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CPR 3 Renal Exam > Robbins Reading Ch. 20 > Flashcards

Robbins Reading Ch. 20 Flashcards

1
Q

What is Azotemia?

A

biochemical abnormality that referes to elevation of BUN and Creatinine, usually related to GFR

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2
Q

What can cause prerenal azotemia?

A
  • hypoperfusion of kidneys
    • hypotension or fluid loss or shock
  • heart failure
  • cirrhosis
  • absence of parenchymal damage
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3
Q

What causes Postrenal azotemia?

A
  • urine flow is obstructed idstal to kidney
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4
Q

What is the term for when azotemia begins showing clinical signs and symptoms with the abnormal labs?

A

Uremia

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5
Q

What is Nephritic syndrome?

A
  • glomerular disease dominated by acute onset of gross or microscopic hematuria with dysmorpihic RBC’s and rec cell casts on UA, diminished FGR, proteinuria, and htn
  • inflammation in the glomeruli
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6
Q

What characterizes Nephrotic syndrome?

A
  • due to glomerular disease characterized by heavy proteinuria more than 3.5 gm/day
  • also hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria
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7
Q

What characterizes Acute Kidney Injury?

A
  • rapid decline in GFR, within hours to days, also presents with dysregulation of fluid and electrolyte balance & retention of metabolic waste products
    • severe forms can present as oligouria or anuria
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8
Q

What defines CKD?

A
  • diminished GFR persistently less than 60 for 3 months from any cause &/or albuminuria
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9
Q

Renal tubular defects are doinated by ___, ___, and ____.

A

Renal tubular defects are doinated by polyuria, nocturia, and electrolyte disorders.

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10
Q

What causes renal tubular defects?

A
  • result of disease that directly affect tubular structures or those that cause defects in function
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11
Q

What characterizes UTI’s? (whats found in urine)

A

bacteriuria and pyruia

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12
Q

What are the manifestations of nephrolithiasis?

A
  • spasms of severe pain known as renal colic
  • hematuria
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13
Q

Most commonly CKD is the end result and major cause of death from renal disease in what two diseases?

A

Diabetes and hypertension

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14
Q

What collagen makes up the GBM?

A

Type IV

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15
Q

What causes hypercellularity in inflammatory diseases of the glomerulus?

A
  • proliferation of mesangial or endothelial cells
  • Infiltration of leukocytes
    • this in combination with proliferation of mesangial or endothelial cells in known as endocapillary proliferation
  • Formation of crescents
    • accumulation of leukocytes and mesangial/endothelial cells
    • plasma proteins leak into urinary space and are exposed to procoagulatnts leading to fibrin deposition- this is trigger for crescent formation but true mechanism is unknown
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16
Q

What are the four basic tissue reactions to glomerulopathies?

A
  • hypercellularity
  • basement membrane thickening
  • hyalinosis
  • sclerosis
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17
Q

What are the three ways thickening of glomerular basememnt membrane is seen on EM?

A
  • deposition of amprphous electone dense material such as immune complexes on BM, could also be fibrin, amyloid, cryoglobulins, and fibrillary proteins
  • Increased synthesis of protein components of basememtn membrane
  • FOrmation of additional layers of basement membrane
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18
Q

What is hyalinosis and how does it look under light microscopy?

A
  • accumulation of material that is homogenous and eospinohilic
  • If extensive the depositis can obliteralte lumens of the glomerular tuft
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19
Q

What is sclerosis? What parts does it involve in the kidney?

A
  • deposition of extracecllular collagenous matrix confined to mesangial areas
  • can be confined to mesangial areas (diabetic glomerulosclerosis) or inolve capillary loops
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20
Q

What cell types are critical for the glomerular filtration barrier and if injured lead to leakage of proteins into urinary space?

A

Podocytes

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21
Q

What are the two types of antibody associated injuries in the kidney? Which one is predominate?

