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Nayla Foundations Exam 5 > Glomerular diseases > Flashcards

Glomerular diseases Flashcards

1
Q

What does “segmental” vs “global” mean

A

segmental is only a portion of the glomerulus is involved

global is the entire glomerulus is involved

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2
Q

What does “focal” vs “diffuse” mean

A

Focal is some of the glomeruli are involved

Diffuse is all (or most) of the glomeruli are involved

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3
Q

What are the 3 parts of the filtration membrane

A
  1. Capillary endothelium
  2. Basement membrane
  3. Podocytes of glomerular capsule
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4
Q

What are the functions of the kidney

A 
control water balance in the body 
control RBC production 
control blood actidity 
filter blood and pass waste into bladder 
control blood pressure
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5
Q

What are adult protein levels

A

average normal physiologic: 80 mg/day

pathologic proteinuria: >150 mg/day

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6
Q

What is the smallest plasma protein

A

albumin; makes up 20-40% of physiologic proteinuria
It is filtered more than other plasma proteins, so you’re more likely to get “microalbuminuria” before you reach “proteinuria”

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7
Q

What is Microalbuminuria

A

excretion of 30-300mg albumin/day

Macroalbuminuria is >300mg/day

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8
Q

What is nephrotic range proteinuria

A

daily excretion >3.5g protein per day

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9
Q

What is the MCC of pathologic proteinuria

A

Glomerular disease: altered permeability= injury of all 3 levels of filtration membrane
first to leak out is albumin, then other proteins

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10
Q

Other pathologic causes of proteinuria include

A

Overflow proteinuria: overproduction of small proteins overwhelms reabsorption in the proximal tubule
Tubular proteinuria: tubulointerstitial dz causes decreased ability of proximal tubule to reabsorb proteins

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11
Q

How are glomerular diseases categorized

A

Nephrotic vs Nephritic

Primary vs Secondary

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12
Q

All glomerular diseases cause

A

glomerular damage

hypoalbuminemia (low if blood because excess excreted)

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13
Q

What is the gold standard definitive dx for glomerular diseases

A

Biopsy!

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14
Q

What is Nephritic syndrome

A

There is an immune response in the capillaries leading to glomerular damage= blood cells pass through

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15
Q

What are possible findings in nephritic syndrome

A 
Edema (LE>UE) 
Hematuria (coca cola) 
Granular casts 
WBC in urine
Proteinuria (<3.5g=subnephrotic) 
HTN (2/2 NA retention and no filtration) 
Azotemia 
High creatinine 
Oliguria (low urine output, glomerulus cant filter as much) 
Periorbital edema 
pale puffy face 
swollen lips
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16
Q

What is rapidly progressive glomerulonephritis

A

severe injury to capillary wall, basement membrane, and bowmans capsule
*very severe, occurs at the end of the “Nephritic syndrome” spectrum and causes renal failure in weeks-months

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17
Q

What are the primary causes of Nephritic Syndromes

A 
post infectious GMN 
IgA nephropathy 
Henoch-Schonlein purpura 
Pauci-immune glomerulonephritis 
Good Pasteur's
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18
Q

What is post-infectious GMN

A

immune mediated glomerular injury due to GABHS (pyogenes)

-immune complexes w/ strep antigens deposited 1-3 weeks after a strep infection

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19
Q

What are findings in P.I. GMN

A

oliguria
edema (protein cant stay in the capillary so fluid leaks out)
HTN
**coca cola urine

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20
Q

Lab findings in P.I. GMN are

A

UA- RBC, red cell casts, and proteinuria

-ASO titers high (unless they took abx)

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21
Q

What is the prognosis of P.I. GMN

A

in kids, good

in adults, not so great- can lead to RPGN or CKD

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22
Q

How do you treat P.I. GMN

A

Supportive! anti-HTN, salt restriction, diuretics prn

Steroids do NOT improve outcome

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23
Q

What is the MC glomerular disease world-wide

A

IgA nephropathy/ Berger’s disease

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24
Q

What occurs in IgA nephropathy

A

IgA deposits in the glomerular mesangium cause an inflammatory response
MC: kids/young adult, M>W

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25
Q

What are is your classic symptom of IgA nephropathy

A

coca cola urine 1-3 days after a URI or GI infection

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26
Q

What will IgA nephropathy labs show

A

hematuria
proteinuria
high IgA but normal complement levels

27
Q

What is the prognosis of IgA nephropathy

A

1/3 remit spontaneously
20-40% develop CKD
rest have chronic microscopic hematuria and stable SrCr for life

28
Q

What is the most favorable prognostic indicator in IgA nephropathy

A

Proteinuria <1g/day

29
Q

How can you treat IgA nephropathy

A

If proteinuria 1-3.5g: STEROIDS

If higher: ACE/ARB

30
Q

What is target BP in IgA nephropathy

A

<130/80

31
Q

What is Henoch-Schonlein purpura

A

IgA deposits in vessel walls causing systemic small vessel vasculitis (similar to IgA nephropathy)
MC in kids with inciting infection, like group A strep

