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Glossary of system path renal

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Created by billychoi85

Proteinuria (“foamy” urine)

Heavy proteinuria; low serum albumin; peripheral edema; hyperlipidemia

Nephrotic syndrome

Gross (“cola-colored” urine) or microscopic
Hematuria, hypertension, renal failure


Nephritic syndrome

Elevated BUN, serum creatinine
Acute (days-weeks) or chronic (months-years)


Renal failure

postural (disappears on lying down)

also get when exercise, fever, hypertension



Proteinuria
Minimal change disease
Membranous glomerulopathy
Focal segmental glomerulosclerosis

these are all



primary renal disease
Diabetic nephropathy
Systemic lupus erythematosus
Amyloidosis
HIV, HBV, HCV, other infections

these are all




secondary renal disease
Massive swelling in eyes and in lower extremeties

#1 cause of NS in children



Minimal change disease
glomerulus by light microscopy appear normal.
podocytes Fused and form a net of epithelium instead of mobile.
Like flat tire and not doing job well.





Minimal change disease
Thickened GBM membranes with “spikes”

GBM are abnormal – thickened and spike projections

membranous glomerulonephritis
Immunofluorescence microscopy shows deposits of IgG and C3

membranous glomerulonephritis
membranous glomerulonephritis secondary causes are
NSAIDs; penicillamine; gold; captopril
SLE
HBV and HCV infection
tumors (older patients)




Hematuria + renal insufficiency + hypertension + central (pulmonary) edema =

Nephritic syndrome
Strep throat to nephritic syndrome =

#1 cause.

Low serum C3, normal C4

antigen binding to antibody so level of C3 going down.





RBC casts
nephritic syndrome
Complement (C3) deposits in capillary wall/mesangium

Electron microscopy
Deposits (“hump-like”) in capillary wall


nephritic syndrome: post-strepococcal infection
Pathogenesis: abnormally glycosylated IgA molecules stick in mesangium, leading to inflammation, and hematuria

IgA nephropathy
Produce lot of diluted urine – can’t satisfy thirst.
polyuria
Renal tubulo-interstitial diseases
BUN/serum creatinine rise
Two main causes:
Ischemia (reduced blood flow)
Toxins (drugs)


Acute tubular necrosis (ATN)
Causes:
Shock, severe heart failure, crush injury, sepsis
Pathology:
Flattening of tubular epithelium
Sloughing of cells



Acute tubular necrosis (ATN)
Polarizable calcium oxalate inclusions

Toxic ATN: acute oxalate nephropathy
Interstitial edema, inflammatory cells, tubulitis
Eosinophils!




Acute Allergic Interstitial Nephritis
Clinical: back pain, fever, renal insufficiency, pyuria
Most cases (85%) E.coli; other fecal flora
Route of infection:
Ascending (bladder g ureter)
Blood-borne



Acute pyelonephritis
Related to:
Obstruction
Reflux
Repeated infections
Obstruction leads to hydroureter and hydronephrosis (dilatation of the ureter and pelvis)



Chronic pyelonephritis
Kidney’s shrunken. Filled with urine.

Hydronephrosis
Higher urine pH = more likely to form Ca stones.

Renal calculi (stones)
Not single layer. Mass of cells. Lot of lipids - clear
in kidney
renal cell carcinoma
Thickened GBM and defective – leak proteins



diabetes
Chronic renal failure leads to:
gPO4 retention and reduced 1,25-Vit D synthesis/tendency to lower Ca++ levels
gincreased PTH synthesis (secondary hyperparathyroidism)



Renal osteodystrophy
Tri-laminar basement mbr has 3 layers
1. Thin fenestrated endothelial layer
2. glomerular basement mbr GBM (collagen type IV, proteoglycan like heparin sufate, fibronectin) : intact structure
3. visceral epi cell (podocytes) contains foot processes and filtration slits bridged by a thin diaphragm



• gross hematuria : RBC in the urine
• proteinuria less than 3-3.5g/ 24 hrs
• HTN : in later disease course
• edema +/- : peripheral or experienced in the lung?
• Azotemia : elevated BUN and creatinine



