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Renal ERIN > renal III > Flashcards

renal III Flashcards

1
Q

what type of anion gap is present in renal tubular acidosis?

A

normal anion gap

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2
Q

Defect in distal renal tubular acidosis (type I)

A

inability of alpha-interacalated cells to secrete H ->no new HCO3- > metabolic acidosis

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3
Q

What will the urine pH be in distal renal tubular acidosis (type I)?

A

> 5.5

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4
Q

What will the serum K be in distal renal tubular acidosis (type I)?

A

decreased

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5
Q

what causes distal renal tubular acidosis (type I)?

A

Amphotericin B toxicity, analgesic nephorpathy, congenital anomalies, autoimmune diseases (sjogrens, RA)

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6
Q

What may be a complication of distal renal tubular acidosis (type I)

A

risk of calcium phosphate kidney stones (due to increased urine pH)

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7
Q

Proximal renal tubular acidosis (type II) defect

A

Defect in PCT bicarbonate reabsorption -> bicard excretion in urine -> metabolic acidosis

The alpha intercalated cells aciidify the urine but not enough to overcome the increased excretion of bicard to prevent metabolic acidosis

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8
Q

Proximal renal tubular acidosis (type II) urine pH?

A

<5.5

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9
Q

Serum potassium in proximal renal tubular acidosis (type II)

A

decreased - loss of HCO leads to diuresis and volume contraction -> increased aldosterone

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10
Q

treatment for proximal renal tubular acidosis (type II)

A

Sodium bicarbonate

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11
Q

Causes of proximal renal tubular acidosis (type II)

A

Fanconi syndrome, multiple myeloma, carbonic anyhydrase inhibitors

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12
Q

complications of proximal renal tubular acidosis (type II)

A

hypophosphatemic rickets (in fanconi syndrome)

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13
Q

defect in hyperkalemic tubular acidosis (type 4)

A

Hypoaldosteroneism or aldosterone resistance -> decreased NH3 synthesis in PCT and decreased NH4 excretion

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14
Q

What is the urine ph in hyperkalemic tubular acidosis (type 4)?

A

<5.5

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15
Q

What is the serum K in hyperkalemic tubular acidosis (type 4)?

A

increased

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16
Q

Causes of hyperkalemic tubular acidosis (type 4)

A

decreased aldosterone production (diabetic, hyporenisinism, ACE inhibitors, ARBS, NSAIDs, heparine, adrenal insufficiency) or aldosterone resistance (K sparing diuretics, nephropathy due to obstruction, TMP-SMX)

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17
Q

How is H+ normally excreted?

A

It joins with a buffer - either titrable acids (phosphate) or to ammonia

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18
Q

What is ammonia synthesized from?

A

glutamine

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19
Q

whats the formula for the urine anion gap ?

A

Na + K -Cl

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20
Q

What do casts in the urine indicate?

A

they indicate that hematuria/pyuria is of glomerular or renal tubular origin

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21
Q

will you see casts in urine with bladder cancer/kidney stones?

A

noooo

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22
Q

will you see casts in acute cystitis?

A

pyruria

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23
Q

in what conditions will you see RBC casts in?

A

glomerulonephritis, hypertensive emergency

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24
Q

what conditions will you see WBCs in?

A

tubulointerstital inflammation, acute pyelonephritis, transplant rejection

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25
Q

In what conditions will you see fatty casts (oval fat bodies)

A

nephrotic syndrome

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26
Q

what sign will you see with fatty casts?

A

maltese cross

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27
Q

when will you see granular casts?

A

acute tubular necrosis

28
Q

When will you see waxy casts?

A

end-stage renal disease or chronic kidney disease

29
Q

When will you see hyaline casts?

A

Non specific finding, may actually be normal

30
Q

Protein levels in nephritic disease?

A

<3.5 grams/day

31
Q

Protein levels in nephrotic diseasE?