A
  • Abs reacting within the the glomoerulus
    • major form of injury- not circulating like previously thought
  • depositon of circulating Ag-Ab complexes in glomerulus
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22
Q

What is the “classic example” of glomerular injury resultilng from the locatl formation of immune complexes? This disorder is an AI disease caused by antibodies to tissue components with an unclear trigger

A

Membranous nephropathy

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23
Q

What antigen underlies most cases of primary human membranous nephropathy?

A

PLA2R aka M type phospholipase A2 receptor

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24
Q

What kind of immune deposition will be seen on immunoflourescence with membranous nephropathy?

A

Granular

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25
Q

Secondary forms of membranous nephropathy can be experimentally induced by ___&___.

A

drugs and graft vs host disease

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26
Q

What kind of immunoflourescent pattern will be seen in anti-glomerular basement membrane induced glomerulonephritis?

A

Diffuse linear pattern

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27
Q

What other basement membranes do anti GBM antibodies corss react with?

A

lung alveoli (good pastures)

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28
Q

What complement pathway is activated in dense-deposit disease aka membranoproliferative glomerulonephritis?

A

alternative complement pathway

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29
Q

How do neutrophils cause damage to kidneys and what brings neutrophils in?

A
  • they enter glomerulus as result of complement activation and Fc mediated activation
  • they release oxygen free radicals and arachidonic acid metabolistes which reduce GFR
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30
Q

How do platelets contribute to glomerular injury?

A

release eicosanoids and other mediators that contribute to cascular injury and proliferation of glomerular cells

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31
Q

How do resident glomerular cells contribute to injury of kidney?

A
  • mesangial cells produce inflammatory mediators, ROS, chemokines etc.. that initiates inflammatory responses
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32
Q

____ stimulates mesangial cells to produce oxidants, proteases, and other mediators. In the absence of neutrophils ___ can cause proteinuria.

A

C5b-C9 stimulates mesangial cells to produce oxidants, proteases, and other mediators. In the absence of neutrophils C5b-C9 can cause proteinuria.

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33
Q

What growth factor is involved with mesangial cell proliferation?

A
  • PDGF
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34
Q

Loss of what cells with a limited capacity to replicate are features of glomerular injury including focal and segmental glomerulosclerosis and diabetic nepropathy.

A

Podocytes

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35
Q

Losing what structure in the glomerular basement membrane is key to proteinuria occuring?

A

normal slit diaphragms

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36
Q

What mutations cause rare hereditary forms of nephrotic syndrome?

A
  • nephrin
  • podocin
  • both components of slit diaphragm
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37
Q

What happens when GFR is reducced to around 30-50% of its normal function and nephrons are destroyed?

A

Progression to ESRD will occur over time at a steady rate

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38
Q

What is focal segmental glomerulosclerosis?

A
  • progressive fibrosis involving portions of glomeruli that develops after many types of renal injury and leads to proteinuria and functional impairment
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39
Q

What initiates the glomerulosclerosis?

A

adaptive change by the unaffected glomeruli of the diseased kidney

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40
Q

What is the most successful intervention to FSGS?

A

Renin angiotensin system inhibitors which will reduce intraglomerular htn

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41
Q

What is tubulointerstitial fibrosis?

A
  • Tubular damage and interstitial inflammation and is a component of many of many acute and chronic glomerulonephropathies
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42
Q

What is Acute proliferative glomerulonephritis? (aka poststreptococcal, postinfectious glomerulonephritis)

A
  • diffuse proliferation of glomerular cells associated with influx of leukocytes, lesions are usually caused by immune complexes
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43
Q

What is poststreptococcal glomerulonephritis?

A
  • immune complexes containing streptococcal antigens and specific antibodies formed din situ
  • appears 1-4 weeks after streptococcal infection most frequently in kids aged 6-10
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44
Q

What will strep antibodies and serum complement levels be in poststreptococcal GN patients?

A
  • elevated titers of Abs against strep antigens
  • serum complement levels are low showing that activation and consumption of complement is occuring
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45
Q

What is the streptococcal angigenic componenet responsible for the immune reaction in post streptococcal GN?

A

Streptococcal pyogenic exotoxin B (SpeB)

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46
Q

Describe the histology seen with Poststrep GN.

