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MSII - Unit 5 > Renal Pathology > Flashcards

Renal Pathology Flashcards

1
Q 
Aminoglycosides (e.g. streptomycin)
heavy metals
myoglobinuria from muscle injury
ethylene glycol 
radiocontrast dye and urate

are some common causes of _____________

A

acute tubular necrosis

nephrotoxic ATN

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2
Q

What can allopurinol be used to prevent if given prior to initiation of chemotherapy?

A

tumor lysis syndrome

urate induced nephrotoxic acute tubular necrosis leading to acute renal failure

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3
Q

What is the expected BUN:Cr ratio and [FENa] % in

Nephrotoxic ATN?

A

Interstitial tubular necrosis results in failure to reabsorb nitrates

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4
Q

What disease is associated with an inherited defect in collagen type IV?

A

Alport Syndrome

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5
Q

How does Alport syndrome present on histology?

A

thinning and splitting of the glomerular basement membrane (due to X-linked inherited Type IV collagen deficiency)

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6
Q

What defines IgA nephropathy?

A

IgA immune complex deposition in MESANGIUM of glomeruli

MOST COMMON NEPHROPATHY

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7
Q

What population is affected the most by IgA nephropathy (aka Berger disease)?

What are hematological/urinary findings in IgA nephropathy?

A

children

episodic, gross, or microscopic hematuria with RBC casts – USUALLY following mucosal infections! that SLOWLY progresses to renal failure.

(IgA = anti-mucosal parasites/infections - increased IgA = > complex formation and deposition in mesangium of glomerulus –> inflammation and bleeding –> microscopic protinurea, hematurea, RBC casts)

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8
Q

What renal pathology presents after beta-hemolytic group A strep infection of the skin (impedigo) or infection of the nasopharynx?

A

post-streptococcal glomerulonephritis

usually infection is with M-protein presenting strains!

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9
Q

How does post-streptococcal glomerulonephritis present clinically (hematologic/urinary findings)?

A

2-3 weeks after upper respiratory tract or skin infection

  • hematurea (cola-colored urine)
  • oliguria
  • hypertension
  • periorbital edema

usually resolves in children, can lead to rapidly progressive glomerulonephritis in adults (~25%)

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10
Q

How does post-streptococcal glomerulonephritis present histologically? What is pathognomonic?

A

nephritic syndrome, so hypercellular glomerulonephritis caused by SUBEPITHELIAL immune complex deposition

SUPEPITHELIAL ‘HUMPS’ of immune complex

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11
Q

What is the classic finding in rapidly progressing glomerulonephritis?

A

Crescent inflammation of the glomerular mesangium (composed of fibrin and macrophages)

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12
Q

What is Goodpasture syndrome? What is the major pathogenic feature?

A

autoimmune dissease that affects lungs and kidneys

anti-(glomerular) basement membrane antibodies against alpha-3 chain of type IV collagen (present linearly on IF)

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13
Q

Who is affected by Goodpastures syndrome and how do they classically present (hematologic/urinary findings)?

A

young males

hematuria and hemoptysis (kidneys and lungs!)

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14
Q

What is the most common type of renal disease in SLE? What is second most common cause?

A

diffuse proliferative glomerulonephritis marked by SUBENDOTHELIAL immune complex and granular IF staining

membranous nephropathy

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15
Q

What distingishes Goodpastures syndrome from and Wegener’s granulomatosis?

A

Both have hemoptosis and hematuria, and rapidly progressive glomerulonephritis (associated with glomerular crescents)

NASAL/SINUS INFECTIONS, lack of IF findings, c-ANCA, are sign of Wegners!

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16
Q

What distingishes Churge Strause syndrome and microscopic polyangitis from Wegener’s granulomatosis?

A

All are auto-immune mediated with hemoptosis, hematuria and rapidly progressive glomerulonephritis

Churg-Stauss and microscopic polyangitis have p-ANCA,
Wegener’s has cANCA

17
Q

What distingishes Churge Strause syndrome from microscopic polyangitis?

A

Both have hemoptosis and hematuria, and rapidly progressive glomerulonephritis

Only Churg Strauss has granulomatous inflamation, eosinophilia, and asthma

18
Q

Where in the kidney does amyloid deposit in systemic amyloidosis? What is the consequence?

A

mesangium, nephrotic syndrom

19
Q

What are the features of renal disease in diabetes melitus?

A

glycosylation of vascular basement membrane and HYALINE ARTERIOSCLEROSIS of glomerular EFFERANT arteriole

High filtration injury leads to microalbuminuria and effentual progression to nephrotic syndrome characterized sclerosis of mesangium for formation of KIMMELSTEIL-WILSON nodules

ACE inhibitors are protective because ATII acts to further contrict efferant arteriole

20
Q

What type of renal syndrome is marked by:

Hypoalbuminemia - pitting edema
hypogammaglobulinemia - increased risk of infection
hypercoagulatable state - loss of anti-thrombin III
Hyperlipidemia and hypercholesteremia - fatty casts in urine

A 
nephrotic syndromes
Include:
Minimal change disease
focal segmental glomerulosclerosis
membrenous nephropathy
membranoproliferative nglomerulonephritis
diabetes mellitus - 
systemic amyloidosis
21
Q

Who are most affected?

