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95 Cards in this Set

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Nephritic Clinical Symptoms
Hematuria, proteinuria, hypertension. RBC casts, and acanthocytes are pathognomonic
Nephrotic clinical sympotoms
Proteineria, hypocomplementemia, hyperlipidemia, edema, > 3.5 gm protein/day
Prerenal azotemia
Increased BUN w/o tubular necrosis - from decreased GFR
Chronic Renal Failure - Na balance
Na excess & Hypervolemia
Chronic Renal Failure and K balance
Little chenge unless GFR < 5mL
Chronic Renal Failure: CV & Pulm abnormalities
CHF, Pulmonary Edema, Hypertension,
Chronic Renal Failure: Hematologic Abn.
Dec RBC #, WBC function, clotting.
Minimal Change Disease: Epidemiology
Especially found in children
Minimal Change Disease: LM
Normal
Minimal Change Disease: IF
IgM (maybe)
Minimal Change Disease: EM
Effacement of podocytes, no immune dep.
Minimal Change Disease: Definition
Fusion of Epithelial foot processes, typically ~1wk after infection. Explosive edema, foam cells.
FSGS:LM
Segmental sclerosis of glomeruli
FSGS: IF
Focal & Segmental IgM, C1q
FSGS: EM
Foot process fusion, sclerosis, hyalinosis
Membranous nephropathy: Epidemiology
Most common nephritis in adults, male, esp 40, 60 (nephrotic), assoc. w/ renal vein thrombosi
Membranous Nephropathy: LM
(late) GBM thickening
Membranous Nephropathy: IF
Granular, IgG, C3
Membranous Nephropathy: EM
Supepithelial deposits, GBM expansion
Membranoporliferative Definition
Complement mediate (type I: classic & alternate, type II(DDD): alternate) nephritic/nephrotic disease.
Membranoproliferative: Epidemiology
2nd, 3rd decade.
Membranoproliferative: LM
Hypercellular glomeruli, duplicated GBM's (tramtracks)
Membranoproliferative: IF
Type 1: C3, IgG, IgM. Type II: C3 in capillary and mesangium
Membranoproliferative: EM
Type 1: Subendo Type II: Dense GBM
IgA Nephropathy: Definition
Nephritic disease - IgA deposits in Mesangium. Red or cola colored urine 1-2 d after infection.
Iga Nephropathy: LM
Focal proliferative w/ diffuse mesangial widening
Goodpastures (anti-GBM): Definition
Ab's against GBM that can also affect lung. Assoc. w/ smoking, hydrocarbon exposure, cocaine. (NEPHRITIC)
Wegeners Definition
P-ANCA abs cause Nephritic, pauci immune disease
Microscopic Polyangiitis
P or C ANCA abs cause Nephritic, pauci immune disease.
Churg Straus
Eosinophilia causes nephritic disease.
Post infectious GN
Nephritic disease 1-2 weeks after infection (esp Strep).
Post infectious GN - Clinical Signs
Periorbital Edema, Urine RBC's, RBC casrs, hypocomplementemia
Post infectious GN - IF
IgG/C3
Post infectious GN - EM
Electron dense humps
Post Infectious GN - LM
Hypercellular glomeruli w mesangial proliferation
Alports (Hereditary Nephritis)
Genetic disorder in Type IV collage (a-5 chain) causes Nephritic
Alports - EM
Irregular thickening of BM , foam cells
SLE GN (LM, EM)
Renal depositions in lupus (LM: wire loops, EM: fingerprints). 5 types
Diabetic Nephropathy LM/EM
Hypertrophy of mesangial matrix. Kimmelsteil wilson nodules, glomerulosclerosis, thickening of BM.
3 primary and 2 pathognomonic
Diabetic Retinopathy
ALWAYS found w/ diabetic nephropathy.
Nephritic Syndrome: Pathognomonics
RBCs in urine, acanthocytes.
Crescents in glomeruli indicate:
RPGN
Preferential passing in slit membrane
Negatives, acids blocked.
Causes of FSGS
SO HARM (sickle/sleep apnea, obesity, HIV, addiction, addiction, reflux, minimal change
SLE Membranous vs Diffuse
Membranous : Karryhrexis wire loops, crescents, diffuse segmental prolif, subeNdothilial prolife DIFFUSE: Mesangial Prolif, SubePithelial
Membranoproliferative - risk factors
CIVLL (Chronic infection, virus, leuk, lymph
thyroidization of tubules
indicative of chronic pyelonephritis.
