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134 Cards in this Set
- Front
- Back
Glomerular diseases induced by NSAIDs (2)
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-Minimal Change Disease
-Membranous Nephropathy |
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Pulmonary-Renal Syndromes (4)
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-Goodpastures (Anti-GBM)
-Granulomatous Vasculitis (c-ANCA) -SLE (Lupus) -HS Purpura (type of IgA Nephropathy) |
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Renal diseases that primarily affect people over the age of 50
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Pauci-immune RPGN
MicroPAN amyloidosis |
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Secondary causes of IgA Nephropathy (4)
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-HS Purpura
-Chronic liver disease -Celiac's Disease -Inflammatory Bowel Disease |
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Presentations of IgA Nephropathy (3)
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-Macroscopic hematuria coupled to upper respiratory infection
-Asymptomatic microscopic hematuria with <1g proteinuria -Nephrotic (less common) |
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Renal diseases proceeding upper respiratory infections (3)
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-IgA Nephropathy
-HS Purpura -PSGN |
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Viral renal diseases (3)
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-HIV: FSGS (Collapsing)
-Hep B: Vasculitis (microPAN) -Hep C: MPGN Type I (Type II is usually primary due to C3 NeF) |
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mechanism of hyperlipidemia in nephrotic syndrome (2)
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-less albumin = more chol. produced
-LCAT (enzyme that helps chol. return to the liver) lost to filtration |
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Hypercoaguability in nephrotic syndrome (explain)
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loss of clotting inhibitors (protein S, antithrombin 3) to filtration
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Clinical presentation: MCD vs FSGS (4)
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a.Hematuria
b.Renal function (elevated creatinine) c.HTN d.Selective vs non-selective proteinuria |
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Non-nephritic causes of hematuria (2)
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a.Urinary blood clots
b.Kidney stone (post-renal obstruction) |
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Glomerular disease caused by malignancy (3)
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a.Membranous Nephropathy
b.MCD (lymphoma) c.MPGN |
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Renal diseases that affect people over 50: (4)
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a.Amyloidosis
b.C-ANCA + Granulomatous vasculitis (pauci-immune) c.MicroPAN vasculitis (pauci-immune) d.Membranous Nephropathy (especially if 2’ to malignancy) |
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Renal diseases that affect males more than females: (6)
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a.Amyloidosis
b.Fabry’s (X-linked) c.Membranous d.IgA Nephropathy e.MPGN Type I (young male smoker) f.Alport's (mainly X-linked) |
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Nephrotic Diseases (5)
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-Minimal Change Disease
-FSGS (HIV Nephropathy) -Membranous (lupus V) -Amyloidosis -MPGN Type I |
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Renal diseases that present with intense pain (3)
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-PCKD (flank)
-Fabry's (distal limb neuropathy) -Sickle cell nephropathy (colic if clots obstruct; can present w/ painless hematuria) |
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Disease associated with lysosomal defect
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Fabry's
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Complement activation in Membranoproliferative Glomerular Nephritis (MPGN)
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a.Type I = low levels of C3, C1q, C4
b.Type II = low levels of C3 for a longer time |
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Gender/Age/Race risk factors for Goodpastures
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a.Gender = Male
b.Age = 30s c.Race = N/A |
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differences between types I and II Rapidly Progressive Glomerular Nephritis (RPGN) Disease Examples = ?
EM findings = ? IF findings = ? |
a.Disease example? I = Goodpastures, II= Lupus
b.EM findings? I = nothing, II = deposits in loops/mesangium c.IF findings (what location is being stained and how is it staining)? I = linear IgG loops/mesangium, II = granular loops/mesangium |
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Epithelial crescents will be stained and capillary loops will not be stained when _____ is used.
