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
In what conditions will you see fatty casts (oval fat bodies)
nephrotic syndrome
26
what sign will you see with fatty casts?
maltese cross
27
when will you see granular casts?
acute tubular necrosis
28
When will you see waxy casts?
end-stage renal disease or chronic kidney disease
29
When will you see hyaline casts?
Non specific finding, may actually be normal
30
Protein levels in nephritic disease?
<3.5 grams/day
31
Protein levels in nephrotic diseasE?
>3.5 grams/day
32
Pathophys and labs seen in nephritic syndrome
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
list the nephritic diseases
``` Acute poststreptococcal glomerulonephritis Rapidly progressive glomerulonephritis IgA nephropathy (berger disease) alport syndrome membranoproliferative glomerulonephritis ```
34
explain the pathophys of nephrotic syndrome
podocyte disruption -> charge barrier imapired -> massive proteinuria with hypoalbuminemia, hyperlipidemia and edema
35
examples of nephrotic diseases
``` Focal segmental glomerulosclerosis Minimal change disease Membranous nephropathy Amyloidosis Diabetic glomerulonephropathy ```
36
What are some examples of nephritic-nephrotic syndrome?
diffuse proliferative glomerulonephritis | membranoproliferative glomerulonephritis
37
What causes minimal change disease?
loss of heparan sulfate (loss of - charge in BM)
38
People with nephrotic syndrome are at an increased risk of clotting, why?
decreased ATIII
39
what will be found in the urine of someone with nephrotic disease?
frothy urine | Fatty casts
40
why is nephrotic syndrome associated with a hypercoagulable state?
AT III. is lost in urine
41
why does nephrotic syndrome cause an increased risk of infection?
loss of immunoglobluins
42
What is minimal change disease (lipoid nephrosis)
Most common cause of nephrotic syndrome in children
43
What is the cause of minimal change disease?
Often idiopathic but may be triggered by recent infection/immunization (triggered by cytokines) Rarely it may be secondary to lymphoma
44
Treatment of minimal change disease?
corticosteroids
45
What will you see on light microscopy of someone with minimal change disease?
normal glomeruli
46
What will you see on IF of MCD?
nothing
47
What will you see on EM of MCD?
effacement of podocyte foot processes
48
What is the most common cause of nephrotic syndrome in African-americans and Hispanics?
Focal segmental glomerulosclerosis
49
What causes Focal segmental glomerulosclerosis?
idiopathic or secondary to other conditions (HIV, sickle cell, heroin abuse, massive obesity, interferon treatment,congenital)
50
how does Focal segmental glomerulosclerosis respond to steroids?
has an inconsistent response
51
what may Focal segmental glomerulosclerosis progress to?
CKD
52
what will be seen on LM of Focal segmental glomerulosclerosis?
segmental sclerosis and hyalinosis
53
what will be seen on IF of Focal segmental glomerulosclerosis?
usually negative but may be positive for nonspecific focal deposits of igM, C3, C1
54
What will be seen on EM of focal segmental glomerulosclerosis ?
effacement of foot processes similar to minimal change disease
55
What is the cause of primary membranous nephropathy (aka membranous glomerulonephritis)?
when autoantibodies form to phospholipase A2 receptor expressed on podocytes (primary form)
56
What is the cause of secondary forms of membranous nephropathy (aka membranous glomerulonephritis)?
secondary to drugs or infections, SLE or solid tumours
57
what is seen on LM of membranous nephropathy (aka membranous glomerulonephritis)?
diffuse capillary and GBM thickening (from immune complex deposition)
58
what is seen on IF of membranous nephropathy (aka membranous glomerulonephritis)?
granular appearnce due to immune complex deposition
59
What is seen on EM of membranous nephropathy (aka membranous glomerulonephritis)?
spike and dome appearance of subepithelial deposits
60
What is the most commonly involved organ in amyloidosis?
The kidney
61
what will be seen on LM in amyloidosis?
Congo red stain will show apple-green bifringence under polarized light due to amyloid deposit in mesangium
62
what does amyloidosis cause in the kidney ?
nephrotic syndrome
63
What is the most common cause of end stage renal disease in the USA?
diabetic glomerulonephropathy
64
explain the pathophys of diabetic glomerulonephropathy?
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
what will you see on LM of diabetic glomerulonephropathy?
mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis. (kimmelstiel-wilson lesions)