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nephriticnephroticnephropathynephritis Flashcards

1
Q

What are the four defining features of nephrotic syndrome?

A
  • proteinuria > 3g/day
  • hypoalbuminemia
  • hyperlipidemia
  • edema
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2
Q

Which renal condition is often associated with solid tumor cancers, NSAIDs, Hep B/C infections, or autoimmune diseases?

A

Membranous nephropathy

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3
Q

What demographic groups are most often affected by membranous nephropathy?

A

Mostly caucasian men aged 50-60 yo

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4
Q

What is the clinical presentation of membranous nephropathy?

A

Swelling of extremities over days to weeks

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5
Q

What urine findings are associated with membranous nephropathy?

A
  • significant proteinuria
  • oval fat bodies, lipid/fatty casts with maltese crosses on polarized light
  • dyslipidemia
  • serum creatinine may be normal or elevated
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6
Q

What are the kidney biopsy findings associated with membranous nephropathy? LM, silver stain, IF, and EM

A

LM: thick GBM
Silver stain: Spike and dome pattern
IF: Granular IgG stain
EM: sub-epithelial immune-complex deposits

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7
Q

What is the treatment of membranous nephropathy?

A

RAAS blockade, salt restriction, diuresis, and immunosuppressive therapy if proteinuria is high

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8
Q

What diagnosis is suggested by a patient with 3.5 g/d of proteinuria, bilateral lower extremity edema, and a kidney biopsy with sub-epithelial immune-complex deposits on electron microscopy?

A

Membranous nephropathy

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9
Q

What renal pathology is associated with HIV infection, lithium medication use, reduced renal mass, or hyperfiltration injury?

A

Focal segmental glomerulosclerosis

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10
Q

What is the clinical presentation of focal segmental glomerulosclerosis?

A

HTN is common, edema is often present but not always, hematuria may be present but not always

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11
Q

What are the urinalysis findings associated with focal segmental glomerulosclerosis?

A
  • elevated creatinine (possible but not always present)
  • proteinuria (usually nephrotic range, but can be sub-nephrotic)
  • hematuria (not always present)
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12
Q

What are the kidney biopsy findings associated with focal segmental glomerulosclerosis? LM, IF, EM

A

LM: One or more lesions of segmental sclerosis on light microscopy
IF: Scant or non-specific staining of IgM, C3, or C1q
EM: Podocyte foot process effacement (focal or diffuse)

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13
Q

What is the treatment for focal segmental glomerulosclerosis?

A
  • treat underlying conditions/stimuli

- steroids, calcineurin inhibitors, or cellcept

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14
Q

What demographic(s) are commonly associated with minimal change disease?

A

Children < 6yo

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15
Q

What is the clinical presentation of minimal change disease?

A

Sudden-onset, “explosive” swelling that involves the face and extremities. May follow infection.

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16
Q

What are the urine findings associated with minimal change disease?

A
  • significant proteinuria
  • sometimes hematuria
  • oval fat bodies, lipid/fatty casts (with maltese cross)
  • renal function usually normal, sometimes constitutes AKI
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17
Q

What are the biopsy findings associated with minimal change disease? LM, IF, EM

A

LM/IF: normal

EM: diffuse podocyte foot process effacement

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18
Q

What is the treatment of minimal change disease?

A

Responsive to steroids usually. Next resort is calcineurin inhibitors, cyclophosphamide, and cellcept.

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19
Q

What is the most common cause of nephrotic-range proteinuria?

A

Diabetes

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20
Q

What are the main criteria associated with nephritic syndrome?

A
  • hematuria with dysmorphic RBCs and/or RBC casts

- proteinuria < 3g/day (sub-nephrotic)

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21
Q

What are the three major categories of nephritic syndromes?

A
  • immune-complex mediated
  • pauci-immune
  • anti-GBM disease
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22
Q

What is the mechanism of anti-GBM disease?

A

Autoantibodies binding to type IV collagen in the glomerular basement membrane (can also involve lungs with the alveolar basement membrane)

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23
Q

What is the clinical presentation of anti-GBM disease?

A

Ill-appearing patient with malaise, weight loss, often with hemoptysis/hypoxia if lung involvement

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24
Q

What are the urine findings associated with anti-GBM disease?

A
  • hematuria with dysmorphic RBCs and casts
  • proteinuria <3 g/day
  • often quickly rising serum creatinine
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25
Q

What are the kidney biopsy findings of anti-GBM disease? LM and IF

A

LM: diffuse crescentic glomerulonephritis
IF: linear IgG stain

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26
Q

What is the treatment of anti-GBM disease?

A

Steroids + cyclophosphamide + plasmapheresis

“aggressive disease requires aggressive treatment”

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27
Q

What is the classic clinical scenario associated with post-infectious GN?