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Trichome
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Membranoproliferative Glomerular Nephritis (MPGN) microscopy findings
LM = ? IF = ? EM = ? |
a.LM (2)
i.Lobular appearing capillary loops ii.“Tram-Tracking” (separation of endothelium and epithelium of GBM) b.IF: “tree trunks (mesangium) and branches (capillary loops)” c.EM (Type I and Type II) i.Type I = mesangial interposition within GBM ii. Type II = Dense deposits within GBM |
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Clinical differences in the two types of Membranoproliferative Glomerular Nephritis (MPGN)
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a.Type I = more nephrotic
b.Type II = more nephritic |
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Describe the H/E, IF, and EM findings of PSGN
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a.H/E: hypercellular glomeruli, WBCs, Diffuse glomerular involvement
b.IF: “camel hump” staining of IgG underneath the podocytes c.EM: subepithelial deposits |
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Lamellar (zebra) bodies are specific for _____ Disease.
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Fabry's
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Lenticonus lens defect is specific for _____ Disease
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Alport's
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Membranous Glomerulonephritis: where are the immune complexes made and where do they reside?
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a.In-situ (made on site)
b.Subepithelial or Membranous Deposits |
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Describe the IF findings of Membranous Glomerulonephritis
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a.Continuity? Granular (non-continuous)
b.Molecules? IgG and C3 |
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Spiky projections of the GBM are seen in which disease
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Membranous Glomerulonephritis
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Membranous Glomerulonephritis...
a.Diffuse or Focal? b.Thickening of what structure due to which molecules? c.Nephrotic/Nephritic Syndrome? |
a.Diffuse or Focal?
Diffuse b.Thickening of what structure due to which molecules? Capillary loops, Immune complexes c.Nephrotic/Nephritic Syndrome? Nephrotic |
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Name the diseases caused by mutations in the following…
a.Nephrin? b.Podocin? c.Actinin? |
a.Nephrin? MCD
b.Podocin? FSGS c.Actinin? FSGS |
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Classic FSGS immunofluoresence findings (2 molecules) within sclerotic segment of glomerulus:
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a.IgM
b.C3 |
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Three major 2’ causes of FSGS
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a.HIV
b.Obesity c.HTN |
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Analogy time
_______ : Focal :: Global : _______ |
Diffuse : Focal :: Global : Segmental
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Pathology signs of MCD (2 LM, 1 EM):
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a.Loss of brush border in PCT cells (LM)
b.Lipid droplets in tubular cells and urine (LM) c.Podocyte effacement (EM) |
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________ injury leads to proteinuria.
__________ injury leads to hematuria. |
_podocytes_ injury leads to proteinuria.
_capillary/mesangium__ injury leads to hematuria. |
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“Full House” meaning in Lupus
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a.During all classes (especially 2 and above) of lupus, all kinds of Igs are involved in mesangial deposits
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3. Location of deposits in lupus 3,4,5
3 = 4 = 5 = |
3 = subendothelial
4 = subendothelial 5 = subepithelial |
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Thrombi, crescents, tubular injury are all signs of disease _________ in lupus, whereas tubular atrophy, progression to fibrous crescents, and progression to interstitial fibrosis are signs of disease _______.
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a. Activity Level
b. Chronicity |
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Age/Gender/Race risk factors of IgA Nephropathy
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a.Age = 20s/30s
b.Gender = Male c.Race = Asian |
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Microscopy findings in IgA Nephropathy
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a.LM = mesangial hypercellularity
b.IF = Granular IgA deposits c.EM = mesangial deposits |
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Differences between Henoch-Schonlein Purpurua and IgA Nephropathy
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a.Age = HSA affects kids; IgA affects 20s/30s
b.Crescent formation and Glomerular necrosis = only common in HSA c.Extra-renal symptoms = only in HSA |
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9.Infectious endocarditis can present with renal symptoms, most commonly _____
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a.Hematuria
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Skin testing in Alport’s disease (to whom does it apply, and describe possible findings)
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a.Only the X-linked (alpha 5) kind
b.Affected males have almost no staining; female carriers have mosaic staining |
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Thin Membrane Disease is very similar to the recessive forms of Alport’s due to the common defect in _______
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a.Alpha 3/4 Collagen IV chains
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Thickening of the GBM, nodules of collagen IV + ECM that stain black, and mesangial hypercellularity are hallmarks of ________
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Diabetic Glomerular Sclerosis
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Normal width of GBM
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350 nm +/- 50 nm
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Renal presentation/progression in amyloidosis