32
Q

How does Henoch-Schonlein present symptomatically

A

palpable purpura in LE and buttocks
Arthralgias
abdominal Sx (nausea, colic, melena)
low GFR

33
Q

How do you treat Henoch-Schonlein purpura

A

plasma exchange

DMARDS (anti-rheumatic drug)

34
Q

What is Pauci-immune GMN

A

Associated with small vessel vasculitides (Wegener’s granulomatosis, Churg-Strauss, microscopic polyangiitis)

35
Q

What are symptoms of Pauci-immune GMN

A 
fever
malaise
weight loss
purpura 
-If w/ Wegener's, nodular lesions and respiratory tract Sx
36
Q

What do Pauci-immune GMN labs show

A

ANCA antibodies
hematuria
proteinuria

37
Q

How do you treat Pauci-immune GMN

A

high dose steroids

DMARDS (rheum)

38
Q

What is the prognosis of Pauci-immune GMN

A

with Tx: 75% complee remission

w/o Tx: poor prognosis

39
Q

What is Good Pasteur’s syndrome

A

Basement membrane injury 2/2 anti-GBM antibodies (usually s/p URI) leading to Glomerulonephritis + pulmonary hemorrhage
-peak 2-3 or 6-7 decade

40
Q

What are Sx of Good Pasteur’s syndrome

A

hemoptysis
dyspnea
RPGN

41
Q

What will Good Pasteur’s diagnostics show

A

labs: anti-GBM antibodies- hemosiderin macrophages in sputum
CXR: pulmonary infiltrate

42
Q

How do you treat Good Pasteur’s

A
  • Plasma exchange (remove abs)

- Immunosuppressive drugs (steroids, DMARDS) s new abs dont form, and decrease inflammaiton

43
Q

What is Nephrotic syndrome

A

Increased basement membrane permeability causing protein to leak out

44
Q

What components are essential in diagnosing Nephrotic syndrome

A 
Proteinuria >3.5g/d 
Hypoalbuminemia (<3g) 
bland urinary sediment (+/- oval fat bodies) 
Peripheral edema 
HLD
45
Q

What are Sx of Nephrotic syndrome

A

**Peripheral edema

dyspnea (pulm. edema, pleural effusion, diaphragm compromise form ascites)

46
Q

When does peripheral edema develop

A

when serum albumin <2g

Na retention 2/2 renal disease

47
Q

What will Nephrotic Syndrome look like on UA

A

Proteinuria (few cellular elements or casts microscopically)
Oval fat bodies 2/2 HLD

48
Q

What will Nephrotic syndrome blood panel show

A

Hypoalbuminemia (<3g)
Hypoproteinemia (<6g)
HLD (liver compensates for low albumin by making lipids)
low Vit. D, zinc, and copper

49
Q

When can protein malnutrition occur

A

when urinary protein loss >10 g/d

50
Q

How do you treat Nephrotic syndrome

A
  • increase diet protein
  • salt restrict/thiazides/loops (edema)
  • diet and exercise, aggressive statins (HLD)
  • Anticoags if with renal vein thrombosis, PE, or recurrent thromboemboli
51
Q

Why are patients with Nephrotic syndrome hypercoagulable

A

Because one of the things that leaks out is AT-III (anti-thrombin III), as well as protein C and S
without these, you are more prone to clot

52
Q

What are secondary causes of Nephrotic syndrome

A

Minimal change disease
membranous nephropathy
focal segmental glomerulosclerosis

53
Q

What is Minimal change disease

A

increased glomerular permeability due to foot processes thinning out

54
Q

Who is minimal change disease mostly seen in

A

kids! 80% of proteinuria in kids
in kids, M>F
in adults, M=W

55
Q

How do you treat Minimal change disease

A

oral steroids w/ prolonged taper (adults up to 16 wks)

-likely relapse after stopping steroids, but rarely progress to ESRD

56
Q

Most complications from minimal change disease arise from

A

long term steroid therapy!

57
Q

What is the MCC of primary nephrotic syndrome in adults

A

Membranous nephropathy- an idiopathic immune mediated glomerulonephropathy causing immune complexes to deposit into capillary walls= increased permeability

58
Q

How does membranous nephropathy present

A 
edema 
frothy urine (from protein) 
venous thromboemboli (low AT-III, pro C&amp;S)
59
Q

How do you treat membranous nephropathy

A

ACE/ARB to decrease urine protein (if BP >125/75)

60
Q

What is the prognosis of membranous glomerulonephropathy

A

if subnephrotic, good

if nephrotic, 30% recover spontaneously- the rest need steroids + 6 months of conservative care if w/ renal failure

61
Q

What is focal segmental glomerulosclerosis

A

podocyte injury leads to increased permeability

Sx is proteinuria (and nephrotic syndrome Sx)

62
Q

What causes FSGS

A

primary renal dz: idiopathic, or genetic alterations in africans
secondary: obesity, HTN, HIV, analgesic/biphosphate exposure, or chronic urinary reflux

63
Q

How do you treat FSGS

A

Diuretics
Statins
ACE/ARB
If it’s a primary cause: steroids w/ 16 week taper

Nayla Foundations Exam 5 (7 decks)

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