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Renal > SM 212 Pathophysiology and Clinical Aspects of Nephrotic Syndrome > Flashcards

SM 212 Pathophysiology and Clinical Aspects of Nephrotic Syndrome Flashcards

1
Q

What are the two components of filtration?

A

Permissive and Restrictive functions are parts of filtration

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2
Q

What is the permissive aspect of filtration?

A

Filtration is permissive in the sense that it allows filtration of small molecules

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3
Q

What is the restrictive aspect of filtration?

A

Filtration is restrictive in the sense that it prevents passage of larger molecules such as Ig’s and plasma proteins into the urine

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4
Q

What must be normal to prevent Ig’s and plasma proteins from entering the urine?

A

Large molecules are restricted from filtration only if the glomerular basement membrane is normal

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5
Q

What constitutes “normal” proteinuria?

A

Some minor proteinuria is normal, and includes plasma proteins as well as proteins from tissue

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6
Q

What is intermittent proteinuria?

A

Proteinuria that comes and goes

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7
Q

What is postural proteinuria?

A

Proteinuria that only occurs while standing

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8
Q

What is persistent proteinuria?

A

Proteinuria that is due to kidney damage and occurs constantly

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9
Q

What type of proteinuria is pathological?

A

Persistent proteinuria

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10
Q

What is permselectivity?

A

The clearance of a molecule to the ratio of the clearance of creatinine

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11
Q

Explain the shape of the permselectivity curve?

A

The curve is sharp early indicating high permselectivity for small sized molecules and rapidly flattens out indicating low permselectivity for large sized molecules

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12
Q

What are the key components of the glomerular tuft?

A

Epithelial podocytes + glomerular basement membrane + endothelial cells

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13
Q

Which cell forms the basement membrane, the podocytes or the endothelial cells?

A

Both podocytes and endothelial cells form the basement membrane

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14
Q

What is the first part of the filtration barrier for particles attempting to enter the urine from blood?

A

The fenestrated endothelium, coated by a glycocalyx

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15
Q

What is the purpose of the glycocalyx?

A

It covers the fenestrated endothelium and acts as a sludge to further slow the entrance of large molecules through the slit processes

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16
Q

What is the second part of the filtration barrier for particles attempting to enter the urine from blood?

A

After crossing the fenestrated endothelium, the glomerular basement membrane acts as the second barrier

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17
Q

How does the glomerular basement membrane act as a filter?

A

It has functional pores that slow down movement of large particles

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18
Q

What is the third part of the filtration barrier for particles attempting to enter the urine from blood?

A

The podocyte is the final part of the filtration barrier, after the fenestrated endothelium and the porous glomerular membrane

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19
Q

Does each podocyte support a single capillary?

A

Nope; each podocyte forms foot processes on several capillaries

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20
Q

What roles do podocytes play?

A

Regulate permselectivity
Structural support
GBM secretion/remodelling

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21
Q

How do podocytes foot processes form a slit process network?

A

The foot processes wrap around capillaries and form interdigitated slits

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22
Q

Why is the permselectivity curve sigmoidal?

A

While large molecules are strongly impermeable and small molecules are strongly permeable, intermediate sized molecules may or may not pass through the glomerular barriers depending on how they enter/their shape/etc., so the curve is sigmoidal

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23
Q

What factors effect glomerular handling of macromolecules?

A

Size and charge

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24
Q

Why are negatively charged ions like chloride able to pass through the anionic charge barrier?

A

These ions are too small to interact with the barrier

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25
Q

Rank the clearance of positive, neutral, and negatively charged molecules through the glomerular membrane?

A

Positive > Neutral > Negative clearance in terms of clearance through the glomerular membrane

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26
Q

What is the idea of the glomerular polyanion?

A

Lots of anions in the glomerular membrane that make the membrane less permeable to negatively charged molecules

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27
Q

Describe the charge barrier across the glomerular basement membrane and why it arises?