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a.Proteinuria
b.Progression to uremia, renal failure |
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2 chemicals that stabilize amyloid fibrils
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a.SAP (serum amyloid protein, an acute phase c-reactive protein)
b.Gylcosaminoglycans (GAGs) |
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Two forms of AL amyloidosis
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a.Primary: just messing up of the proteins
b.Immunoproliferative: B cells are spitting out Ab’s like crazy |
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Two forms of PAN (BV Inflammation)
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a.Classic: medium-small artery involvement; no glomerular disease; could affect kidneys via infarct/aneurysm
b.Micropan: capillaries, more likely to have nephritic presentation; M > F; 60s; |
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strange (isn't seen in any other renal disease we covered) symptom of sickle cell nephropathy
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increased GFR (may explain proteinuria)
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2 determining factors for giving treatment to Membranous nephropathy patients
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1. gender (males at higher risk)
2. proteinuria |
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Diseases that affect African Americans more than other ethnicities (4)
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-Lupus
-Sickle Cell Nephropathy -Polycystic Kidney Disease -FSGS |
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extra-renal presentation of PCKD (4)
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Diverticulosis
Benign GI cysts Berry Aneurysms Mitral Valve Prolapse |
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Diagnostic criteria for PCKD
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US/CT
2 cysts in each kidney (30-60) 1 cyst in each kidney (under 30) |
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name all the cystic kidney diseases (not including pediatric urinary obstruction disease) (4)
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-PCKD
-Simple Cysts (aging, benign) -Acquired (smaller kidneys than PCKD) -Medullary (teens, ESRD, bad news) |
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Name the cystic kidney diseases (not including pediatric urinary obstruction diseases) (4)
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PCKD
Simple cysts Acquired Medullary |
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Extra-renal PCKD features (4)
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Berry aneurysms
Diverticulosis GI cysts MV prolapse |
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Kidney specific problems in PCKD (4)
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rupture
bleeding enlargement of kidney infection |
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PCKD: age of symptom onset
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mean = 45 years
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Medullary cystic KD
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the worst one; teens with ESRD; autosomal dominant
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earliest symptom in Alport's (male or female carrier)
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hematuria (if in female carrier, microscopic)
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PCKD dx:
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US/CT
30-60: two cysts in each kidney under 30: one cyst in each kidney +60: probably simple aging cysts, benign |
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extra-renal features of fabry's
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corneal opacities, Left ventricular hypertrophy, purple rashes, distal limb pain (neuropathy)
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extra-renal features of Alport's
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hearing loss (90% @ 40)
anterior lenticonus, platelet abnormalities |
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Two factors that, when increased, lead to sickling of RBCs in sickle cell disease
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1. osmolarity
2. [H+] |
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most consistent, early feature of sickle cell kidney nephropathy
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conc. defect (max urine osmolarity ~400)
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Classic signs of allergic (non-NSAID) AIN (3)
Which drugs cause it? |
-Allergy (eosinophils/rash/fever)
-Mild proteinuria -Hematuria (microscopic, without RBC casts b/c the glomerulus is fine) -Recent antibiotic/diuretic/PPI/allopurinol use |
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Distinguishing features of NSAID AIN (from normal allergy AIN) (3)
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-lymphocytes instead of eosoinophils
-glomerular involvement -nephrotic-range proteinuria |
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ways to explain high eosinophils in urine/blood (3)
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1. AIN
2. cholesterol emboli 3. contrast-induced |
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Three general types of CIN (covered in class)
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1. Analgesia
2. Oxalate 3. Metals |
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Sterile pyruia: what is it and how is it revelant to CIN
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urine containing pus that doesn't yield a culture sample
found in analgesic CIN |
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presenting factors of analgesic CIN
age? urine findings? systemic features? |
Age = 30-70
Urine findings = [+] protein [-] hematuria, bacteria (sterile pyuria) Systemic = HTN, back/head pain |
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Diagnostic sign of analgesic CIN
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[imaging] small, lobulated kidneys with papillary calcifications
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analgesic CIN: synergy of negative effects due to ______ and ______.
