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CKD part 2 Flashcards

1
Q

What is nephritic disease?

A
  • inflammation/immune
  • Urine sediment with hematuria +/- RBC casts
  • Proteinuria <3 g/d
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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
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3
Q

What are symptoms of nephritic syndrome?

A

HTN
Cola-colored urine (hematuria)
oliguria

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4
Q

what are symptoms of nephrotic syndrome?

A

hypoalbuminemia
hyperlipidemia
massive proteinuria
peripheral edema

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5
Q

broad term for glomerular diseases in the nephritic spectrum

A

glomeruloneprhitis

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6
Q

What is the general cause of glomeruloneprhitis?

A

inflammatory process affecting glomeruli, causing acute or chronic renal dysfunction

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7
Q

what are causes of glomeruloneprhitis?

A

immune complex deposition
pauci-immune
anti-glomerular basement membrane
C3 glomerulopathy
monoclonal Ig

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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
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9
Q

what are causes of immune complex deposition?

A

IgA nephropathy, infections, endocarditis, lupus, nephritis, membranoproliferative, cryoglobinemic

streptococcal infections are associated in particular

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10
Q

what causes anti-GBM associated glomerulonephritis?

A

autoantibodies against GBM that may be confined to kidney or involve lungs as well

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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

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12
Q

what happens in c3 glomerulopathy?

A

c3 complement proteins lodge in the glomerular basement membrane causing destruction

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13
Q

what is the cause of c3 glomerulopathy?

A

abnormal alternative complement pathway

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14
Q

type of glomerulonephritis where excessive antibodies lodge in GBM and/or tubular basement membrane

A

monoclonal Ig-mediated glomerulonephritis

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15
Q

what causes monoclonal Ig-mediated glomerulonephritis?

A

monoclonal gammopathies (multiple myeloma, MGUS)

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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

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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”
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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

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19
Q

what are red blood cell casts a sign of?

A

heavy glomerular bleeding, tubular stasis

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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

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21
Q

What test would you consider if there is no CI to find the pattern of inflammation in glomerulonephritis?

A

renal biopsy

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22
Q

How is glomerulonephritis treated?

A
  • Manage HTN
  • Manage volume overload if present
  • Antiproteinuric therapy (ACE/ARB)
  • high dose corticosteroids or cytotoxic agents
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23
Q

What additional therapy could be added for goodpasture or pauci-immune glomerulonephritis?

A

plasma exchange

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24
Q

what usually causes postinfectious glomerulonephritis?

A

GABHS

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25
Q

how soon after infection does postinfectious glomerulonephritis usually occur?

A

7-10 days on average, 1-3 weeks after infection

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26
Q

what are s/s of postinfectious glomerulonephritis?

A

vary from asymptomatic hematuria to nephritic syndrome

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27
Q

what lab findings are present with postinfectious glomerulonephritis?

A
  • serum: low complement; high ASO titer (unless previous abx)
  • Urine: hematuria, subnephrotic proteinuria, RBC casts
  • Biopsy: humps of immune complex deposits **definitive dx*
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28
Q

what is the treatment of postinfectious glomerulonephritis?

A
  • treatment of infection
  • Supportive care: antihypertensives, salt restriction, diuretics
  • steroids do not improve outcome
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29
Q

what is the prognosis of postinfectious glomerulonephritis?

A
  • children often recover; adults may progress to CKD
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30
Q

what is the most common primary glomerular disease worldwide?

A

IgA nephritis (Berger’s disease)

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31
Q

what population is berger’s disease (IgA nephritis more common in?

ou

A

males, children and young adults

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32
Q

what are s/s of IgA nephritis (Berger’s disease)

A
  • gross hematuria
  • often with mucosal viral infection
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33
Q

what are lab values in IgA nephritis (Berger’s disease)?

A
  • Serum: normal complement; no confirming serum test
  • Urine: hematuria, proteinuria
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34
Q

how is IgA nephritis (Berger’s disease) treated?

A
  • 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
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35
Q

what is the prognosis of IgA nephritis (Berger’s disease)?

A

33% spontaneous remission

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36
Q

what is henoch-schonlein purpura?

A
  • systemic small-vessel vasculitis MC systemic vasculitis of childhood
  • Associated with IgA deposition in vessel walls
  • Often associated with inciting infection
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37
Q

What population is henoch-schonlein purpura more common in?

A

males and children

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38
Q

what are s/s of henoch-schonlein purpura?

A
  • palpable purpura in lower extremities and buttocks
  • arthralgias
  • abdominal symptoms (nausea, colic, melena)
39
Q

what are lab results for henoch-schonlein purpura?

A
  • serum: normal complement; no confirming serum test
  • urine: hematuria, proteinuria
40
Q

how is henoch-schonlein purpura treated?

A

no direct treatment successful
* supportive care: hydration, rest, pain relief

41
Q

what is the prognosis of henoch-schonlein purpura?

A
  • may make full recovery over several weeks or progress to CKD
42
Q

what is the MCC of nephrotic glomerular disease?

A

DM

43
Q

what is the nephrotic range of proteinuria?

A

> 3 g/day

44
Q

what are general s/s of nephrotic syndrome?

A
  • 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
Q

what are urinalysis lab findings for nephrotic syndrome?

A
  • 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
Q

what labs can be used to check for proteinuria in nephrotic syndrome?

A
  • urine dipstick- only detects albumin
  • spot urine protein: urine Cr ratio
  • 24 hour urine for protein
47
Q

what are serum lab findings for nephrotic syndrome?

A
  • hypoalbuminemia
  • hypoproteinemia
  • hyperlipidemia
  • elevated ESR
  • vitamin D, zinc, copper deficiency
48
Q

when would you order a renal biopsy of a patient with suspected nephrotic syndrome?

A

adult with new-onset idiopathic nephrotic syndrome

not if long-standing DM or other obvious cause

49
Q

what is treatment of nephrotic syndrome?

A

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
Q

when is hypercoagulability usually seen in nephrotic syndrome?

A
  • serum albumin <2 g/dL causing urinary loss of antithrombin, protein C, and protein S and increased platelet activation
51
Q

what is the MCC of proteinuric renal disease in children?

A

minimal change disease

52
Q

what are s/s of minimal change disease?

A

full-blown nephrotic syndrome with thromboembolic events, hyperlipidemia, and protein malnutrition

53
Q

how is minimal change disease treated?

A
  • corticosteroids - prednisone

rarely progresses to ESRD

54
Q

What is the most common primary nephrotic syndrome in adults?

A

Membranous nephropathy

55
Q

Why does membranous nephropathy occur?

A
  • Immune complex deposition
  • May be secondary to carcinoma, HBV, HCV, syphilis, endocarditis, autoimmune disease, NSAIDs, captopril
56
Q

what are s/s of membranous nephropathy?

A
  • may be asymptomatic
  • edema, frothy urine
  • higher risk of hypercoagulable state, esp. renal vein thrombosis
  • subnephrotic proteinuria (30%)
57
Q

what are types of secondary nephrotic syndrome?

A
  • amyloidosis
  • diabetic nephropathy
57
Q

what is treatment of membranous nephropathy?

A
  • ACE/ARB
  • Immunosuppressive agents
  • transplant
57
Q

what causes amyloidosis?

A
  • extracellular deposition of amyloid protein
58
Q

what are s/s of amyloidosis?

A
  • proteinuria
  • decreased GFR
  • nephrotic syndrome
  • kidneys often enlarged
  • s/s of other chronic inflammatory disease
59
Q

how is amyloidosis treated?

A
  • manage underlying disease

overall 5 year survival <5%

60
Q

What is the MC cause of ESRD in the US?

A

diabetic nephropathy

61
Q

what are s/s of diabetic nephropathy

type of secondary nephrotic syndrome

A
  • usually develops 10 years after DM onset
  • Early: hyperfiltration with increased GFR
  • Later: microalbuminuria
  • Progression: albuminuria
62
Q

what is treatment of diabetic nephropathy?

A
  • strict glycemic control
  • control HTN with ACE/ARB

as soon as microalbuminuria is seen

63
Q

disorders mainly affecting renal tubules and interstitium and usually not glomeruli/renal vessels

A

tubulointerstitial disease

64
Q

how does acute interstitial nephritis present?

