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CPR > Renal Pathology > Flashcards

Renal Pathology Flashcards

1
Q

What is the most common cause of tubulointerstitial nephritis (TIN)?

A

Acute pyelonephritis

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2
Q

What changes can occur in the kidney if bacterial pyelonephritis is left untreated?

A

It will progress to chronic pyelonephritis, characterized by scarring and fibrosis –> thyroidization, and tubular atrophy. These changes lead to hypertension and renal failure.

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3
Q

What is this process called and what is it a result of?

A

Thyroidization of the kidney due to chronic pyelonephritis.

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4
Q

What the hell is the difference between tubulointerstitial nephritis (TIN) and acute interstitial nephritis/interstitial nephritis (AIN/IN)?

A

TIN is a general term for inflammation of the tubules or interstitium. AIN/IN is inflammation not caused by bacteria; usually caused by a hypersensitivity reaction to drugs.

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5
Q

Name the drugs that have the potential to cause what is seen in the photo. What is this disease called?

A

Intersitial nephritis - caused by penicillins (esp. methicillin), NSAIDs, sulfonamides

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6
Q

What is the cause of analgesic nephropathy? Briefly describe the pathogenesis of the disease and the morphological changes that occur in the kidney as a result.

A

Due to chronic use of acetaminophen + aspirin for >3 years.

Pathogenesis: NSAIDs inhibit COX, so there is no PGE2 synthesis by macula densa cells –> no vasodilation of the afferent arteriole to increase GFR.

Reduced blood flow due to an inability to make PGE2 and vasodilate ultimately leads to papillary necrosis.

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7
Q

Name four substances that have the potential to cause acute tubular necrosis (ATN).

A

Aminoglycosides, heavy metals, contrast dyes, myoglobin (from rhadbomyolysis)

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8
Q

Your patient has a slightly reduced GFR and they got a radiocontrast CT to evaluate renal function. They develop acute kidney failure. Biopsy shows the following. What is your Dx?

A

Acute tubular necrosis (ATN)

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9
Q

Can severe hypotension cause acute tubular necrosis?

A

Yeah

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10
Q

You have been managing a patient with resistant hypertension and note an increase in their serum creatinine. Check the pic. What is that called?

A

Hyalinosis

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11
Q

Describe two vascular changes in the kidneys that can occur in the setting of malignant hypertension (>180/120).

A

Fibrinoid necrosis (plasma proteins getting squeezed out of the arteriole) and onion skin lesions (intimal thickening and smooth m. and collagen proliferation).

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12
Q

Name the mutated genes and their corresponding chromosomes involved in autosomal dominant polycystic kidney disease (ADPKD).

A

PKD1 on chromosome 16

PKD2 on chromosome 4

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13
Q

Describe the morphological changes that occur in the kidneys of a patient with ADPKD.

A

Both kidneys become enlarged, with cysts that destroy the renal parenchyma

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14
Q

Name two major comorbidities associated with ADPKD.

A
  1. Berry aneurysms
  2. Polycystic liver disease
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15
Q

Is ADPKD common?

A

Yeah!

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16
Q

What is the genetic mutation involved in autosomal recessive polycystic kidney disease (ARPKD)? What is the typical outcome from this disorder?

A

PKHD1 fibrocystin gene mutation

Non-functioning kidneys in the fetus –> oligohydramnios –> lung hypoplasia and death

If fetus survives to birth, there is usually also congenital hepatic fibrosis needing a transplant.

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17
Q

Can patients with ESRD on prolonged dialysis develop a cystic kidney disease?

A

Yeah

18
Q

Very simply, what is nephrotic syndrome?

A

Podocyte damage –> lots of proteins leak into the filtrate

19
Q

Name four clinical findings suggestive of nephrotic syndrome.

A

1) Proteinuria –> 2) Hypoalbuminuria leading to 3) Edema
4) Hyperlipidemia cuz the liver thinks that will make up for the loss of protein

20
Q

Name five differential diagnoses for nephrotic syndrome.

A

Glomerular-specific diseases:

  1. Minimal change disease
  2. Focal segmental glomerular sclerosis
  3. Membranous glomerulopathy

Systemic diseases:

  1. Diabetic nephropathy
  2. Lupus
21
Q

Which glomerular disease is the most common cause of nephrotic syndrome in kids? How is it treated and what is usually the outcome?

A

Minimal change disease. Treat w/ steroids, typically resolves completely.

22
Q

Describe the microscopic pathological changes of minimal change disease that can be seen on microscopy.

A

On light microscopy, shit looks normal.

On EM, you can see podocyte foot effacement (the feet look like they have coalesced).

23
Q

Focal segmental glomerular sclerosis (FSGS) causes ________ syndrome clinically and is seen predominantly what patient population?