What are the negative effects of each analgesic? Where do they occur in the kidney? |
NSAID, acetominophen
NSAIDs = ischemia due to lower GFR 2' to decreased prostaglandins Acetaminophen = oxidative damage 2' to reduced levels of glutathione MEDULLARY fibrosis |
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Conditions that indicate Fanconi's (or a Fanconi-like) syndrome
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1. Positive glucose dipstick (probably hyperglycemia, but could be Fanconi's if pediatric)
2. Cadmium-induced CIN 3. pRTA |
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where does class II MHC fit into the schematic for AIN?
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tubular insult > MHC II upregulation > T-lymphocytes/Macrophages > edema, fibrosis, renal decline
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Negative effects of high [oxalate]
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1. bone dz
2. arthritis 3. heart conduction problems |
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type II 1' oxalosis
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hepatic enzyme defect causes increased NAD+, drives glycoxylate metabolism toward oxalate
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type I 1' oxalosis
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hepatic enzyme defect prevents conversion of glyoxylate to glycine, shunting it to a different (oxalate) pathway
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decreased absorption of _____ ties up _____ and allows oxalate to be reabsorbed in the _______
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decreased absorption of _fat_ ties up _Ca2+_ and allows oxalate to be reabsorbed in the _colon__
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Analgesic CIN increases one's risk for (3)
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HTN
Athersclerosis Urinary tract cancer |
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mechanisms for damage in lead-induced CIN (3)
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-decreased cellular respiration
-cortical atrophy -impaired excretion of uric acid |
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clinical presentation of lead-induced CIN (3)
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HTN
Gout min. 5-10 years Pb2+ exposure |
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Histology of lead-induced CIN
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similar to hypertensive nephrosclerosis
-tubular/interstitial changes -late in course glomerular changes -PCT damage |
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2 features that would confirm CIN 2' to Cd2+ (assuming prolonged exposure)
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-lots of metabolites in urine (Fanconi-like)
-kidney stones (hypercalciuria) |
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Analgesic CIN increases one's risk for (3)
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HTN
Athersclerosis Urinary tract cancer |
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mechanisms for damage in lead-induced CIN (3)
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-decreased cellular respiration
-cortical atrophy -impaired excretion of uric acid |
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clinical presentation of lead-induced CIN (3)
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HTN
Gout min. 5-10 years Pb2+ exposure |
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Histology of lead-induced CIN
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similar to hypertensive nephrosclerosis
-tubular/interstitial changes -late in course glomerular changes -PCT damage |
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2 features that would confirm CIN 2' to Cd2+ (assuming prolonged exposure)
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-lots of metabolites in urine (Fanconi-like)
-kidney stones (hypercalciuria) |
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Analgesic CIN increases one's risk for (3)
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HTN
Athersclerosis Urinary tract cancer |
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mechanisms for damage in lead-induced CIN (3)
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-decreased cellular respiration
-cortical atrophy -impaired excretion of uric acid |
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clinical presentation of lead-induced CIN (3)
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HTN
Gout min. 5-10 years Pb2+ exposure |
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Histology of lead-induced CIN
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similar to hypertensive nephrosclerosis
-tubular/interstitial changes -late in course glomerular changes -PCT damage |
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2 features that would confirm CIN 2' to Cd2+ (assuming prolonged exposure)
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-lots of metabolites in urine (Fanconi-like)
-kidney stones (hypercalciuria) |
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Analgesic CIN increases one's risk for (3)
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HTN
Athersclerosis Urinary tract cancer |
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mechanisms for damage in lead-induced CIN (3)
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-decreased cellular respiration
-cortical atrophy -impaired excretion of uric acid |
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clinical presentation of lead-induced CIN (3)
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HTN
Gout min. 5-10 years Pb2+ exposure |
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Histology of lead-induced CIN
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similar to hypertensive nephrosclerosis
-tubular/interstitial changes -late in course glomerular changes -PCT damage |
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2 features that would confirm CIN 2' to Cd2+ (assuming prolonged exposure)
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-lots of metabolites in urine (Fanconi-like)
-kidney stones (hypercalciuria) |
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differentiating acquired from genetic oxalosis
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acquired = later in life, usually with anatomical bowel resection or increased oxalate intake
genetic = presents earlier in life (childhood) |
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renal disease with prominent lipid droplets in PCT epithelial cells
