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From Flashcardlet > Renal First Aid > Flashcards

Renal First Aid Flashcards

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0
Q

What is the mesonephros?

A

the interim kidney during the first trimester

it contributes to the male genital system later on

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1
Q

When does the pronephros appear?

A

week 4, then degenerates

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2
Q

What is the metanephros?

A

the permanent kidney

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3
Q

When does the metanephros appear?

A

fifth week of gestation; nephrogenesis continues through 32-36 week of gestation

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4
Q

What is the ureteric bud?

A

DERIVATION caudal end of mesonephros
GIVES RISE TO ureter, pelvises, calyses, collecting buds
Fully canalized by 10th week.

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5
Q

What is the metanephric mesenchyme?

A

tissue that interacts with ureteric bud –> induction of differentiation and formation of glomerulus through to distal convoluted tubule

NOTE if this interaction between the metanephric mesenchyme and the ureteric bud does not occur properly, several congenital malformations of the kidney may occur

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6
Q

What is last to canalize?

A

ureteropelvic junction

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7
Q

What is the most common site of obstruction (hydronephrosis) in the fetus?

A

ureteropelvic junction

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8
Q

What is Potter’s syndrome?

A

oligohydramnios –> compression of fetus –> limb deformities, facial deformities, and pulmonary hypoplasia

Potter’s syndrome is incompatible with life.

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9
Q

What is the cause of death in Potter’s syndrome?

A

pulmonary hypoplasia

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10
Q

What are the causes of Potter’s syndrome?

A

ARPKD
posterior urethral valves
bilateral renal agenesis

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11
Q

What is a horseshoe kidney?

A

inferior poles of both kidneys fuse; during the ascent from the pelvis in development, the horseshoe kidney gets trapped under the inferior mesenteric artery

This is the most common congenital renal anomaly.

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12
Q

With what is a horseshoe kidney associated?

A

Turner syndrome

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13
Q

What causes a multicystic dysplastic kidney?

A

abnormal interaction between ureteric bud and metanephric mesenchyme –> nonfunctional kidney consisting of cysts and connective tissue

if unilateral, a multicystic dysplastic kidney is generally asymptomatic; the opposite kidney will undergo compensatory hypertrophy

if bilateral, distinguish from inherited polycystic kidney disease

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14
Q

How and when is multicystic dysplastic kidney commonly diagnosed?

A

prenatally via ultrasound

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15
Q

Do the ureters course under or over the uterine artery / vas deferens (females vs males)?

A

under

–Water under the bridge–

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16
Q

Which kidney is taken in a donor transplant?

A

left, as it has a longer renal vein

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17
Q

How much of the total body weight is nonwater mass?

A

40%

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18
Q

How much of the total body weight is water?

A

60%

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19
Q

Of the total body water, how much is intracellular fluid?

A

2/3

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20
Q

Of the total body water, how much is extracellular fluid?

A

1/3

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21
Q

Of the extracellular fluid, how much is plasma volume?

A

1/4

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22
Q

Of the extracellular fluid, how much is interstitial volume?

A

3/4

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23
Q

What percentage of the body weight is total body water, intracellular fluid, and extracellular fluid, respectively?

A

60% total body water
40% ICF
20% ECF
–60-40-20 rule–

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24
Q

Is potassium higher intracellularly or extracellularly?

A

intracellular

–HIKIN’: HIgh K INtracellular–

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25
Q

What is used to monitor plasma volume?

A

radiolabeled albumin

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26
Q

What is used to monitor extracellular volume as a whole?

A

inulin

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27
Q

What is normal osmolarity?

A

290 mOsm/L

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28
Q

What is the composition of the glomerular filtration barrier?

A

fenestrated capillary endothelium (size barrier)
fused basement membrane with heparan sulfate (negative charge barrier)
epithelial layer consisting of podocyte foot processes

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29
Q

What is the function of the glomerular filtration barrier?

A

filtration of plasma according to size and net charge

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30
Q

What happens to the glomerular filtration barrier in nephrotic syndrome?