A

The glomerular polyanion allows for cations to pass through while restricting cations, resulting in a predominantly negative urinary space and a neutral vascular space (after and prior to filtering)

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28
Q

What is the difference between diffusion and convection?

A

Diffusion refers to the equilibration of concentration gradients

Convection is “solvent drag” that pulls solute, regardless of size/charge, through a membrane partition

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29
Q

What determines the relative contribution of Diffusion and Convection to glomerular filtration?

A

The relative contribution of Diffusion and Convection is determined by whether or not filtration equilibrium is reached

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30
Q

Does high flow promote or inhibit filtration equilibration?

A

High flow inhibits filtration equilibration between hydrostatic and oncotic pressure across the glomeruli, leading to net filtration and Convection

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31
Q

Does low flow promote or inhibit filtration equilibration?

A

Low flow promotes filtration equilibration and allows time for equilibration to occur between hydrostatic and oncotic pressure across the glomeruli, favoring Diffusion over Convection

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32
Q

What is the autoregulation of blood flow in the kidney?

A

Constant perfusion at a wide range of blood pressures due to glomerulotubular feedback

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33
Q

What factors mediate autoregulation?

A

RAAS, neural control, metabolic buildup of vasoactive metabolites

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34
Q

What factors can modulate the passage of macromolecules through the glomerular membrane?

A

Hypertension = excessive filtration pressure
Fluid overload = filtration disequilibrium = favors convection
Dehydration = hemoconcentration, increased diffusion of protein
Sepsis = podocyte dysfunction alters slit diaphragm

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35
Q

Does HTN promote or inhibit macromolecule transport through the glomerular membrane?

A

Excessive filtration pressure favors macromolecule transport

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36
Q

Does fluid overload promote or inhibit macromolecule transport through the glomerular membrane?

A

Fluid overload prevents filtration equilibrium from being reached and favors Convection to drag protein across the filtration barrier

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37
Q

Does dehydration promote or inhibit macromolecule transport through the glomerular membrane?

A

Dehydration causes hemoconcentration of macromolecules that promotes diffusion of macromolecules across the filtration barrier

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38
Q

Does sepsis promote or inhibit macromolecule transport through the glomerular membrane?

A

Sepsis causes podocyte dysfunction alters the slit diaphragm function

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39
Q

Broadly speaking, what factors effect glomerular protein filtration?

A

Size (small)
Charge (anionic repulsion)
Glomerular capillary pressure
Macromolecular shape and deformability

40
Q

How do the tubules normally handle protein?

A

The PCT normally reabsorbs protein via absorptive endocytosis via non-specific binding to Cubulin and Megalin

41
Q

How does the PCT relate to proteinuria?

A

PCT failure to reabsorb protein is a potential cause of proteinuria, and may occur when excess protein crosses the GBM

42
Q

What is Fanconi Syndrome?

A

Amino aciduria
Glycosuria
Phosphaturia
Proximal RTA

43
Q

What is Beta2 Microglobulin?

A

A protein that is part of MHCI which is freely filtered by the glomerulus and degraded by the PCT

44
Q

How does Glomerular dysfunction effect protein levels in the serum and urine?

A

Glomerular dysfunction prevents passage of proteins through the GBM leading to high serum and low urine

45
Q

How does Tubular dysfunction effect protein levels in the serum and urine?

A

Tubular dysfunction prevents passage of proteins through the GBM leading to low serum and high urine

46
Q

Is the amount of protein in pathologic proteinuria fixed?

A

The absolute amount of protein in proteinuria is fixed and varies little with time, since it depends solely on the permeability of the GBM

47
Q

Is the concentration of protein in pathologic proteinuria fixed?

A

The concentration of protein in proteinuria is varied, since it depends on the amount of volume being excreted

48
Q

What underlying abnormality of proteinuria suggest?

A

Increased glomerular permeability to proteins

Decreased tubular reabsorption of proteins

49
Q

What are the two broad causes of fixed proteinuria?