Nephritic syndrome
• no cells in urine
• proteinuria more than 3-3.5g/ 24 hrs: massive protein loss
• edema
• +/- HTN
• Azotemia



Nephrotic syndrome
injury to one particular layer= visceral epi layer
anti-glom basement antibody -> floating in the circulation -> attaching diffusely across the endo lining
Anti-GMB antibody induced nephritis

Goodpasture syndrome

• immunofluorescence deposits of IgG and C3
• linear pattern


Anti-GMB antibody induced nephritis
weakness, fatigue and edema/swelling around his eyes and both legs. He also noted dark tea or cola colored urine
BP 170/100 Physical exam + for periorbital edema and leg edema


Anti-GMB antibody induced nephritis
• idiopathic
• secondary to other disease/ infections : bacterial infection, endocarditis
• hepatitis B+ C
• SLE : hard to make diagnosis,
• solid tumors in older pts
• drugs : NSAIDS, penicillamine, Gold, Captopril




Membranous GN
immunofluorescent die that was put on the antibody -> see where is the damage -> patchy, not linear, random throughout the sample
Immune complex Glomerulo-nephritis
• Kidney biopsy shows patchy membranous staining
• On EM see electron dense deposits (EDD) along sub-epithelial aspect of basement membrane


Immune complex Glomerulo-nephritis
antibody -> import in Wegner\'s granulomatosis : can get presentation with glomerulo nephritis (gross hematuria, glomerulo hemorrhage)
ANCA GN
• nothing coming to the epi lining or 2nd lining
ANCA GN
after strep infection
• Young child develops malaise, fever, nausea, oliguria(small amt) + cola colored urine
• Periorbital edema and mild-moderate HTN(not always)
• Subepithelial deposit
• Treat with steroids



Post infectious GN

Post strep granular immunofluorescence
o granular, patchy
o some reactivity against antigen in our kidney


recent impetigo
fatigue and cola colored dark urine.
• BP 160/90 first time-> high
• Physical showed periorbital edema and pitting edema to abdomen
• Urine ++blood and +protein, Azotemia



post-strep glomerulo-nephritis
o huge crescents
o fills Bowman\'s space -> filtration is altered


• rapid progression to renal failure
Crescent formation :
1. post strep GN
2. Goodpasture
3. SLE
• Crescent = RPGN
• Does not point to particular disease!
• Crowded so unhappy!






• Biopsy: sclerosis in JG cells
• •No autoantibodies
• •IgM and C3 focal deposit in hyaline
• •Confused with MCD; podocyte injury* and parietal epithelial cell
• Lesion not a disease****



Focal sclerosis
Weak, Fatigue, Sallow, Pale
uremic (build up lots of toxic)
• crystal diffuse into skin
• Anorexia
• platelet not functioning normally
• itching, bruising








ESRD (end state renal disease)
Nail changes :
• discoloration of proximal nail
• loss of lunula



ESRD (end state renal disease)
o happen to the podocytes : 3rd layer
o looks like normal kidney
foot process of podocytes damage : no longer convoluted

Minimal change disease : MCD
• 3 yr old girl was brought to pediatrician’s office for swelling around the eyes and legs
• No recent illnesses. No fever. BP normal
• Labs CBC, electrolytes, Creatinine and BUN all normal, hypoalbuminemia and hyperlipidemia

Minimal change disease : MCD
• Arcus in 15 yr old boy
• Premature arcus senalis hypercholesterolemia
o blue eye, ring around, periphery at the edge of iris
o low albumin and high fat in blood




Chronic nephrotic syndrome :
• Cushingoid features
• Moon facies
• Buffalo hump on neck
• Purple striae




Chronic steroids for nephrotic syndrome :
• Prominent mesagial IgA deposits + complement activates alternative complement pathway
• Increased cellularity of endothelium
• Increased incidence in Asians



IGA nephropathy : Berger\'s disease
• Urine ++blood, no WBC, no bacteria, no crystals
• Urine is cola colored
• Increased mesangial cells

IGA nephropathy : Berger\'s disease

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