CKD part 2 Flashcards
(94 cards)
1
Q
What is nephritic disease?
A
- inflammation/immune
- Urine sediment with hematuria +/- RBC casts
- Proteinuria <3 g/d
2
Q
What is nephrotic spectrum?
A
- Bland urine sediment (no cells or casts)
- Proteinuria (at least 300 mg/d, often >3 g/day)
- O for protein
3
Q
What are symptoms of nephritic syndrome?
A
HTN
Cola-colored urine (hematuria)
oliguria
4
Q
what are symptoms of nephrotic syndrome?
A
hypoalbuminemia
hyperlipidemia
massive proteinuria
peripheral edema
5
Q
broad term for glomerular diseases in the nephritic spectrum
A
glomeruloneprhitis
6
Q
What is the general cause of glomeruloneprhitis?
A
inflammatory process affecting glomeruli, causing acute or chronic renal dysfunction
7
Q
what are causes of glomeruloneprhitis?
A
immune complex deposition
pauci-immune
anti-glomerular basement membrane
C3 glomerulopathy
monoclonal Ig
8
Q
what happens in immune complex deposition?
A
- antigen-antibody complexes lodge in glomerular basement membrane
- complement activation to resolve complexes causes GBM destruction
9
Q
what are causes of immune complex deposition?
A
IgA nephropathy, infections, endocarditis, lupus, nephritis, membranoproliferative, cryoglobinemic
streptococcal infections are associated in particular
10
Q
what causes anti-GBM associated glomerulonephritis?
A
autoantibodies against GBM that may be confined to kidney or involve lungs as well
11
Q
what is the term for the syndrome that is anti-GBM-associated glomerulonephritis that impacts both the kidneys and lungs?
A
goodpasture’s syndrome
12
Q
what happens in c3 glomerulopathy?
A
c3 complement proteins lodge in the glomerular basement membrane causing destruction
13
Q
what is the cause of c3 glomerulopathy?
A
abnormal alternative complement pathway
14
Q
type of glomerulonephritis where excessive antibodies lodge in GBM and/or tubular basement membrane
A
monoclonal Ig-mediated glomerulonephritis
15
Q
what causes monoclonal Ig-mediated glomerulonephritis?
A
monoclonal gammopathies (multiple myeloma, MGUS)
16
Q
what is involved in pauci-immune glomerulonephritis?
A
small vessel vasculitis associated with ANCAs that can manifest in other body areas as well
17
Q
what are general findings of glomerulonephritis?
A
- inflammatory damage to glomeruli –> fall in GFR, eventually with uremic s/s with salts and water retention
- Edema and HTN common, first seen in scrotum and periorbital
- Heavy glomerular bleeding –> gross hematuria and “cola-colored urine”
18
Q
what are lab findings with glomerulonephritis?
A
- Serum Cr rises over days to months
- Urinalysis: hematuria, moderate proteinuria (usually <3 g/d)
- Urine sediment: RBCs, WBCs, RBC casts
RBCs often dysmoprphic from crossing damaged glomerulus
19
Q
what are red blood cell casts a sign of?
A
heavy glomerular bleeding, tubular stasis
20
Q
What would lab findings that suggest certain causes of glomerulonephritis be?
A
- low complement levels in C3 complex and immune complex glomerulonephritis
- ASO titers for a recent streptococcal infection (immune complex deposition)
- anti-GBM antibodies (anti-GBM associated glomerulonephritis)
- P-ANCA and C-ANCA levels (Pauci-immune glomerulonephritis)
- SPEP (monoclonal gammopathies)
Inflammatory markers- ESR, CRP, ANA
21
Q
What test would you consider if there is no CI to find the pattern of inflammation in glomerulonephritis?
A
renal biopsy
22
Q
How is glomerulonephritis treated?
A
- Manage HTN
- Manage volume overload if present
- Antiproteinuric therapy (ACE/ARB)
- high dose corticosteroids or cytotoxic agents
23
Q
What additional therapy could be added for goodpasture or pauci-immune glomerulonephritis?
A
plasma exchange
24
Q
what usually causes postinfectious glomerulonephritis?
A
GABHS
25
how soon after infection does postinfectious glomerulonephritis usually occur?
7-10 days on average, 1-3 weeks after infection
26
what are s/s of postinfectious glomerulonephritis?
vary from asymptomatic hematuria to nephritic syndrome
27
what lab findings are present with postinfectious glomerulonephritis?
* serum: low complement; high ASO titer (unless previous abx)
* Urine: hematuria, subnephrotic proteinuria, RBC casts
* Biopsy: humps of immune complex deposits **definitive dx*
28
what is the treatment of postinfectious glomerulonephritis?
* treatment of infection
* Supportive care: antihypertensives, salt restriction, diuretics
* steroids do not improve outcome
29
what is the prognosis of postinfectious glomerulonephritis?