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Minimal change disease
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Minimal change disease IF findings
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nothing
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Common (3) and less common (3) 2' causes of FSGS
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Common = obesity/HTN/sickle cell Dz; Less common = de novo (transplant), UTI, Obstruction
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mutations in these genes can result in which diseases: alpha-actinin, podocin, nephrin
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alpha-actinin and podocin = FSGS; nephrin = Minimal Change
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histological differences between classic and collapsing FSGS (with respect to cap loops and podocytes)
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Classic = sclerosed cap loops + podocyte loss (peripheral damage); Collapsing = collapsed cap loops + podocyte proliferation (central damage)
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Etiologies of collapsing FSGS (3)
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HIV (infects podocytes) mainly, but also CMV and Hep C
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IF findings of FSGS
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sclerotic areas + mesangium have IgM and C3
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Membranous Glomerulonephritis mechanism
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IgG binding to endogenous glomerular antigens
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the relatively small fraction of 2' membranous GN cases are due to (3)
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Hepatitis B, Lupus, Malignancy
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IF findings of Membranous GN
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Diffuse, granular deposits of IgG (M+A if lupus) and C3 in a capillary loop pattern
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EM findings of Membranous GN
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subepithelial/intramembranous dense deposits + podocyte effacement (loss)
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Heymann Nephritis
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animal model for membranous GN; inject PCT brush border antigens (megalin); get anti-megalin Abs
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negative prognosis predictor in FSGS
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proteinuria > 10g/day and HTN
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negative prognosis predictor in APSGN
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presence/abundance of glomerular crescents
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glomerular diseases and types of proteinuria (2)
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MCD is selective (albumin) and FSGS is non-selective
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FSGS Tx
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Primary FSGS = corticosteroids; Secondary FSGS = ACEi
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presentations of FSGS
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HTN = 30%; microscopic hematuria = 50%; less severe proteinuria/edema than MCD; renal decline = 30%
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example of a glomerular disease with normal serum complement levels despite local complement activation
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Membranous
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Membranous Glomerulonephritis LM findings (2)
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silver stain shows spikes on GBM; capillary loop thickening;
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negative prognostic factors for Membranous (3)
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proteinuria > 10g/day. HTN, male (same as FSGS except for gender)
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ASPGN LM findings (3)
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ALL OF THESE ARE DIFFUSE, DAMAGE IS EVERYWHERE: capillary thrombi (maybe); endocapillary proliferation w/ neutrophils; enlarged caps
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ASPGN IF findings
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Granular deposits of IgG/M and C3 in mesangium/GBM
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ASPGN EM findings
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subepithelial "humps"
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to be a RPGN, must have this histological finding:
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LM: diffuse (more than 50%) of glomeruli featuring cellular crescents (indicate acute process)
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goodpasture's tx (2)
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cytotoxics (kill lymphocytes) and plasmaphoresis (remove problematic antibodies)
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common MPGN LM findings (2)
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endocapillary proliferation and "tram-tracking" (splitting of GBM)
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MPGN Type I histo findings
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Type 1 = IgG and C3/4 granular diffuse deposition (IF) and mesangial interposition or subendothelial deposits (EM)
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MPGN Type II histo findings
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Type 2 = continuous (non-immune complex) material that looks like another membrane or layer (EM); granular irregular linear C3 deposition (IF)
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Differences between Types I and II MPGN (age, presentation, pathology, EM, complement, etiology)
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Type I = children, immune complexes, often due to HepC; nephrotic, C4/1q depression, mesangial interposition and endothelial deposits on EM; Type II = young children; C3 NeF; duplication of GBM on EM; nephritic presentation
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Lupus EM findings by class
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3/4 = subendothelial; 5 = subepithelial
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transition from Lupus II to Lupus III as seen on IF
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just mesangial (tree trunk) staining on II; III has loop + mesangial staining (more global)
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