Reflux chronic pyelonifrites - organization
Polar. (obstructive has multiple scars)
Cavitary Ring Shadow
Analgesic induced nephropathy.
Which type of diabetes is more like to cause nephropathy?
Type I
Where do high affinity antibodies end up in the glom.
mesangium
Where fo high valency antigens end up in the glomerulus
Mesangium
Where do deposits end up in antigen excess
Capillary wall
What disease is from circulating immune complexes depositing?
Lupus.
Which diseases activate the alternate pathway (C3_
Post Strep, Lupus, IgA, MP
Who's got C3NeF
MP II
Flea bitten kidney (petechial hemorrhage)
Post Infectious GN
Which lupus has more decrease in complement
Diffuse
Clinical presentation of acute renal failure
Hyperkalemia, Oliguria, Acidosis, Creatine (inc), Dec Urine
What is Ang II's effect on GFR
Increase via efferent constriction
What are prostaglandin's effect on GFR
Increase via blocking constriction of afferent
Causes of Vascular Intrinsic Renal Failure
HARMS - HUS/TTP, Atheroembolic/antiphospholipd diseas, Radiation, Mal hypertension, Scleroderma
Why do crushing injuris cause ATN?
Myoglobin (and hemoglobin) are nephrotoxic.
Causes of ATN
Toxic, ischemic
Causes of Interstitial Intrinsic Renal Failure
MAID - Malig, Autoimmune, Infect/idio, Drug
Which diuretics are potassium wasting?
Loop
Which adrenergic causes a decrease in K+
Beta agonists
Sevelamer
Phosphate binder
5 levels of kidney disease
GFR 1. >90 2. 60-89 3. 30-59 4. 15-29 5. <15
How are acute and chronic kidney rejection mediated?
Humoral & Cellular, by IgM, C3/C1q
Which renal transplantation rejections are irreversible?
Hyperacute and chronic
What is indicitave of hyperacute rejection?
PMN infiltration, sludging, fibrin.
What is indicitave of actue rejection?
Petechiae, lymphocytes, monocytes, perivascular infiltration, tubulitis
What is indicative of chronic rejection
Plasma cells, mesangial expansion, fibrosis, fibrointimal prolif
Explain cyclosporin toxicity
Acute changes: Necroses,vacuolar degeneration, cellular infiltration, HUS. Chronic - Hyalinization, fibrosis
Which (2) diseases are most likely to recur in a renal transplant
MPII, IgA
Which disease is most likely to occur in a transplant (not recur)
Membranous GN
What is characteristic of ischemic ATN
Hypotension, Patchy lesions, tubulorrhexis, casts
What is characteristic of toxic ATN
Diffuse lesions.
What causes toxic ATN
MAOI - Metals, Ab's, Organix Solvents, Immunosuppresants
What are the phases of ATN
Oliguric (hyperkalemia, acidosis, fluid retention), Early diuretic (hypokalemia, fluid loss), late diuretic (recovery)
What distinguishes hematogenous from reflux pyelonephritis?
Reflux is polar.
What's indicative of Analgesic Nephropathy?
Necrosis of papillae, cavetary ring shadow
How is Drug Induced TIN mediate
NSAID's causea Type I Hypersens response (IgE) --> Histology shows eosinophils
What clinically differentiates Malignant Hypertension from Benign Hypertension
Presence of renin in malignant hypertension, and malignant hypertensive patients are younger
Onion skin lesions in vessels are indicative of which hypertension?
Malignant.
3 classes of disease that cause secondary hypertenstion
Glomerular, Tubulointerstitial, Vascular
What are the differences in the cysts in dom vs rec polycystic kidney
Dom - all over. Rec - Just in collecting duct (fusiform)
Fibrocystin mutation is what disease
ARPKD
Clinical presentations of medullary sponge
HIS BAG - Hematuria, infection, stones, benign, asymptomatic, gravel
Nephrocystin mutation is which disease
Medullary cystic disease complex
MCDC clinical manifestations
Nephronophthisis, Uremia, CRF, Salt wasting, Polyuria
What genes are involved in ADPKD?
PKD1,2,3
EGFR and ADPKD
EGFR dedifferentiates into fetal form and presents on the luminal side in ADPKD
How do you treat ADPKD
Tyrosine Kinase inhibition