A

A child who had pharyngitis with group A beta-hemolytic strep infection approximately 10-14 days ago

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28
Q

What is the clinical presentation of post-infectious GN?

A
  • symptom onset 1-2 weeks after strep pharyngitis (or longer for impetigo)
  • fever, malaise
  • HTN, edema, sometimes oliguria and gross hematuria
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29
Q

What are the urine findings of post-infectious GN?

A
  • hematuria with dysmorphic RBCs and casts
  • proteinuria
  • elevated serum creatinine
  • low complement levels
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30
Q

What are the kidney biopsy findings associated with post-infectious GN? LM, IF, EM

A

LM: glomerular hypercellularity or proliferation
IF: lumpy-bumpy appearance of IgG, IgM, and C3 staining
EM: large sub-epithelial immune complex deposits (“humps”)

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31
Q

What is the treatment for post-infectious GN?

A

Usually just treat lingering infection, possibly add steroids if severe

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32
Q

What demographic group(s) are most likely affected by lupus nephritis?

A

Women > men, usually child-bearing age

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33
Q

What is the clinical presentation of lupus nephritis?

A
  • edema, HTN

- systemic lupus signs (rash, joint pain, muscle pain, ulcers, pleuritis, pericarditis)

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34
Q

What are the urine findings of lupus nephritis?

A
  • hematuria (usually microscopic)
  • proteinuria (variable amount, can be nephrotic range)
  • +ANA, +anti-dsDNA
  • low complement levels
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35
Q

What is the treatment of lupus nephritis with mild kidney involvement?

A

Supportive, focused on systemic SLE management

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36
Q

What is the treatment of lupus nephritis with active inflammation/necrosis on biopsy?

A

High-dose steroids and immune modulators (cyclophosphamide, cellcept)

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37
Q

What condition is known as IgA vasculitis?

A

Henoch-Scholein purpura

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38
Q

What is the clinical presentation of IgA nephropathy?

A

Presents 1-2 days post-URI or GI illness with gross hematuria and hypertension

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39
Q

What are the urine findings of IgA nephropathy?

A
  • gross or microscopic hematuria with dysmorphic RBCs and/or casts
  • normal or elevated serum creatinine
  • normal serum complement levels
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40
Q

What are the kidney biopsy findings of IgA nephropathy? LM, IF, EM

A

LM: mesangial proliferation
IF: IgA deposits
EM: mesangial/paramesangial immune-complex deposits

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41
Q

What is the treatment for IgA nephropathy with mild proteinuria?

A

ACE-I or ARB +/- fish oil and low-salt diet

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42
Q

What is the treatment of IgA nephropathy with high proteinuria?

A

Treat with ACE-I or ARB +/- fish oil and low salt diet as well as steroids

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43
Q

What is the treatment of IgA nephropathy with rapidly rising serum creatinine?

A

Cyclophosphamide (with maintenance care like ACE-I, ARB, fish oil, low salt diet)

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44
Q

What are the urine findings associated with membranoproliferative glomerular nephritis?

A
  • hematuria
  • proteinuria (can be nephritic or nephrotic range)
  • low C3
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45
Q

What are the kidney biopsy findings associated with membranoproliferative glomerular nephritis? LM, PAS stain, IF, EM

A

LM: mesangial proliferation and “lobular” glomeruli
PAS: “tram track” appearance due to GBM splitting
IF: C3 and IgG stain
EM: immune-complex deposits

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46
Q

What is the clinical presentation of granulomatosis with polyangiitis?

A
  • fever, weight loss, malaise
  • nasal crusting, nosebleeds, “saddle nose deformity”
  • chronic sinusitis
  • dyspnea, hypoxia, hemoptysis
  • palpable purpura
  • usually middle-aged/older people
47
Q

What are the urine findings of granulomatosis with polyangiitis?

A
  • hematuria with dysmorphic RBCs and casts
  • variable proteinuria (<3g/day)
  • elevated serum creatinine
    • c-ANCA
48
Q

What are the kidney biopsy findings of granulomatosis with polyangiitis?

A

Necrotizing crescentic glomerulonephritis

49
Q

What is the treatment for granulomatosis with polyangiitis?

A

High dose steroids and cyclophosphamide (depends on level of organ damage)

50
Q

What is the clinical presentation of microscopic polyangiitis?

A
  • fever, weight loss, malaise
  • palpable purpura
  • peripheral nerve involvement
  • hemoptysis, dyspnea, hypoxia
51
Q

What are the urine findings of microscopic polyangiitis?

A
  • hematuria with dysmorphic RBCs and casts
  • proteinuria (< 3g/day)
  • elevated serum creatinine
    • p-ANCA
52
Q

What are the kidney biopsy findings of microscopic polyangiitis?

A

Necrotizing crescentic glomerulonephritis

53
Q

How many patients with diabetes go on to develop nephropathy?