A

Glomerular and Tubular

50
Q

Does protein loss in proteinuria effect specific systems or the entire body?

A

Specific protein loss = specific systems

Generalized protein loss = nephrotic syndrome

51
Q

What does significant loss of plasma protein in nephrotic syndrome lead to?

A

Decreased levels of plasma proteins, peripheral edema, and metabolic abnormalities

52
Q

How is proteinuria defined by grams of protein?

A

3gm/day of protein = Nephrotic Syndrome

53
Q

How is proteinuria defined by ratio?

A

Urine Protein:Creatinine > 2 = Nephrotic Syndrome

54
Q

What are the additional components of true Nephrotic Syndrome, beyond high protein?

A

Hypoalbuminemia
Edema
Hypercholesterolemia

55
Q

How do Nephrosis and Nephritis compare in terms of the inciting derangement?

A

Nephrosis is caused by low serum Albumin

Nephritis is caused by renal inflammation

56
Q

How do Nephrosis and Nephritis compare in terms of resulting physiology?

A

Nephrosis leads to peripheral edema

Nephritis leads to decreased GFR

57
Q

How do Nephrosis and Nephritis compare in terms of vascular effects?

A

Nephrosis leads to decreased intravascular volume

Nephritis leads to increased intravascular volume

58
Q

How do Nephrosis and Nephritis compare in terms of vascular effects?

A

Nephrosis leads to decreased intravascular volume

Nephritis leads to increased intravascular volume

59
Q

How do Nephrosis and Nephritis compare in terms of edema?

A

Nephrosis leads to significant edema

Nephritis leads to mild edema

60
Q

How do Nephrosis and Nephritis compare in terms of causing hypertension?

A

Nephrosis occasionally causes HTN

Nephritis usually causes HTN

61
Q

Which is more likely to cause edema, Nephrosis or Nephritis?

A

Nephrosis is more likely to cause edema than Nephritis

62
Q

Which is more likely to cause HTN, Nephrosis or Nephritis?

A

Nephritis is more likely to cause HTN than Nephrosis

63
Q

How does Nephrosis alter clearance of large molecules?

A

Nephrosis leads to increased clearance of large molecules

64
Q

How do albuminuria and proteinuria relate in nephrotic patients?

A

Two types: primarily albuminuria and generalized proteinuria that leads to hypoalbuminemia

65
Q

Why is the clearance of some macromolecules decreased in nephrotic syndrome?

A

Podocyte effacement involves flattening of the foot processes and decreases the surface area on the capillary available for clearing macromolecules

66
Q

How does podocyte effacement effect the podocytes in nephrotic syndrome?

A

Podocyte effacement = flattening = less surface area because the slits are closer together = decreased clearance

67
Q

Why is albumin excretion increased in Nephrotic syndrome?

A

Albumin excretion increases the charge barrier is lost in the barrier and Albumin itself is relatively small

68
Q

How does Minimal Change Disease lead to Nephrotic Proteinuria?

A

Podocyte effacement leads to charge selectivity

69
Q

How does FSGS lead to Nephrotic Proteinuria?

A

Podocyte dysfunction leads to altered glomerular sieving

70
Q

How does Hyperfiltration lead to Nephrotic Proteinuria?

A

Occurs in diabetes, leads to glomerular hypertrophy and failure

71
Q

How does Inflammation lead to Nephrotic Proteinuria?

A

Disruption of the filtration barrier leads to massive proteinuria

72
Q

Which Nephrotic syndrome is initiated by respiratory infection?

A

Minimal Change Disease

73
Q

Which Nephrotic syndrome tends to remit and relapse?

A

Minimal Change Disease

74
Q

What does Minimal Change Disease look like on labs and physical exam?

A

Labs = albuminuria

Physical Exam = Anascara (total body edema)

75
Q

How is Minimal Change Disease treated?

A

Corticosteroids

76
Q

How does edema occur in Nephrotic syndrome?