Minimal change disease -

focal segmental glomerulosclerosis -

membrenous nephropathy -

membranoproliferative glomerulonephritis (Type I) - *

membranoproliferative glomerulonephritis (Type II) - *

diabetes mellitus -

systemic amyloidosis -

A

Children, (Hodgkins),

black,hispanic,HIV,Heroine,sickle cell,

white adults;HepB,C,SLE,solid tumor, NSAIDS/penecillin

HepC/B virus

C3 nephritic factor-compliment active w/ low serum C3

MPGN - immune complex deposition (Type I = SUBENDOTHELIAL; Type II = INTRAMEMBRENOUS) granular on IF

22
Q

What renal syndrome?

child, kidney damage due to cytokines from T-cells, good steroid response

black,hispanic,HIV,Heroine,sickle cell, (steroid resistant)

Caucasian with C3 convertase autoantibody

A

Minimal change (nephrotic) kidney disease

focal segmental glomerulosclerosis

membranoproliferative flomerulonephritis (Type II)

23
Q

What are similarities and differences between anti-GBM disease (Goodpasture’s) and Alport Syndrome?

A

both affect Type IV collagen

Anti-GBM is autoimmune with auto-antibodies
Alport’s is inherited defect in Type IV collagen that is also associated with sensory hearing loss, ocular disturbance

24
Q

What renal syndrome?

child, kidney damage due to cytokines from T-cells, good steroid response

A

Minimal change disease

25
Q

black,hispanic,HIV,Heroine,sickle cell, (steroid resistant)

affects only some glomeruli and only part of the glomerulus - no immune complex deposits

A

focal segmental glomerulosclerosis

26
Q

“Spike-Dome” subepithelial granular immune complex deposits

NSAIDS or Penicillamine

A

membranous grlomerulonephritis

27
Q

What type of renal pathology could be caused by treatment of Wilson’s disease, rhumatoid arthritis, or cystinurea

A

membranous grlomerulonephritis

  • penicillamine (heavy metal chealator and immunosupressant) also metabolite of penicillin

used to treat too much copper disease (Wilsons) inflammatory joint disease (RA) and prevention of kidney stones (due to cyctinurea - autosomal recessive inherited disorder associated with high cystine in urine due to failure to reabsorp in proximal CT)

28
Q

vesicureteral reflux in children or ureter obstruction is most likely to cause what?

A

chronic peilonephritis - fibrosis of the kidney with cortical scarring and blunted calyces

*scaring at upper and lower poles is characteristic of vesicoureteral reflux (reflux from bladder to kidney, usually due to malformation of ureter angle of insertion into bladder)

29
Q

staghorn caliculus in a kid is made from what?

A

cystine - cystinurea (staghorn stone fills renal calyx, hence caliculus, and requires surgical removal)

30
Q

staghorn caliculus in an adult is made from what?

A

ammonium magnesium phosphate (second most common type of stone) - usually cased by infection with urease postive organism (proteus vulgaris or klebsiella)

alkaline urine lease to formation!

31
Q

Hydrochlorothiazide can be used to treat what type of kidney stone? Why?

A

calcium-oxylate

thiazides are “calcium sparing” diuretics

32
Q

Denys-Drash syndrome is associated with what 4 features?

A

Wilms tumore, progressive glomerular disease, pseudohermaphroditism, mutation of WT1 gene

33
Q

Wilms tumor, neonatal hypoglycemis, muscular hemhypertrophy and orgnaomegaly (including tounge), WT2 gene cluster mutattions (11p15.5) ==> major alteration is IFG-2

A

Beckwith-Wiedemann syndrome

34
Q

Large unilateral flank mass with hematurea and hypertension in a 3 year old

A

Wilms tumor (comprised of blastema - immature mesenchyme)

35
Q

What would a high Antistreptolysin O level indicate? What might it predispose?

A

previous strep infection&raquo_space; post-streptochocal glomerulonephritis

36
Q

Normal BUN

Normal Creatinine

A

normal BUN level for healthy individuals is 7-20 mg/dL in adults, and 5-18 mg/dL in children. Patients on dialysis have higher BUN levels, usually 40-60 mg/dL

A normal result is 0.7 to 1.3 mg/dL for men and 0.6 to 1.1 mg/dL for women. Women usually have a lower creatinine level than men.

37
Q

What would postitive ASO and Anti-DNase B titers indicate?

A

Recent strep infection associated with Post-strepticoccal glomerulonephritis

38
Q

In which conditions would there be hypocomplemantemia?

membranoproliferative glomerulonephritis
IgA nephropathy 
Membranous Glomerulonephropathy 
post-infectious glomerunephritis, 
Lupis nephritis
A

Characteristic of active immune complex glomerulonephritis

seen in membranoproliferative glomerulonephritis
post-infectious glomerunephritis,
Lupis nephritis

NOT in:
IgA nephropathy
Membranous Glomerulonephropathy

MSII - Unit 5 (16 decks)

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