiitis (Churg-Strauss), or renal-limited vasculitis.
    • ANCA vasculitis is most prevalent in individuals >50 years old
    • ANCAs cause disease by activating neutrophils to attack small vessels
    Clin J Am Soc Nephrol 12: 1680–1691, 2017. doi: https://doi.org/10.2215/CJN.02500317
    GN ANCA
    A low C3 with a normal C4 suggest activation of the alternative complement pathway
    https://doi.org/10.1016/j.smim.2019.101331
    Membranoproliferative GN (MPGN).

    Naveed Masani et al. CJASN doi:10.2215/CJN.06410613

    ©2014 by American Society of Nephrology


    Copyrights apply
    Points of action of the different potential causative factors of
    C3G in the complement cascade

    FHR, factor H-related proteins; C3/C5Nef, C3/C5 nephritic factor. https://doi.org/10.1016/j.smim.2019.101331


    Complexity is a challenge
    Enjoy the journey in Nephrology

    You might also like