A
  • enlarged hypercellular glomeruli
  • Electron microscopy shows amorphous electron dense deopsits on epithelial side of membrane and appearance of humps
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47
Q

What are the signs of a kid developing PSGN?

A
  • malaise
  • fever
  • nausea
  • oligouria
  • hematuria (cola colored)
  • 1-2 weeks after recovery from sore throat
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48
Q

What are the signs and sx of an adult developing PSGN?

A
  • sudden appearance of htn or edema
  • elevation of BUN
49
Q

Important lab findings for PSGN?

A

elevations of antistreptococcal antibody titers and decline in serum concentration of C3

50
Q

Prognosis of kids vs adults with PSGN?

A

Kids have a 95% recovery with sodiuim and water balance support. While adults havea 60% quick recovery and some develop chronic glomerulonephritis

51
Q

How does postinfectious GN differ from post streptococcal GN?

A

Postinfectious sometimes produces immune deposits containing IgA rather than IgG

52
Q

What is Rapidly Progressive Glomerulonephritis (RPGN) and what are the signs? Prognosis?

A
  • syndrome associated with severe glomerular injury but doesn’t havea specific etiologic form of glomerulonephritis
  • rapid progressive loss of renal function with severe oligouria and signs of nephritic syndrome
    • death in weeks to months if untreated
53
Q

RPGN histology?

A
  • presence of crescents in most of glomeruli
54
Q

Three classifications of RPGN?

A
  1. Type I anti GBM AB
  2. Type II Immune Complex
  3. Type III Pauci Immune
55
Q

Describe type I RPGN

A
  • linear depositis of IgG and C3 in GBM
    • can cross react with alveoli causing Goodpasture syndrome
  • high prevelance of HLA DRB1
56
Q

Describe type II RPGN

A
  • RPGN type II can be caused by any immune complexe nephritides
    • SLE, postinfectiouis GN, poststreptococcus GN, Lupus nephritis, IgA nephropathym Henoch Schonlein purpura
  • Granular staining
  • Influx of leukocytes and crescent formation
57
Q

Describe Pauci Immune Type III RPGN

A
  • lack of detectable anti GBM Ab’s or immune complexes
  • most do have circulating ANCAs
  • limited to kidneys and idiopathic
58
Q

Histology of Pauci Immune RPGN

A
  • Segmental glomerular nectosis adjacent to glomerular segments uninvolved by inflammatory or proliferative changes is key histology to this
  • Dominated by crescents with fibrin strands between cellular layers
59
Q

What causes nephrotic syndrome? What are the signs?

A
  • Derangement in glomerular capillary walls resulting in increased permability to proteins
  • massive proteinuria
  • hypoalbuminemia
  • generalized edema
  • hyperlipidemia and lipiduria
60
Q

With nephrotic syndrome, what hormone gets comepsatorily secreted?

A

Aldosterone due to the hypovolemia enhanced renin secretion and stimulation of sympathetic system

61
Q

what is the difference between a highly selective proteinuria and a poorly selective proteinuria?

A

Highly selective has mostly low molecular weight proteins such as albumin and poorly selctive has higher molecular weight globulins in addition to albumin

62
Q

What infections are nephrotic patients vulnerable to?

A

staphylococcal and pneumococcal due to loss of immunoglobins

63
Q

What causes nephrotic syndrome in kids under 17 and in adults?

A
  • <17 is a lesion primary to the kidney such as
    • minimal change disease
    • membranous glomerulopathy
    • focal segmental glomerulosclerosis
  • adults is asssociated with a systemic disease such as
    • diabetes
    • amyloidosis
    • SLE
64
Q

What characterizes membranous nephropathy?

A

diffuse thickening of glomerular capillary wall ddue to accumulation of depostis containing Ig along subepithelial side of basement membrane

65
Q

What can cause secondary membranous nephropathy?

A
  • Drugs
  • Underlying maligmant tumoors particularly carcinomas in lung and colon and melanoma
  • SLE
  • Infections
  • other AI disorders
66
Q

What causes Primary (idiopathic) membranous nephropathy?