* children often recover; adults may progress to CKD
30
what is the most common primary glomerular disease worldwide?
IgA nephritis (Berger's disease)
31
what population is berger's disease (IgA nephritis more common in?
## Footnote
ou
males, children and young adults
32
what are s/s of IgA nephritis (Berger's disease)
* gross hematuria
* often with mucosal viral infection
33
what are lab values in IgA nephritis (Berger's disease)?
* Serum: normal complement; no confirming serum test
* Urine: hematuria, proteinuria
34
how is IgA nephritis (Berger's disease) treated?
* Varies on risk for progression
* Low risk- no HTN, normal GFR, minimal proteinuria--> monitor yearly
* High risk- proteinuria >1 g/d, decreased GFR, HTN --> ACE/ARB
35
what is the prognosis of IgA nephritis (Berger's disease)?
33% spontaneous remission
36
what is henoch-schonlein purpura?
* systemic small-vessel vasculitis MC systemic vasculitis of childhood
* Associated with IgA deposition in vessel walls
* Often associated with inciting infection
37
What population is henoch-schonlein purpura more common in?
males and children
38
what are s/s of henoch-schonlein purpura?
* palpable purpura in lower extremities and buttocks
* arthralgias
* abdominal symptoms (nausea, colic, melena)
39
what are lab results for henoch-schonlein purpura?
* serum: normal complement; no confirming serum test
* urine: hematuria, proteinuria
40
how is henoch-schonlein purpura treated?
no direct treatment successful
* supportive care: hydration, rest, pain relief
41
what is the prognosis of henoch-schonlein purpura?
* may make full recovery over several weeks or progress to CKD
42
what is the MCC of nephrotic glomerular disease?
DM
43
what is the nephrotic range of proteinuria?
>3 g/day
44
what are general s/s of nephrotic syndrome?
* subnephrotic proteinuria- little to no s/s
* nephrotic syndrome- peripheral edema, may be in dependent regions, may be generalized
* dyspnea, pleural effusions, ascites can occur
45
what are urinalysis lab findings for nephrotic syndrome?
* proteinuria of 300 g/d of more
* urine sediment with few cells/casts
* If marked HLD, oval fat bodies "grape clusters" or "maltese crosses"
46
what labs can be used to check for proteinuria in nephrotic syndrome?
* urine dipstick- only detects albumin
* spot urine protein: urine Cr ratio
* 24 hour urine for protein
47
what are serum lab findings for nephrotic syndrome?
* hypoalbuminemia
* hypoproteinemia
* hyperlipidemia
* elevated ESR
* vitamin D, zinc, copper deficiency
48
when would you order a renal biopsy of a patient with suspected nephrotic syndrome?
adult with new-onset idiopathic nephrotic syndrome
not if long-standing DM or other obvious cause
49
what is treatment of nephrotic syndrome?
protein loss
* if subnephrotic or mild, dietary protein restriction
* If >10 g/d lost, increase protein intake
* ACE/ARB to lower urine protein excretion
Edema
* dietary salt restriction, diuretics--> larger doses of thiazide or loop diuretics because protein bound
Hyperlipidemia
* diet and exercise; lipid lowering drugs
Hypercoagulability
* anticoagulation x3-6 months min if evidence of thrombosis and ongoing if renal vein thrombosis, PE, recurrent thromboembolism
50
when is hypercoagulability usually seen in nephrotic syndrome?
* serum albumin <2 g/dL causing urinary loss of antithrombin, protein C, and protein S and increased platelet activation
51
what is the MCC of proteinuric renal disease in children?
minimal change disease
52
what are s/s of minimal change disease?
full-blown nephrotic syndrome with thromboembolic events, hyperlipidemia, and protein malnutrition
53
how is minimal change disease treated?
* corticosteroids - prednisone
## Footnote
rarely progresses to ESRD
54
What is the most common primary nephrotic syndrome in adults?
Membranous nephropathy
55
Why does membranous nephropathy occur?
* Immune complex deposition
* May be secondary to carcinoma, HBV, HCV, syphilis, endocarditis, autoimmune disease, NSAIDs, captopril
56
what are s/s of membranous nephropathy?
* may be asymptomatic
* edema, frothy urine
* higher risk of hypercoagulable state, esp. renal vein thrombosis
* subnephrotic proteinuria (30%)
57
what are types of secondary nephrotic syndrome?
* amyloidosis
* diabetic nephropathy
57
what is treatment of membranous nephropathy?
* ACE/ARB
* Immunosuppressive agents
* transplant
57
what causes amyloidosis?
* extracellular deposition of amyloid protein
58
what are s/s of amyloidosis?
* proteinuria
* decreased GFR
* nephrotic syndrome
* kidneys often enlarged
* s/s of other chronic inflammatory disease
59
how is amyloidosis treated?