A

30% of patients

54
Q

What are the four phases of the natural history of diabetic nephropathy?

A

1) hyperfiltration (silent)
2) microalbuminuria
3) macroalbuminuria
4) advanced nephropathy/failure

55
Q

What changes occur at the glomeruli in the silent phase of diabetic nephropathy?

A

Hyperfiltration and hypetrophy, basement membrane thickening

56
Q

How long does the silent phase of diabetic nephropathy last?

A

10 years

57
Q

What is the defining clinical feature of the incipient phase of diabetic nephropathy?

A

Microalbuminuria - small amounts of albumin are spilled from blood into urine (30-300 mg/day)

58
Q

What are the pathological changes associated with the microalbuminuria phase of diabetic nephropathy?

A
  • further thickening of GBM and tubular basement membrane
  • mesangial matrix expansion (collagen, fibronectin)
  • mesangial matrix expansion (diffuse or nodular Kimmelstiel-Wilson lesions)
59
Q

What co-morbidity of diabetes often occurs around the same time as the microalbuminuria phase of diabetic nephropathy?

A

diabetic retinopathy

60
Q

What is the clinically defining feature of overt diabetic nephropathy?

A

Macroalbuminuria in excess of 300 mg/day

61
Q

What is the average rate of GFR decline during the macroalbuminuria phase of diabetic nephropathy?

A

6-12 ml/min/year

62
Q

What is the risk of progression of macroabluminuria phase diabetic nephropathy to ESRD without treatment?

A

50% in 10 years, 75% within 15 years

63
Q

What factors influence hyperfiltration in diabetic nephropathy?

A
  • glomerular hypertrophy
  • afferent arteriolar vasodilation
  • efferent arteriolar vasoconstriction
    (mediated by angiotensin II)
64
Q

What three pathological changes in diabetic nephropathy contribute to proteinuria?

A
  • GBM thickening
  • podocyte damage/detachment/fusion
  • hemodynamic effects, intraglomerular hypertension
65
Q

What pathological features of diabetic nephropathy correlate to reduced GFR?

A
  • mesangial matrix expansion (obliteration of capillary surface area)
  • tubulointerstitial fibrosis (nephron loss and further damage)
66
Q

What is the initial stimulus of diabetic nephropathy?

A

Hyperglycemia

67
Q

How does hyperglycemia contribute to kidney damage in diabetic nephropathy?

A

It leads to production of advanced glycation end products (altered protein structure) or reactive oxygen species (cell damage)

68
Q

What are key cytokines of diabetic nephropathy?

A

TGF-beta (hypertrophic, profibrotic), VEGF, angiotensin-II (profibrotic)

69
Q

What is the goal A1c level in treatment of diabetic nephropathy?

A

Under 7%

70
Q

What are the most recent blood pressure control guidelines for patients with diabetic nephropathy?

A

<130/80

71
Q

Should ACE-I and ARBs be used together to treat diabetic nephropathy?

A

No - studies show that using both together can cause AKI and hyperkalemia

72
Q

What is the function of SGLT2 inhibitors?

A

They block the action of sodium-glucose co-transporters in the proximal tubule, leading to urinary glucose loss and improved management of diabetes

73
Q

What does a dense-pink hyaline appearing nodule in the mesangium suggest?

A

Diabetic nephropathy - Kimmelstiel-Wilson lesion

74
Q

What are the two infectious classes of tubulointerstitial disease?

A

Acute pyelonephritis, chronic pyelonephritis

75
Q

What are four non-infectious classes of tubulointerstitial disease?

A
  • drug-induced interstitial nephritis
  • ishchemia
  • metabolic derangements
  • physical damage
76
Q

What is the pathophysiology of analgesic-induced nephropathy?

A

Acetaminophen/phenacetin = oxidative damage

Aspirin = prostaglandin synthesis inhibitor leading to vasoconstriction and reduction of blood flow to an already ischemic papilla

77
Q

What are the three phases of acute tubular necrosis?

A

Initiation, maintenance, and recovery

78
Q

What are causes of acute tubular necrosis?

A

Ischemia, drug/toxicity, severe glomerular disease, acute papillary necrosis

79
Q

What is postural proteinuria?

A

Observed only when subject assumes an upright position

80
Q

What transmembrane protein crosses the podocyte slit diaphragm?

A

nephrin (2 molecules interlock)

81
Q

What is the mechanism of albuminuria in minimal change disease/nephrotic syndromes?

A

Nephrin slit diaphragms are disrupted, altering slit pore integrity. Loss of cytoskeletal integrity of podocytes leads to disrupted potential charge of EBM, losing the charge selectivity of the filter

82
Q

How does nephrotic syndrome lead to edema?

A

Loss of proteins in the serum leads to fluid retention in the extra-vascular space, which depletes volume for the heart and for kidney perfusion. This triggers a vicious cycle of RAAS activation due to perceived hypovolemia

83
Q

Why is lipid production increased in nephrotic syndrome?