A
  • Autoimmune diseased linked to HLA DQA1 and caused by antibodies to renal autoantigens
67
Q

What mediates the capillary wall injury in glomeruli with primary membranous nephropathy?

A
  • C5b-9 complex, it activate4s glomerular epithelial and mesangial cells inducing them to release proteases and oxidants causing injury and increased protein leakage
  • Complement is activated by IgG4, but it is not known how because this doesn’t typically induce complement pathway, but it is the principal immunoglobin deposited in this disease
68
Q

Under light microscopy how does membranous nephropathy look?

A

Uniform diffuse thickening of glomerular capillary wall

69
Q

What is minimal change disease?

A
  • benign disorder charcterized by diffuse effacement of foot processes of visceral epithelial cells detectable only by electron microscopy in glomeruli that appear normal on light microscopy
70
Q

What is the most frequent cause of nephrotic syndrome in kids?

A

minimal change disease

71
Q

What features of minimal change diease point to immunologic etiology?

A
  • clincial assoc. with respirtatory infections and prophylacric immunizations
  • response to corticosteroids or other immunosuppressives
  • association with other atopic disorders
  • increase prevelance of HLA haplotypes
    • Increase indicence of disease in those with hodgkins lymphoma
72
Q

What is the principal lesion in minimal change disease?

A

visceral epithelial cells that show a uniform and diffuse effacement of foot processes

73
Q

How is the diagnosis of minimal change dosease made?

A

When there is presence of effacement of foot processes on podocytes associated with normal glomleruli on light microscopy

74
Q

Clinical features of minimal change disease?

A
  • highly selective (meaning mostly albumin) massive protienuria, but renal function remains good
  • NO htn or hematuria
  • Dramatic response to corticosteroids
75
Q

what is the nmost common cvause of nephrotic syndrome in adults in the US?

A
  • focal segmental glomoerulosclerosis
76
Q

Break down the meaning of the name focal segmental glomeruloscleoris?

A
  • sclerosis of some but not all glomoeruli, this is what the “focal” part means
  • in the affected glomeruli only a portion of the capillary tuft is involved, this is where “segmental” comes in
77
Q

Clinical signs of FSGS?

A
  • acute or subactue onset of nephrotic or non nephrotic proteinuria
  • Hypertension
  • Microscopic hematuria
  • azotemia
78
Q

How do focal segmental glomerulosclerosis and minimal change disease differ?

A
  • FSGS has higher incidence of hematuria, reduced GFR and htn
  • Proteinuria is more nonselective in FSGS
  • Poor response to corticosteroids unlike minimal change
    • progression to CKD
79
Q

What is the hallmark histologic change seen on FSGS?

A

epithelial damage with effacement of foot processes

80
Q

What was the first gene to be identified related to FSGS?

A

NPHS1 on chromosome 19q13 encoding the protein nephrin which is a key componenet of the slit diaphragm

81
Q

Autosomal recessive FSGS results from a mutation in what gene/protein?

A
  • Mutations in NPHS2 gene encoding the protein podocin
    • podocin is also part of the slit diaphragm
      • this results in syndrome of steroid resistant nephrotic syndrome of childhood onset
82
Q

What protein mutation leads to autosomal dominant FSGS which has an insidous onset and high rate of progression to renal insufficiency?

A

Podocyte actin binding protein

83
Q

In those of African descent, what is strongly asociated with an increased risk of FSGS and renal failure and what does this polymorphism protect against?

A

APOL1 on chromosome 22, it has resistance to trypanosome infection

84
Q

What is Membranoproliferative glomerulonephritis (MPGN) and what are the two groups its catergorized into?

A
  • patteron of immune mediated injury and not a specific disease
  • Type I characterized by deposition of immune complexes containing IgG and complement
    • Type II called dense deposit disease where complement activation is the most important factor
85
Q

How is MPGN characterized histologically?

A
  • alterations in GBM, proliferation of glomerular cells, leukocyte inflitration and presence of deposits in mesangial regions and glomerular capillary walls
86
Q

Describe the morphology of glomeruli seen on histology in MPGN.