* manage underlying disease
## Footnote
overall 5 year survival <5%
60
What is the MC cause of ESRD in the US?
diabetic nephropathy
61
what are s/s of diabetic nephropathy
| type of secondary nephrotic syndrome
* usually develops 10 years after DM onset
* Early: hyperfiltration with increased GFR
* Later: microalbuminuria
* Progression: albuminuria
62
what is treatment of diabetic nephropathy?
* strict glycemic control
* control HTN with ACE/ARB
as soon as microalbuminuria is seen
63
disorders mainly affecting renal tubules and interstitium and usually not glomeruli/renal vessels
tubulointerstitial disease
64
how does acute interstitial nephritis present?
* acute renal failure, most due to medication
65
how does chronic tubulointerstitial disease present?
* indolent
* tubular dysfunction
66
what is the predominant pathology behind chronic tubulointerstitial disease?
* interstitial fibrosis
* tubular atrophy
67
what are causes of chronic tubulointerstitial disease?
* obstruction uropathy (MC)
* vesicoureteral reflux (2nd MC)
* analgesic nephropathy
* renal ischemia, glomerular disease
68
what can cause obstructive uropathy leading to chronic tubulointerstitial disease?
prolonged obstruction of urinary tract due to:
* prostatic disease
* ureteral calculi
* cancer of cervix, colon, or bladder
* retroperitoneal tumors or fibroids
69
what is vesicoureteral reflux?
retrograde flow of urine when voiding
70
how much analgesic does a patient have to consume to be at risk for analgesic nephropathy?
min 1 g/d for 3+ years
71
what is the pathophysiology of obstructive uropathy?
1. backflow of urine
2. extravasation into interstitum
3. inflammation, fibrosis
4. damage, scarring
72
what are s/s of obstructive uropathy?
vary with underlying cause, location/degree of obstruction
* hydronephrosis
* pain-if acute complete obstruction
* bladder distension- may or may not be present
* HTN- may be present
* urine output- may be normal, oliguria or anuria, polyuria
73
why would a patient with obstructive uropathy have polyuria?
decreased ability to concentrate urine
73
why might a patient with obstructive uropathy have oliguria or anuria?
decreased GFR and obstruction
74
what would be seen on UA of a patient with obstructive uropathy?
often benign, may see hematuria, pyuria
75
What would serum creatinine of a patient with obstructive uropathy be?
elevated
76
how can obstructive uropathy be diagnosed?
imaging with US
can use CT but not first line
## Footnote
SHOULD BE DONE IN ALL PATIENTS WITH AKI OF UNKNOWN CAUSE AND ALL CKD PTS TO R/O OBSTRUCTION
77
if you suspect a stone or PCKD, what imaging should be done?
noncontrast CT
78
how is obstructive uropathy treated?
relief of obstruction
79
why should you relieve a obstruction ASAP?
prolonged --> further tubular damage --> renal scarring
removing will not restore renal function or stop progression
80
when does vesicoureteral reflux tend to occur and why?
during childhood
incompetent, misplaced vesicoureteral sphincter --> retrograde flow of urine while voiding
## Footnote
leads to inflammatory response and scarring
81
what is the presentation of vesicoureteral reflux?
* frequent UTIs especially young children
* HTN
82
what will labs show for vesicoureteral reflux?
* varying elevations in BUN/Cr
* Urine: mild-moderate proteinuria
* voiding cystourethrogram
* hydronephrosis, renal scarring on US
83
what is a voiding cystourethrogram?
* radiopaque dye instilled in bladder
* pt voids while x-ray is taken
84
how does a US of an adult with vesicoureteral reflux present?
* asymmetric small kidneys
* irregular outlines
* thin cortices
* areas of compensatory hypertrophy
85
how is vesicoureteral reflux treated?
* maintaining sterile urine in childhood
* surgical reimplantation of ureters for high-grade reflux
* control of HTN-ACE/ARB preferred
86
what analgesic was especially associated with analgesic nephropathy?
phenacetin
87
what is seen on renal biopsy of analgesic nephropathy?
tubulointerstitial inflammation and papillary necrosis
88
what are lab findings of analgesic nephropathy?
* urine: hematuria, proteinuria, polyuria, pyuria, sloughed papillae in urine
* imaging findings: CT small, scarred kidney with papillary calcifications
* IVP: ring shadow or golfball on a tee
## Footnote
"ring shadow"/"golfball on a tee" = contrast in area of sloughed papillae
89
how is analgesic nephropathy treated?
* renal function may stabilize or improve if analgesics stopped
90
what autoimmune disorders can cause autoimmune interstitial nephritis?
* amyloidosis
* cryoglobinemia
* igA nephropathy
* Renal transplant rejection
* Anti-GBM antibody syndrome
* sarcoidosis
* sjogren syndrome
* SLE
91
what are clinical