A

> 3.5 grams/day

32
Q

Pathophys and labs seen in nephritic syndrome

A

due to GBM disruption.
Hypertension and increased BUN and creatinine, oliguria, hematuria, RBC casts in urine.
Proteinuria (in subnephrotic range) except for severe cases

33
Q

list the nephritic diseases

A 
Acute poststreptococcal glomerulonephritis 
Rapidly progressive glomerulonephritis
IgA nephropathy (berger disease)
alport syndrome
membranoproliferative glomerulonephritis
34
Q

explain the pathophys of nephrotic syndrome

A

podocyte disruption -> charge barrier imapired -> massive proteinuria with hypoalbuminemia, hyperlipidemia and edema

35
Q

examples of nephrotic diseases

A 
Focal segmental glomerulosclerosis
Minimal change disease
Membranous nephropathy
Amyloidosis
Diabetic glomerulonephropathy
36
Q

What are some examples of nephritic-nephrotic syndrome?

A

diffuse proliferative glomerulonephritis

membranoproliferative glomerulonephritis

37
Q

What causes minimal change disease?

A

loss of heparan sulfate (loss of - charge in BM)

38
Q

People with nephrotic syndrome are at an increased risk of clotting, why?

A

decreased ATIII

39
Q

what will be found in the urine of someone with nephrotic disease?

A

frothy urine

Fatty casts

40
Q

why is nephrotic syndrome associated with a hypercoagulable state?

A

AT III. is lost in urine

41
Q

why does nephrotic syndrome cause an increased risk of infection?

A

loss of immunoglobluins

42
Q

What is minimal change disease (lipoid nephrosis)

A

Most common cause of nephrotic syndrome in children

43
Q

What is the cause of minimal change disease?

A

Often idiopathic but may be triggered by recent infection/immunization (triggered by cytokines)
Rarely it may be secondary to lymphoma

44
Q

Treatment of minimal change disease?

A

corticosteroids

45
Q

What will you see on light microscopy of someone with minimal change disease?

A

normal glomeruli

46
Q

What will you see on IF of MCD?

A

nothing

47
Q

What will you see on EM of MCD?

A

effacement of podocyte foot processes

48
Q

What is the most common cause of nephrotic syndrome in African-americans and Hispanics?

A

Focal segmental glomerulosclerosis

49
Q

What causes Focal segmental glomerulosclerosis?

A

idiopathic or secondary to other conditions (HIV, sickle cell, heroin abuse, massive obesity, interferon treatment,congenital)

50
Q

how does Focal segmental glomerulosclerosis respond to steroids?

A

has an inconsistent response

51
Q

what may Focal segmental glomerulosclerosis progress to?

A

CKD

52
Q

what will be seen on LM of Focal segmental glomerulosclerosis?

A

segmental sclerosis and hyalinosis

53
Q

what will be seen on IF of Focal segmental glomerulosclerosis?

A

usually negative but may be positive for nonspecific focal deposits of igM, C3, C1

54
Q

What will be seen on EM of focal segmental glomerulosclerosis ?

A

effacement of foot processes similar to minimal change disease

55
Q

What is the cause of primary membranous nephropathy (aka membranous glomerulonephritis)?

A

when autoantibodies form to phospholipase A2 receptor expressed on podocytes (primary form)

56
Q

What is the cause of secondary forms of membranous nephropathy (aka membranous glomerulonephritis)?

A

secondary to drugs or infections, SLE or solid tumours

57
Q

what is seen on LM of membranous nephropathy (aka membranous glomerulonephritis)?

A

diffuse capillary and GBM thickening (from immune complex deposition)

58
Q

what is seen on IF of membranous nephropathy (aka membranous glomerulonephritis)?

A

granular appearnce due to immune complex deposition

59
Q

What is seen on EM of membranous nephropathy (aka membranous glomerulonephritis)?

A

spike and dome appearance of subepithelial deposits

60
Q

What is the most commonly involved organ in amyloidosis?

A

The kidney

61
Q

what will be seen on LM in amyloidosis?

A

Congo red stain will show apple-green bifringence under polarized light due to amyloid deposit in mesangium

62
Q

what does amyloidosis cause in the kidney ?

A

nephrotic syndrome

63
Q

What is the most common cause of end stage renal disease in the USA?

A

diabetic glomerulonephropathy

64
Q

explain the pathophys of diabetic glomerulonephropathy?

A

hyperglycemi- > nonenzymatic glycation of tissue proteins ->mesangial expansion -> GBM thickening and increased permeability

Hyperfiltration -> glomerular hypertrophy and glomerular scarring leading to further progression of nephropathy

65
Q

what will you see on LM of diabetic glomerulonephropathy?

A

mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis. (kimmelstiel-wilson lesions)

Renal ERIN (5 decks)

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