A

Increased hepatic lipoprotein synthesis, urinary loss of HDL,anddecreased lipoprotein lipase activity

84
Q

Why do patients with nephrotic syndromes have altered hemostasis?

A

Loss of clotting factors in the urine (proteinuria)

85
Q

Why are nephrotic patients often more susceptible to infection?

A

Loss of immunoglobulins in urine (proteinuria)

86
Q

Why do patients with nephrotic syndrome get bone disease?

A

They lose vitamin D in the urine, which leads to bone degradation from low calcium levels

87
Q

Why do some nephrotic syndrome patients develop anemia?

A

Loss of iron-binding proteins in the urine (proteinuria)

88
Q

What two nephrotic syndromes result from podocytopathy?

A

Minnimal change disease, focal segmental glomerulosclerosis

89
Q

What two renal disorders result from chronic primary renal inflammation?

A
  • membranoproliferative glomerulonephritis

- membranous nephropathy

90
Q

What is the cause of fragmented red blood cells?

A

Shear stress in microvasculature with thrombi

91
Q

What is the cause of thrombocytopenia?

A

Platelet consumption in thrombi

92
Q

What 4 features of the glomerular microvascular bed make it susceptible to injury?

A

1) fenestrations
2) high capillary pressure
3) continual exposure to toxins and complement activation because of high blood flow
4) death of glomerular endothelium exposes underlying glomerular basement membrane, which is extremely pro-thrombotic

93
Q

What are three factors that protect the glomerular microvascular bed?

A

1) high levels of VEGF in the glomerulus (blood vessel growth factor)
2) complement regulatory proteins (factor H)
3) ADAMTS13 that breaks down vWF multimers to limit platelet aggregation

94
Q

What is the pentad of thrombitic thrombocytopenic purpura?

A

Hemolytic anemia, thrombocytopenia, neurologic symptoms, kidney injury, fever

95
Q

What is the cause of thrombotic thrombocytopenic purpura?

A

Extremely low ADAMTS13 activity, which leads to large multimers of vWF that increase platelet activation and thrombus formation

96
Q

What is the normal function of ADAMTS13?

A

It cleaves large circulating multimers of vWF

97
Q

What is the treatment for thrombotic thrombocytopenic purpura?

A

Plasmapheresis and exchange (remove antibody and/or give back the enzyme)

98
Q

What is the cause of typical HUS?

A

Shiga-toxin from E Coli O157:H7

99
Q

What is the mortality of typical HUS?

A

12% ESRD, 25% longterm renal sequelae

100
Q

What is the mechanism of shiga toxin?

A

It enters systemic circulation, binds to Gb3 receptor on glomerular endothelial cells and leads to platelet thrombi

101
Q

What is the treatment of typical HUS?

A

Supportive care, plasmapheresis, and eculizimab

102
Q

What is the prevalence of atypical HUS?

A

10% of cases not attributed to shiga-toxin

103
Q

What are causes of atypical HUS?

A

Familial or sporadic causes of abnormal complement regulation, most commonly defects in factor H

104
Q

What is the most common cause of atypical HUS?

A

Mutations in the gene encoding factor H or auto-antibodies to factor H (a regulator of complement activation)

105
Q

What is the treatment for atypical HUS?

A

Plasmapheresis and exchange to remove auto-antibody and/or give back factor H to deficient patients, also therapies to block complement activation (eculizimab)

106
Q

How can strep pneumo cause HUS?

A

It has neuraminidase production that acts on antigen exposed on surface of endothelial cells

107
Q

What are characteristics of preeclampsia?

A

TMA, hypertension, thrombotic microangiopathy in kidney, neurologic features, hemolytic anemia, thrombocytopenia, and edema

108
Q

What is HELLP syndrome?

A

A disorder related to anti-VEGF that has features of
Hemolytic anemia
Elevated Liver enzymes
Low Platelets

109
Q

When does preeclampsia occur?

A

Usually after the 20th week of pregnancy

110
Q

What are three risk factors for preeclampsia?

A

First pregnancy, twins, molar pregnancy

111
Q

What is the pathophysiology of preeclampsia?

A

High circulating levels of sFlt1 (soluble VEGF receptor 1) that binds VEGF and reduces its activity, resulting in hypertension, damage to glomerular endothelium, and other vascular beds resulting in thrombi formation

112
Q

What is the treatment for preeclampsia?

A

Delivering the baby, MgSO4 for neurologic symptoms, blood pressure control

113
Q

What are the side-effects of anti-VEGF drugs?

A

Hypertension, kidney injury with glomerular endotheliosis, platelet-rich thrombi

114
Q

What are ant-VEGF drugs used for?

A

Treatment for diabetic retinopathy

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