A

the charge barrier is lost –> albuminuria, hypoproteinemia, generalized edema, hyperlipidemia

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31
Q

What is the equation for clearance?

A 
Cx = (UxV)/Px 
This is the volume of plasma from which the substance is completed cleared per unit time.
Cx = clearance of X in mL/min
Ux = urine concentration of X
Px = plasma concentration of X
V = urine flow rate
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32
Q

If Cx (clearance) is less than GFR, what is happening to substance X?

A

net tubular resorption

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33
Q

If Cx (clearance) is more than GFR, what is happening to substance X?

A

net tubular secretion

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34
Q

If Cx = GFR, what is happening to substance X?

A

no net secretion or reabsorption

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35
Q

What is the equation for glomerular filtration rate (GFR)?

A

Normally, GFR is approximately 100 mL/min
Kf = filtration constant
Pg = hydrostatic pressure within the glomerular capillary
Pb= hydrostatic pressure within Bowman’s capsule
πg = colloid osmotic pressure within the glomerular capillary
πb = colloid osmotic pressure within Bowman’s capsule; normally 0

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36
Q

Why is inulin clearance used to calculate GFR?

A

it is freely filtered and is neither reabsorbed nor secreted

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37
Q

Does creatinine clearance overestimate, underestimate, or equal GFR?

A

slightly overestimates GFR, as creatinine is moderately secreted by the renal tubules

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38
Q

What do incremental reductions in GFR denote?

A

stages of chronic kidney disease

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39
Q

How is ERPF (effective renal plasma flow) calculated?

A 
ERPF = (Upah x V) / Ppah 
ERPF = Cpah
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40
Q

What is used to estimate ERPF?

A

PAH clearance; it is both filtered and actively secreted in the proximal tubule. All PAH entering the kidney is excreted.

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41
Q

How is RBF calculated?

A

RBF = RPF / (1-HCT)

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42
Q

What is the relationship between ERPF and RPF?

A

ERPF underestimates true RPF by ~10%

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43
Q

What is the equation for filtration fraction?

A

FF = GFR / RPF

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44
Q

What is the normal FF?

A

20%

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45
Q

What is the equation for filtered load?

A

filtered load = GFR x plasma concentration

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46
Q

What dilates the afferent arteriole?

A

prostaglandins dilate afferent arteriole –> increased RPF, increased GFR
This maintains FF.

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47
Q

What blocks the effect of prostaglandins on the afferent arteriole?

A

NSAIDs

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48
Q

What constricts the efferent arteriole?

A

Angiotensin II constricts efferent arteriole –> decreased RPF, increased GFR
This increases FF.

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49
Q

What blocks the effect of angiotensin II on the afferent arteriole?

A

ACE inhibitors (block the formation of AII in and of itself)

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50
Q

What is affected in renal artery stenosis?

A

the afferent artery; renal artery stenosis decreases GFR and FF.

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51
Q

What are the effects of afferent arteriole constriction on RPF, GFR, and FF?

A

RPF decreased
GFR decreased
FF unchanged

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52
Q

What are the effects of afferent arteriole constriction on RPF, GFR, and FF?

A

…

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53
Q

What are the effects of efferent arteriole constriction on RPF, GFR, and FF?

A

RPF decreased
GFR decreased
FF increased

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54
Q

What are the effects of increased plasma protein concentration on RPF, GFR, and FF?

A

RPF unchanged
GFR decreased
FF decreased

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55
Q

What are the effects of decreased plasma protein concentration on RPF, GFR, and FF?

A

RPF unchanged
GFR increased
FF increased

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56
Q

What are the effects of constriction of ureter on RPF, GFR, and FF?

A

RPF unchanged
GFR decreased
FF decreased

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57
Q

How is filtered load calculated?

A

filtered load = GFR * Px

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58
Q

How is excretion rate calculated?

A

excretion rate = V * Ux

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59
Q

How is reabsorption rate calculated?

A 
Reabsorption = filtered - excreted
Reabsorption = (GFR * Px) - (V * