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PHA 521 > Glomerular and Cystic Kidney Disease > Flashcards

Glomerular and Cystic Kidney Disease Flashcards

1
Q

Functional Role of the Kidney

A

control the balance of water in the body

control red blood cell production (erythropoietin)

control acidity of the blood

filter blood and pass waste products for excretion

control blood pressure (RAAS)

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2
Q

What is the average urine PHYSIOLOGIC protein excretion in adults

A

~80mg/day

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3
Q

What level of protein excretion qualifies as PATHOLOGIC proteinuria

A

150mg or greater over 14 hours

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4
Q

Albumin

A

smallest plasma protein

20-40% of physiologic proteinuria

filtered more readily than other globulins/plasma proteins

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5
Q

Microalbuminuria

A

excretion of 30-300 mg/day of albumin

too small to be detected by routine dipstick screening

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6
Q

Macroalbuminuria

A

excretion of albumin >300mg/day

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7
Q

Nephrotic range proteinuria

A

daily excretion of 3.5+g of protein

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8
Q

Glomerular Disease

A

MCC of pathologic proteinuria

alteration of glomerular permeability –> injury to podocytes, BM, capillary endothelium, mesangium –> pathologic proteinuria

initially: excess albumin
eventual progression to larger proteins

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9
Q

Overflow Proteinuria

A

overproduction of smaller proteins overwhelms reabsorptive ability of proximal tubule –> pathologic proteinuria

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10
Q

Tubular Proteinuria

A

tubulointestinal disease –> diminished reabsorptive capacity of the proximal tubule –> pathologic proteinuria

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11
Q

Classifications of Glomerular Disease

A

nephritic or nephrotic

primary or secondary

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12
Q

Glomerular Disease

A

cause some degree of glomerular damage

urinary loss of proteins –> hypoalbuminemia

DEFINITIVE DIAGNOSIS/GOLD STANDARD: biopsy

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13
Q

Nephritic Syndrome: definition

A

inflammatory process w/ associated immunologic response –> renal glomeruli damage –> blood cell passage

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14
Q

Nephritic Syndrome: clinical presentation

A 
edema (IS THIS EXTREMITY OR FACE)
hematuria (coca cola urine) (dysmorphic RBC and casts)
occasional WBC
subnephrotic proteinuria
HTN 
azotemia
rising creatinine
oliguria
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15
Q

Rapidly Progressive Glomerulonephritis

A

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

most severe of the nephritic spectrum

progresses to renal failure in wks/mos

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16
Q

Nephritic Syndrome: Primary

A

post infectious glomerulonephritis
IgA nephropathy
Henoch Schonlein purpura
Pauci immune glomerulonephritis (ANCA assn)
anti glomerular BM glomerulonephritis (good pastures)

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17
Q

Post Infectious Glomerulonephritis

A

group A beta hemolytic streptococci

immune mediated glomerular injury - deposition of immune complexes

1-3wk after strep infxn (pharyngitis, impetigo)

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18
Q

Post Infectious Glomerulonephritis: clinical presentation

A

oliguria
edema
variable hypertension

coca cola urine

UA: RBCs, red cell casts, proteinuria

ASO titer high (unless blunted by abx)

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19
Q

Post Infectious Glomerulonephritis: prognosis

A

children: good
adults: less favorable (severe disease RPGN, develop CKD)

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20
Q

Post Infectious Glomerulonephritis: Treatment

A

treat underlying infxn

supportive

  • anti hypertensives (ACE-I, ARB)
  • salt restriction
  • diuretics (loop)

**steroids are of no benefit

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21
Q

IgA Nephropathy

A

aka Berger’s disease

IgA deposition in glomerular mesangium –> inflammatory response

MC primary glomerular disease world wide

children, young adults
M>F

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22
Q

IgA Nephropathy: clinical presentation

A

variable
follows URI or GI infxn

hematuria (coca cola urine 1-3d from illness onset)
proteinuria
INC IgA levels
NORMAL complement levels

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23
Q

IgA Nephropathy: prognosis

A

1/3: spontaneous remission
20-40%: CKD
remainder: chronic microscopic hematuria + stable creatinine

most unfavorable prognostic indicator:
proteinuria > 1g/d

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24
Q

IgA Nephropathy: Treatment

A

corticosteroids (if proteinuria 1-3.5g/d)

ACE-I or ARB (if severe proteinuria)

target BP: <130/80

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25
Q

Henoch Schonlein Purpura

A

systemic small vessel associated w/ IgA deposition in vessel walls

children
assn w/ inciting infxn (group A strep)

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26
Q

Henoch Schonlein Purpura: clinical presentation

A

palpable purpura in LE and buttock

arthralgias

abdominal sx (nausea, colic, melena)

dec GFR (w/ nephritic presentation – some may have enough damage that leads to nephrotic)

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27
Q

Henoch Schonlein Purpura: treatment

A

no definitive treatment

**some successful indications w/ plasma exchange (plasmapheresis) and DMARDs

DMARDs: disease modifying antirheumatic drugs

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28
Q

Pauci-Immune Glomerulonephritis

A

ANCA associated

seen w/ small vessel vasculitis

  • granulomatosis w/ polyangiitis
  • eosinophilic granulomatosis w/ polyangiitis
  • microscopic polyangiitis
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29
Q

Pauci-Immune Glomerulonephritis: clinical presentation

A

fever
malaise
weight loss
purpura

granulomatosis w/ polyangiitis:

  • respiratory tract sx
  • nodular lesions that can bleed
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30
Q

Pauci-Immune Glomerulonephritis: diagnostics

A

Labs:

  • ANCA positive (antineutrophil cytoplasmic antibodies)
  • hematuria
  • proteinuria
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31
Q

Pauci-Immune Glomerulonephritis: treatment

A

high dose corticosteroids

DMARDs

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32
Q

Anti-Glomerular Basement Membrane Glomerulonephritis

A

aka goodpasture syndrome

glomerulonephritis + pulmonary hemorrhage

BM injury from anti GBM antibodies

1/3: no lung injury
2/3: lung injury

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33
Q

Anti-Glomerular Basement Membrane Glomerulonephritis: epidemiology

A

bimodal peak incidence

2nd-3rd decade
6th-7th decade

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34
Q

Anti-Glomerular Basement Membrane Glomerulonephritis: clinical presentation

A

preceded by URI
hemoptysis
dyspnea
RPGN

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35
Q

Anti-Glomerular Basement Membrane Glomerulonephritis: diagnostics

A

Labs:

  • hemosiderin laden macrophages in sputum
  • anti-GBM antibodies

CXR:
-pulmonary infiltrates

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36
Q

Anti-Glomerular Basement Membrane Glomerulonephritis: treatment

A

plasma exchange therapy (plasmapheresis)
-removes circulating antibodies

immunosuppresive drugs (corticosteroids, DMARDs)

  • prevents formation of new antibodies
  • controls inflammatory response
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37
Q

Nephrotic Syndrome

A

significantly inc BM permeability

38
Q

Nephrotic Syndrome: essentials of diagnosis

A

urine excretion 3.5+g/24hr

hypoalbuminemia (serum albumin <3g/dL)

bland urinary sediment (oval fat bodies)

peripheral edema

hyperlipidemia

39
Q

Nephrotic Syndrome: clinical presentation

A

PERIPHERAL EDEMA:

  • serum albumin <2 g/dL
  • Na retention
  • initially presents in dependent areas of the body (LE)

DYSPNEA:

  • pulmonary edema
  • pleural effusion
  • diaphragmatic compromise from ascites
40
Q

Nephrotic Syndrome: urinalysis findings

A

proteinuria

oval fat bodies (associated w/ marked HLD)

41
Q

Nephrotic Syndrome: blood chemistry findings

A

dec serum albumin (<3 g/dL)

dec total serum protein (<6g/dL)

HLD
(inc proteinuria –> fall in oncotic pressure –> inc lipid production –>
dec VLDL clearance –> hypertriglyceridemia

dec vitamin D, zinc, copper

42
Q

Nephrotic Syndrome: protein loss considerations

A

daily total dietary protein intake should replace the daily urinary protein losses to avoid negative nitrogen balance

protein malnutrition can occur w/ urinary protein loss >10g/d

43
Q

Nephrotic Syndrome: edema considerations

A

dietary salt restriction

utilize thiazide and loop diuretics (combination, high dose)

44
Q

Nephrotic Syndrome: HLD considerations

A

encourage dietary modifications and exercise

aggressive pharmacologic thearpy

45
Q

Nephrotic Syndrome: hypercoaguable state considerations

A

serum albumin < 2 –> hypercoaguable

low antithrombin III, protein C, protein S –> inc platelet activation

prone to renal vein thrombosis

46
Q

Nephrotic Syndromes

A

minimal change disease
membranous nephropathy
focal segmental glomerulosclerosis

47
Q

Minimal Change Disease: pathogenesis

A

inc levels of glomerular permeability

foot process effacement

48
Q

Minimal Change Disease: epidemiology

A

MC in children
boy>girl

adults: M=F

49
Q

Membranous Nephropathy

A

MCC of primary nephrotic syndrome in adults

idiopathic immune mediate glomerulopathy

immune complex deposition in glomerular capillary walls –> inc permeability

50
Q

Membranous Nephropathy: clinical presentation

A

variable

asymptomatic

EDEMA W/ FROTHY URINE

high incidence of venous thromboembolism

51
Q

Membranous Nephropathy: diagnostics

A

Labs:

subnephrotic (<3.5 proteinuria) to classic nephrotic (>3.5 proteinuria) syndrome

52
Q

Membranous Nephropathy: treatment

A

ACE-I or ARB
(if BP >125/75)
(reduces urine protein levels)

Corticosteroid therapy
(nephrotic syndrome only)
(if failure to improve w/ 6 mo of conservative treatment)

53
Q

Focal Segmental Glomerulosclerosis

A

inc permeability due to podocyte injury

primary or secondary renal disease

54
Q

Focal Segmental Glomerulosclerosis: primary renal disease

A

idiopathic
some genetic

altered podocyte formation

african descent

children

55
Q

Focal Segmental Glomerulosclerosis: secondary renal disease

A 
obesity
HTN
chronic urinary reflex
HIV infection
analgesic exposure
biphosphonate exposure
56
Q

Focal Segmental Glomerulosclerosis: clinical presentation

A

proteinuria

most w/ overt nephrotic syndrome

57
Q

Focal Segmental Glomerulosclerosis: treatment

A

diuretic (edema)

ACE-I or ARB (proteinuria, HTN)

statin (HLD)

high dose corticosteroid (primary, overt nephrotic)

58
Q

Renal Cyst Development

A

genetic (autosomal dominant polycystic kidney disease) and non-genetic process

childhood and adulthood diseases (acquired renal cysts secondary to chronic renal failure)

59
Q

Renal Cyst Categorization

A 
size
location
septations
calcifications
contents
enhancement
60
Q

Simple Renal Cyst

A

65-70% of all renal masses

observed in normal kidneys

MC incidental finding

little clinical significance

incidence inc w/ age
M>F

no clinical manifestations

61
Q

Simple Renal Cyst: characteristics

A

develop in cortex and medulla

solitary/multiple
unilateral/bilateral

<1cm->10cm

round/oval

lined by single epithelial layer

fluid filled

clear to straw colored fluid

62
Q

Simple Renal Cyst: potential complications

A

obstruction of calyxes or renal pelvis

rupture
(flank pain, hematuria)

infection –> renal abscess
(insidious fever, vague lumbo-abdominal pain, +/-hematuria or pyuria)

hypertension
(compression of renal parenchyma –> angiotensin dependent HTN)

63
Q

Simple Renal Cyst: US criteria for simple cyst

A

sharply demarcated w/ smooth thin walls

no echoes (anechoic) w/in mass

enhanced back wall indicating good transmission through the cyst

64
Q

Simple Renal Cyst: US criteria for complex cyst

A

thick walls and/or septations

calcifications

solid components

mixed echogenicity

vascularity

65
Q

Simple Renal Cyst: diagnostics

A

first line: US

CT w/ and w/out contrast if US is equivocal or c/w complex cyst

66
Q

Bosniak Classification of Renal Cysts: Category I

A

sharply demarcated w/ smooth thin walls
homogenous fluid
no contrast enhancement

simple cyst
benign
image in 6-12 months

67
Q

Bosniak Classification of Renal Cysts: Category II

A 
closely resemble simple cyst
few thin septa
few calcifications
<3cm diameter, well marginated
no contrast enhancement

complex cyst
benign
imagine in 6-12months

68
Q

Bosniak Classification of Renal Cysts: Category IIF

A

more complicated than II
multiple thin septa
thickened walls, calcifications
>3cm diameter

complex cyst
likely benign (5% malignant)
repeat imaging in 3-6months

69
Q

Bosniak Classification of Renal Cysts: Category III

A

indeterminate cystic masses
thickened irregular walls or septa
measurable enhancement

complex cyst
40-60% malignant
monitor in older patients
excise in younger patients

70
Q

Bosniak Classification of Renal Cysts: Category IV

A

category III + soft tissue enhancing components adjacent to cyst wall

complex cyst
85-100% malignant

71
Q

Acquired Renal Cysts

A

MC reason: chronic renal failure

inc risk of development w/ dialysis

inc incidence w/ duration of dialysis

may inc RCC risk

72
Q

Acquired Renal Cysts: diagnostic criteria

A

bilateral involvement
> 4 cysts
<0.5-2/3cm diameter

73
Q

Acquired Renal Cysts: clinical presentation

A

small to normal sized kidneys

asymptomatic

74
Q

Acquired Renal Cysts: screening consideration

A

yearly screening after 3-5yrs of dialysis

US vs. CT w/ and w/out contrast

75
Q

Simple or Complex Renal Cyst: treatment

A

excision (Bosniak classification)

acute/intermittent pain:

  • acetaminophen
  • NSAID

persistent pain:

  • percutaneous aspiration w/ injection of sclerosing agent
  • laparoscopic unroofing
76
Q

Autosomal Dominant Polycystic Kidney Disease: etiology

A

autosomal dominant

  • PKD1 mutation: aggressive, MC
  • PKD2 mutation: slow growing

5% spontaneous

mutation –> obstructed tubules –> cyst formation –> fluid accumulation –> enlargement –> separate from nephron –> compression of neighboring renal parenchyma –> progressive compromise of renal function

77
Q

Autosomal Dominant Polycystic Kidney Disease: clinical presentation

A

clinically silent

irreversible decline in renal function (begins in 4th decade)

HTN
pain
hematuria (microscopic)
proteinuria

78
Q

Autosomal Dominant Polycystic Kidney Disease: initial presentation

A

30’s-40’s

pain
(abdominal, flank, back, chest, combination)

large palpable kidneys

frequent UTIs or recurrent nephrolithiasis

79
Q

Autosomal Dominant Polycystic Kidney Disease: diagnostics

A

US
(for screening and monitoring)

Labs:
CBC
CMP
UA
genetic screening
80
Q

Autosomal Dominant Polycystic Kidney Disease: associated manifestations

A

hepatic cysts (estrogen sensitive)

pancreatic/splenic cysts

cerebral aneurysms

mitral valve prolapse

colonic diverticula

81
Q

Autosomal Dominant Polycystic Kidney Disease: treatment

A

no definitive treatment

treat HTN

  • ACE-I or ARB
  • low Na diet
  • limit caffeine consumption

pain management

avoid nephrotoxic agents

avoid contact sports

manage complications

ESRD - dialysis or kidney tranplant
UTI - quinolones

82
Q

Medullary Sponge Kidney

A

congenital disorder

MC: sporadic w/ no FH
rare: familial autosomal dominant

not diagnosed until 4th or 5th decade

83
Q

Medullary Sponge Kidney: clinical presentation and characteristics

A

asymptomatic

characterized by:

  • dilation of collecting tubules
  • medullary cysts
84
Q

Medullary Sponge Kidney: complications

A 
nephrolithiasis
UTI
hematuria
dec urinary concentrating ability
renal insufficiency
85
Q

Medullary Sponge Kidney: diagnostics

A 
intravenous pyelography
(brush/linear striations, radiating outward from calyces)

multidetector row CT

86
Q

Medullary Sponge Kidney: treatment

A

no known therapy

good hydration

thiazide diuretiv (if hypercalciuria)

abx (for UTI)

87
Q

Medullary Cystic Disease

A

aka nephronophthisis

autosomal recessive

infantile, juvenile and adolescent forms

progression to ESRD, generally before 20 years of age

88
Q

Medullary Cystic Disease: characteristic findings

A

reduced urinary concentrating ability
(bland urinary sediment, polyuria, polydipsia)

chronic tubulointerstitial nephritis w/ renal cysts after age 9

89
Q

Medullary Cystic Disease: diagnosis

A

clinical

extrarenal manifestations (retinitis pigmentosa)

genetic testing

US
(normal-slight dec in kidney size)
(inc echogenicity w/ loss of corticomedullary differentiation)

90
Q

Medullary Cystic Disease: treatment

A

no specific treatment

supportive care

PHA 521 (12 decks)

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