A

Nephrotic syndrome = low albumin = loss of oncotic pressure = edema throughout the body (Anascara)

77
Q

What is the underfilling model of edema in Nephrotic syndrome?

A

Hypoalbuminemia leads to edema
Edema = lower EABV
Lower EABV = lower glomerular perfusion
Low glomerular perfusion = Renin secretion + RAAS
RAAS = increased sodium reabsorption = Edema

78
Q

How does Renin cause edema in Nephrotic syndrome?

A

Edema from hypoalbuminemia and low oncotic pressure causes less fluid delivery to the JGA releasing Renin

Renin causes thirst and sodium retention which worsens edema

79
Q

Is protein loss the cause of Nephrotic edema?

A

Potentially, proteinuria is associated with edema

80
Q

What is the primary sodium retention model of edema in Nephrotic syndrome?

A

Serine proteases like Plasmin that leak into the Nephron during Nephrotic syndrome activate eNaC

eNaC promotes sodium retention which causes fluid retention and edema

81
Q

How do the underfilling and primary sodium retention models of edema vary?

A

The underfilling model involves low EABV and compensatory high RAAS + Aldosterone

The primary sodium retention model involves activation of eNaC by Serine proteases and fluid retention, with low compensatory RAAS + Aldosterone

82
Q

How do lipid levels rise in Nephrotic syndrome?

A

Nephrotic syndrome causes lipid levels to rise

83
Q

Why do lipid levels rise in Nephrotic syndrome?

A

Since lipids are bound to lipoproteins Albumin, decreased lipoproteins from proteinuria acts as a signal to the Liver to increase lipid production

84
Q

Why does hypercholesterolemia occur in Nephrotic syndrome?

A

Albumin, a transport protein for Cholesterol esters, is lost, inhibiting the conversion of Cholesterol to Cholesterol esters by LCAT and causing cholesterol levels to rise

85
Q

Why does hypercoagulability occur in Nephrotic syndrome?

A

Proteinuria in Nephrotic syndrome causes a decrease in anti-coagulant proteins like Protein S
Dehydration from edema and water loss increases the effective concentration of pro-coagulants

86
Q

What platelet abnormalities accompany Nephrotic syndrome?

A

Altered fibrinolysis
Increased aggregation due to loss of Albumin carrier protein
Glycoprotein charge on platelet and vessel wall

87
Q

Name an anti-coagulant protein factor lost in Nephrotic syndrome?

A

Protein S is an anti-coagulant lost in Nephrotic syndrome

88
Q

How is bone metabolism effected in Nephrotic syndrome?

A

Vitamin D Binding Protein is lost in Nephrotic syndrome leading to decreased Ca absorption and increased PTH to compensate for less Ca, leading to bone loss

89
Q

How does Nephrotic syndrome effect the immune system?

A

Nephrotic syndrome causes immune dysfunction due to urinary loss of opsonizing factors and Immunoglobulins

90
Q

What disease are Nephrotic patients susceptible to and why?

A

Nephrotic patients lose opsonizing factors and antibodies which predisposes Strep. Pneumo immunization, due to that bacterium’s antiphagocytic capsule only being vulnerable to antibodies

91
Q

How does Nephrotic syndrome cause anemia?

A

Nephrotic syndrome can cause loss of Iron binding proteins

92
Q

How does Nephrotic syndrome effect drug metabolism?

A

Nephrotic syndrome leads to the loss of Albumin as a drug carrier protein, altering metabolism

93
Q

What triggers Minimal Change Disease?

A

Immune stimuli like upper respiratory infections and allergies

94
Q

How does Minimal Change Disease present on electron microscopy?

A

Podocyte effacement

95
Q

What disease present with podocyte effacement?

A

Minimal Change Disease and FSGS

96
Q

Is FSGS acquired or genetic?

A

Both; genetic causes due to loss of function in Nephrin and other basement membrane proteins

97
Q

How can diet treat protein or lipid abnormalities in Nephrotic syndrome?

A

It doesn’t

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