A
  • glomeruli are large and hypercellular due to proliferation of cells in the mesangium
  • glomeruli have accentuated lobular appearance due to proliferating mesangial cells and increased mesangial matrix
  • the GBM is thick and shows a double contour or tram track appearance on PAS or silver stain, this is caused by splitting (duplication) of the GBM
87
Q

How is type one MPGN identified on histology?

A

presence of discrete subendothelial electron dense deposits

88
Q

Clinical features of MPGN and prognosis

A
  • present in adolescene or young adults with nephrotic syndrome and a nephritic component with hematuria or more insidiously proteinuria
  • Few remissions can occur but the disease usually follows a slow progressive unremitting course.
  • 50% develop Chronic renal failure in 10 yrs
89
Q

what settings do secondary MPGN occur in with adults?

A
  • Chronic immune complex disorders such as SLE hepatitis, HIV, endocarditis….
  • alpha 1 antitrypsin deficiency
  • Malignant diseases
90
Q

what pathway is excessively activated in Dense deposit disease (aka type II MPGN)? What will serum concentrations look like? What causes this to happen?

A
  • Alternative complememtn pathway
  • They will have consistently decreased serum C3 but normal C1 and C4, also Diminished factor B and properdin serum levels as well (part of alternative path)
  • C3 nephritic factor C3NeF binds alternative path C3 convertase and protects it from inactivation
91
Q

What is the defining feature of Dense Deposit disease on Electron microscopy?

A
  • permeation of lamina densa of GBM by a ribbon like homogenous extremely electron dense material of unknown composition
92
Q

What is the most common type of glomerulonephritis world wide and describe what it is?

A
  • IgA Nephropathy (Berger Disease)
  • Characterized by presence of prominent IgA deposits in mesangial regions and recurrent hematuria
    *
93
Q

Clinical features of IgA nephropathy?

A
  • mild proteinuria
  • nephrotic syndrome occasionally develops
  • diagnosis is made by detection of glomerular IgA depositon
94
Q

what is the cause of IgA nephropathy

A

hereditary or acquired defect in normal formation or attachment of O linked glycans to the hinge region of IgA before they are secreted by B cells

94
Q

what is the cause of IgA nephropathy

A

hereditary or acquired defect in normal formation or attachment of O linked glycans to the hinge region of IgA before they are secreted by B cells

95
Q

What individuals does IgA nephropathy occur more in?

A

Those with celiac disease

95
Q

What individuals does IgA nephropathy occur more in?

A

Those with celiac disease or liver disease

96
Q

Clinical features of IgA nephropathy? Prognosis?

A
  • older children and young adullts
  • gross hematuria after respiratory infection
    • lasts few days but returns every few months
  • +/- proteinuria
  • some delveop nephritic syndrome
  • Many retain renal function for decades, but some progress to chronic renal failure after 20 yrs
97
Q

What is Alport syndrome?

A
  • hemmaturia with progression to chronic renal fialure accompanied by nerve deafness and other eye disorders
  • X linked
98
Q

What is mutated in Alport syndrome

A

Collagen IV

99
Q

How is Benign familial hematuria/Thin basement membrane lesion found and what is prognosis?

A
  • found by routine urinalysis and morphologically by diffuse thinning of GBM
    • Mild to moderate proteinuria is present but renal function remains normal nd prognosis is good
100
Q

Chronic glomerulonephritis histology findings?

A
  • cortex is thinned and increawse in peripelvic fat
  • obliteration of glomeruli eventually results transforming them into eosinophilic masses
  • Arterial and arteriolar scleoris is conspicuous but patients have htn
101
Q

How will patients with chronic glomerulonephritis present?

A
  • loss of appetite
  • anemia
  • vomiting
  • weakness
  • some disease is discovered with proteinuria htn or azotemia

Disease is relentlessly progressive, patients need dialysis or transplant or they will die from this disease

102
Q

What can clincal manifestations of Lupus Nephritis include?

