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Foundations II- Nephrology > Glomerular Diseases > Flashcards

Glomerular Diseases Flashcards

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1
Q

Segmental v. Global?

Focal v. Diffuse?

A

part of glomerulus involved, all of glomerulus involved

some of glomeruli involved, all or almost all of the glomeruli are involved

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2
Q

What are the 3 parts of the filtration membrane of the glomerulus?

A

capillary endothelium

BM

foot processes of podocyte of glomerular capsule

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3
Q

Funcs. of the kidney?

A

Control the balance of water in the body

Control process of RBC production

Control acidity of the blood

Filter blood and pass the waste products to the bladder for excretion as urine

Control BP

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4
Q

Average urine physiologic protein excretion in adults? Pathologic proteinuria?

A

~80 mg/day

150mg or greater in 24 hours

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5
Q

What is the smallest plasma protein?

A

Albumin- filtered more readily than other proteins , can contribute to microalbuminuria

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6
Q

Daily excretion of more than….of protein is termed nephrotic range proteinuria

A

≥ 3.5 g

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7
Q

What is glomerular disease?

A

alteration of glomerular permeability- due to injury of one of the layers of filtration

-initially excess albumin w/ eventual progression to larger proteins

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8
Q

What are two other reasons for pathologic proteinuria?

A

Overflow proteinuria:
Overproduction of smaller proteins overwhelms reabsorptive ability of proximal tubule

Tubular proteinuria:
Tubulointerstitial disease leads to diminished reabsorptive capacity of the proximal tubule

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9
Q

How do we classify glomerular disease?

A

Nephritic syndrome vs. nephrotic syndrome

Primary vs. secondary

All cause some degree of glomerular damage and result in hypoalbuminemia due to urinary loss of proteins

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10
Q

What is the gold standard for definitive dx of glomerular disease?

A

BIOPSY

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11
Q

Describe nephritic syndrome

A

Inflammatory process w/ associated immunologic response leads to renal glomeruli damage

-Degree of damage is significant enough to allow blood cell passage

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12
Q

clinical findings in nephritic syndrome?

A
  • edema: LE, UE, periorbital, puffy pale face
  • hematuria “coca cola”
  • oliguria
  • HTN
  • Azotemia
  • rising Cr over days to month -occasional WBCs
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13
Q

Describe rapidly progressive glomerulonephritis

A

severe injury to the glomerular capillary wall, GBM and Bowman’s capsule

most severe and clinically urgent end of the nephritis spectrum

progression to renal failure in a matter of wks to mos

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14
Q

What are some primary nephritic syndromes?

A

Post Infectious Glomerulonephritis

IgA nephropathy

Henoch-Schönlein purpura

Pauci-immune glomerulonephritis (ANCA-associated)

Anti-Glomerular Basement Membrane Glomerulonephritis (Goodpasture Syndrome)

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15
Q

Etiology of post infectious glomerulonephritis

A

Group A beta hemolytic streptococci

-immune mediate glomerular injury, occurs 1-3 wks after strep infection (pharyngitis, impetigo)

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16
Q

Presentation of post infectious glomerulonephritis?

A

variable presentation

pt typically: oliguric, edematous, variably hypertensive

classic finding: coca cola urine

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17
Q

UA for pt with post infectious glomerulonephritis typically shows…

A

RBCs, red cell casts, proteinuria

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18
Q

Besides UA, what should you check if you suspect post infectious glomerulonephritis?

A

ASO (Antistreptolysin O)

will be high unless immune response has been blunted with abx tx

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19
Q

Px for post infectious glomerulonephritis?

A

good in children, less favorable for adults > prone to develop CKD

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20
Q

Tx for post infectious glomerulonephritis?

A

Supportive!
-Antihypertensives (ACE or ARB), salt restriction, diuretics PRN

NO STEROIDS- don’t improve outcomes

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21
Q

IgA Nephropathy is also known as…

A

Berger’s disease

MC primary glomerular disease world wide

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22
Q

What is IgA nephropathy?

A

IgA deposition in the glomerular mesangium > inflammatory response

-same lesion that’s seen in Henoch-Schonlein purpura

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23
Q

Epidemiology of IgA nephropathy?

A

MCly seen in children and young adults

M > F

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24
Q

Presentation of IgA nephropathy?