A

FSGS causes nephrotic syndrome and is seen mostly in black older teens and young adults

24
Q

Describe the cellular pathological changes that occur in FSGS.

A

Podocytes get injured

Some podocytes die, exposing the underlying basement membrane.

Parietal epithelial cells reach out and attach to the exposed basement membrane.

Fibrosis ensues in these areas.

25
Q

You see a 16 year old black patients who presents with sudden onset of 10 pound weight gain. On exam you note bilateral lower limb edema. You do a UA in the office and it shows 3+ proteinuria. Biopsy shows the following. What is at the top of your DDx?

A

FSGS

26
Q

What is membranous glomerulopathy and what causes it?

A

Primary cause:

Auto-antibodies to PLA2-R on podocytes cause subepithelial injury –> proteinuria/nephrotic syndrome.

Secondary causes:

Malignancies

Drugs (penicillamine, captopril, gold, NSAIDs)

Lupus

Infections (HCV, HBV, syphilis, malaria)

27
Q

What is the histopathological hallmark of membranous glomerulonephritis?

A

Thick capillary walls with subepithelial basement membrane spikes.

28
Q

What is the leading cause of end-stage renal disease in the US?

A

Diabetic nephropathy

29
Q

Name four histopathological changes seen in diabetic nephropathy.

A
  1. Basement membrane thickening
  2. Mesangial cell proliferation
  3. Arterial hyalinosis
  4. Nodular glomerulosclerosis aka Jimmy Kimmelstiel Wilson nodules
30
Q

Your patient with diabetes now has what you suspect to be nephrotic syndrome. To confirm, you get a renal biospy that shows this. What are those things at the arrows? What does the patient have?

A

Kimmelstiel Wilson nodules. The patient has diabetic nephropathy causing nephrotic syndrome.

31
Q

Name four clinical features of nephritic syndrome.

A
  1. Oliguria
  2. Hypertension
  3. Hematuria
  4. Azotemia
32
Q

Describe the typical clinical scenario of post-streptococcal glomerulonephritis. Briefly describe the pathogenesis of the disease.

A

Happens roughly a week after infection with GAS (Strep. pyogenes). Immune complexes deposit in the glomeruli –> inflammation and glomerular capillary rupture –> hematuria

33
Q

Name three tests you could get for a patient that you suspect has post-strep glomerulonephritis.

A

ASO titer will be elevated

UA will show hematuria

Urine microscopy will show RBC casts

34
Q

What are two histopathological findings of post-strep glomerulonephritis?

A

Hypercellularity (inflammatory cell infiltrate) and subepithelial humps from immune complex deposition.

35
Q

Name five potential causes of rapidly-progressing glomerulonephritis (RPGN).

A
  1. Post-strep (most common cause)
  2. Lupus
  3. IgA nephropathy
  4. Goodpasture syndrome (autoantibodies against the GBM)
  5. Pauci-immune (ANCA-associated)
36
Q

What is the histopathological hallmark of RPGN?

A

Crescents: a proliferation of cells between the glomerular tuft and Bowman’s capsule as well as deposition of fibrin in Bowman’s space due to rupture of glomerular capillaries.

37
Q

What is P-ANCA and what diseases is it associated with?

What about C-ANCA?

A

P-ANCA:

peri-nuclear ANCA against myeloperoxidase

Churg-Strauss syndrome and Microscopic polyangiitis

C-ANCA:

cytoplasmic ANCA against PR-3 (proteinase 3)

Granulomatosis with polyangiitis (Wegener’s)

38
Q

Why do some diseases preferentially affect both the lungs and kidneys? Name six such diseases.

A

These organs use similar proteins in their basement membranes, so in systemic diseases damage to both organs occurs.

  1. Goodpasture’s syndrome (anti-GBM syndrome)

ANCA-associated:

  1. Granulomatosis with polyangiitis (Wegener’s)
  2. Microscopic polyangiitis
  3. Eosinophilic polyangiitis (Churg-Strauss syndrome)

Immune complex:

  1. Lupus
  2. Henoch-Schonlein Purpura
39
Q

What specifically causes Goodpasture syndrome? How does it manifest clinically? Name two histopathologic findings.

A

Auto-antibody against the alpha-3 subunit against type IV collagen, expressed in the BM of the lungs and kidneys.

Clinical manifestations:

Pneumonitis with hemoptysis

RPGN

Histopathology:

Crescentic morphology

Linear immunofluorescence

40
Q

What causes Alport syndrome? How does it manifest clinically?

A

Mutation in type 4 collagen gene (COL4A5)

Clinical manifestations:

Nephritic syndrome

Hearing loss

Problems with the lenses of the eyes

CPR (27 decks)

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