A
  • recurrent microscopic or gross hematuria, nephritic syndrome, rapidly progressive glomerulonephritis, nephrotic syndrome, acute and chronic renal failure, and htn
103
Q

What is HSP? (signs/sx, ages, what is deposited)

A
  • Purpuric skin lesions
    • extensor surfaces of UE and LE & butt
  • Abdominal pain
  • Intestinal bleeding
  • Arthralgia
  • Renal abnormalities
    • hematuria, nephritic syndrome, nephrotic syndrome
  • Affects kids most commonly 3-8
  • IgA is deposited in mesangium
104
Q

What is fibrillary glomerulonephritis? What do patients present with and what occurs with a transplant?

A
  • characteristic fibrillar deposits in the mesangium and glomeruolar capillary walls that resemble amyloid fibrils but do NOT stain with congo red
  • Patients develop nephrotic syndrome hematuria and progressive renal insufficiency
    • recurs with transplants
105
Q

What is acutre tubular inijury?

A
  • acute renal failure and morphologic evidence of tubular injury in the form of necrosis of tubular epithelial cells
  • reversible
  • due to isschemia or direct toxic injury to tubuoles by endogenous or exogenous agents
106
Q

What factors can predispose tubules to toxic injury?

A
  • increased surface area for tubular reabsorption
  • active transport systems for ions and organic acids
  • high rate of metabolism and oxygen consumption
107
Q

What are the three stages of ATI?

A
  1. Initiation phase lasts 36 hrs, only indication of renal involvement is slight decline in urine output with rise in BUN
  2. Maintenance phase sustained decreases in urine output, salt and water overload, rising BUN, hyperkalemia, metabolic acidosis, uremia
  3. Recovery phase steady increase in urine volume, hypokalemia, becomes a problem due to potassium being lost in urine, increased risk of infection, most patients who reach this phase recover
108
Q

Descibe the histologic appearance of Acute tubuloiniterstitial nephritis?

A
  • rapid clinical onset with histology that shows interstitial edema with leukocyte infiltration of interstitium and tubules
109
Q

Chronic interstitial nephritis histology?

A
  • iinifiltartion with monocuclear leukocytes
  • priminent interstitial fibrosis
  • widespread tubular atrophy
110
Q

How are chronic and acut tubulointerstitial nephritis distinguished from glomerular diseases clinically?

A
  • absence of nephritic or nephrotic syndromes
  • presence of defects in tubular function
    • polyruia or nocturia, salt wasting, metabolic acidosis
111
Q

What is pyelonephritis?

A
  • Complication of urinary tract infections leaading to inflammation in the tubules interstitium and renal pelvis
112
Q

What causes UTI’s?

A
  • 85% are gram negative bacilli
    • E. coli, proteus, klebsiella, enterobacter (order most common to less common)
113
Q

What is the most common cause of pyelonephritis?

A
  • Ascending infection
    • colonization of distal urethra
    • urethra to bladder
    • bladder to kidneys
      • urinary tract obstruction and stasis of urine
      • Vesicoureteral reflux
      • Intrarenal reflux
114
Q

How does urinary tract obstruction or urine stasis lead to pyelonephritis?

A
  • any organism introduced to the bladder is usually voided but when the urine is stagnant the bacteria can multiply leading to infection
    • seen in those with BPH, tumors, calculi, or neurogenic bladder dysfunction
115
Q

How can vesicoureteral reflux lead to pyelonephritis?

A
  • urine is not supposed to flow backwards up into the ureter, but with an incompetent valve when pressures rise in the bladder leakage of urine backwards occurs
    • often due to congenital absence or shortening of intravesical portion of ureter, so ureter isn’t compressed during urination
    • bacteria may also be able to induce inflammation to promote reflux
116
Q

what is intrarenal reflux?

A
  • Another way urine moves from bladder to kidneys
  • there are open ducts at the tips of the renal papillae that allow the infected urine to travel backwards through
  • most commonly occurs in the upper and lower poles of kidney where papillae are flattened
117
Q

Hallmarks of acute pyelonephritis on histology?

A
  • patchy intersitial suppurative inflamation
  • intratubular aggregates of neutrophils
  • neutrophilic tubulitis
  • tubular necorisis

CPR 3 Renal Exam (14 decks)

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