Study These Flashcards
A

usually follows a URI or GI infection

coca cola urine 1-3 days after illness onset

25
Labs for pt with IgA nephropathy typically reveal...
Labs consistent with nephritic syndrome hematuria, proteinuria, increased IgA levels, complement levels normal
26
Px for pts with IgA nephropathy? What is a favorable prognostic indicator?
1/3 > spontaneous remission 1/3 > CKD 1/3 chronic microscopic hematuria and stable Sr Cr proteinuria <1g/d
27
Tx for IgA nephropathy?
corticosteroids if proteinuria 1.0-3.5g/day ACE or ARBs if severe proteinuria Target BP <130/80
28
What is Henoch-Schonlein purpura?
systemic small vessel vasculitis assoc. with IgA deposition in vessel walls, similar to IgA nephropathy
29
Epidemiology of Henoch-Schonlein purpura?
MC in children assoc. with an inciting infection such as a group A streptococcus
30
Classic presentation of Henoch-Schonlein purpura?
palpable purpura in the LE and buttock area with arthralgias and abd sxs (N, colic, melena) Decrease in GFR is common with a nephritic presentation but some may incur enough damage that leads to nephrotic presentation
31
Tx for Henoch-Schonlein purpura?
no definitive tx but plasma exchange and DMARDs (anti rheumatic drugs) may help
32
What is Pauci-immune glomerulonephritis (ANCA-associated) seen with?
small vessel vasculitides -Wegner granulomatosis - churg-Strauss disease - mircoscopic polyaniitis/polyarteritis
33
S/S of pauci-immune glomerulonephritis?
those of a systemic inflammatory disease - fever, malaise, weight loss, purpura - 90% of those with Wegner granulomatosis have respiratory tract sxs with nodular lesions that can bleed
34
Labs for pauci-immune glomerulonephritis?
ANCA + UA: hematuria and proteinuria
35
Proteinuria: - Nephritic range? - Nephrotic range?
2g/day 4g/day
36
Tx for pauci-immune glomerulonephritis?
high dose corticosteroids! DMARDs with tx: 75% remission without: poor px
37
Describe Goodpasture syndrome (Anti-glomerular BM glomerulonephritis)
Glomerulonephritis + pulmonary hemorrhage (2/3) basement membrane injury from anti-GBM antibodies
38
Peak incidence for goodpasture syndrome occurs in which age range?
2nd-3rd decade 6th-7th decade
39
S/S of goodpasture syndrome?
onset follows URI in most cases hemoptysis and dyspnea RPGN
40
Work up for goodpasture syndrome?
Anti-GBM abs in 90% of pts Sputum: hemosiderin-laden macrophages CXR: pulmonary infiltrates
41
Tx for goodpasture syndrome?
Plasma exchange therapy Immunosuppressive drugs > prevents formation of new abs and controls inflammatory response -corticosteroids, DMARDs
42
Describe Nephrotic syndrome
significantly increased basement membrane
43
Essential components for dx of nephrotic syndrome?
Urine protein excretion ≥ 3.5 g per 24 hours Hypoalbuminemia (serum albumin < 3 g/dL) Bland urinary sediment: oval fat bodies may be seen Peripheral edema Hyperlipidemia
44
S/S of nephrotic syndrome?
peripheral edema* dyspnea (pulmonary edema, pleural effusions)
45
UA in pt with nephrotic syndrome may reveal... Blood chemistries...
proteinuria from an alteration of the GBM, oval fat bodies > assoc. with marked hyperlipidemia decreased serum albumin, hyperlipidemia in >50% with early nephrotic syndrome
46
In patients with nephrotic syndrome, loss of binding proteins in the urine can cause them to be deficient in...
Vitamin D, Zinc, and Copper
47
Tx for nephrotic syndrome
Increase dietary protein Edema: salt restriction, Thiazide and loop diuretics used frequently Tx hyperlipidemia: mod/high dose Statin Those with serum albumin <2 can become hypercoagulable, may need anticaogs
48
What are some nephrotic syndromes?
Minimal Change Disease Membranous nephropathy Focal Segmental Glomerulosclerosis (FSGS)
49
Describe minimal change disease
increases level of glomerular permeability, foot process effacement mainly seen in children
50
S/S of minimal change disease?
classic nephrotic syndrome: peripheral edema, massive proteinuria, hypoalbuminemia, hyperlipidemia
51
Tx for minimal change disease?
oral corticosteroids with prolonged taper, relapse is common upon discontinuation of steroids progression to ESRD is rare
52
MC cause of primary nephrotic syndrome in adults?
membranous nephropathy
53
Describe membranous nephropathy
Idiopathic immune mediated glomerulopathy Immune complex deposition in glomerular capillary walls results in increased permeability
54
Clinical presentation for membranous nephropathy?
Clinical presentation is variable: - Asymptomatic - Edema w/ frothy urine - High incidence of venous thromboembolism labs range from subnephrotic to classic nephrotic
55
Tx for membranous nephropathy
targets reduction of urine protein levels with ACE or ARB if BP > 125/75 corticosteroid therapy initiated in pts with failure to improve with 6 months of conservative care
56
Describe focal segmental glomerulosclerosis (FSGS)
Increased permeability due to podocyte injury -primary > mostly idiopathic -secondary > obesity, hypertension, chronic urinary reflux, HIV infection, analgesic or bisphosphonate exposure
57
Initial clinical presentation for focal segmental glomerulosclerosis?
proteinuria -80% of children and 50% of adults present with overt nephrotic syndrome
58
Tx for focal segmental glomerulosclerosis?
Diuretics for edema ACE/ARB to reduce proteinuria & HTN Statins for hyperlipidemia Corticosteroids for those w/ primary cause & overt nephrotic syndrome: high dose then taper

Foundations II- Nephrology (7 decks)

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