A
  • acute renal failure, most due to medication
65
Q

how does chronic tubulointerstitial disease present?

A
  • indolent
  • tubular dysfunction
66
Q

what is the predominant pathology behind chronic tubulointerstitial disease?

A
  • interstitial fibrosis
  • tubular atrophy
67
Q

what are causes of chronic tubulointerstitial disease?

A
  • obstruction uropathy (MC)
  • vesicoureteral reflux (2nd MC)
  • analgesic nephropathy
  • renal ischemia, glomerular disease
68
Q

what can cause obstructive uropathy leading to chronic tubulointerstitial disease?

A

prolonged obstruction of urinary tract due to:
* prostatic disease
* ureteral calculi
* cancer of cervix, colon, or bladder
* retroperitoneal tumors or fibroids

69
Q

what is vesicoureteral reflux?

A

retrograde flow of urine when voiding

70
Q

how much analgesic does a patient have to consume to be at risk for analgesic nephropathy?

A

min 1 g/d for 3+ years

71
Q

what is the pathophysiology of obstructive uropathy?

A
  1. backflow of urine
  2. extravasation into interstitum
  3. inflammation, fibrosis
  4. damage, scarring
72
Q

what are s/s of obstructive uropathy?

A

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
Q

why would a patient with obstructive uropathy have polyuria?

A

decreased ability to concentrate urine

73
Q

why might a patient with obstructive uropathy have oliguria or anuria?

A

decreased GFR and obstruction

74
Q

what would be seen on UA of a patient with obstructive uropathy?

A

often benign, may see hematuria, pyuria

75
Q

What would serum creatinine of a patient with obstructive uropathy be?

A

elevated

76
Q

how can obstructive uropathy be diagnosed?

A

imaging with US
can use CT but not first line

SHOULD BE DONE IN ALL PATIENTS WITH AKI OF UNKNOWN CAUSE AND ALL CKD PTS TO R/O OBSTRUCTION

77
Q

if you suspect a stone or PCKD, what imaging should be done?

A

noncontrast CT

78
Q

how is obstructive uropathy treated?

A

relief of obstruction

79
Q

why should you relieve a obstruction ASAP?

A

prolonged –> further tubular damage –> renal scarring
removing will not restore renal function or stop progression

80
Q

when does vesicoureteral reflux tend to occur and why?

A

during childhood
incompetent, misplaced vesicoureteral sphincter –> retrograde flow of urine while voiding

leads to inflammatory response and scarring

81
Q

what is the presentation of vesicoureteral reflux?

A
  • frequent UTIs especially young children
  • HTN
82
Q

what will labs show for vesicoureteral reflux?

A
  • varying elevations in BUN/Cr
  • Urine: mild-moderate proteinuria
  • voiding cystourethrogram
  • hydronephrosis, renal scarring on US
83
Q

what is a voiding cystourethrogram?

A
  • radiopaque dye instilled in bladder
  • pt voids while x-ray is taken
84
Q

how does a US of an adult with vesicoureteral reflux present?

A
  • asymmetric small kidneys
  • irregular outlines
  • thin cortices
  • areas of compensatory hypertrophy
85
Q

how is vesicoureteral reflux treated?

A
  • maintaining sterile urine in childhood
  • surgical reimplantation of ureters for high-grade reflux
  • control of HTN-ACE/ARB preferred
86
Q

what analgesic was especially associated with analgesic nephropathy?

A

phenacetin

87
Q

what is seen on renal biopsy of analgesic nephropathy?

A

tubulointerstitial inflammation and papillary necrosis

88
Q

what are lab findings of analgesic nephropathy?

A
  • 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

“ring shadow”/”golfball on a tee” = contrast in area of sloughed papillae

89
Q

how is analgesic nephropathy treated?

A
  • renal function may stabilize or improve if analgesics stopped
90
Q

what autoimmune disorders can cause autoimmune interstitial nephritis?

A
  • amyloidosis
  • cryoglobinemia
  • igA nephropathy
  • Renal transplant rejection
  • Anti-GBM antibody syndrome
  • sarcoidosis
  • sjogren syndrome
  • SLE
91
Q

what are clinical

A

GU (3 decks)

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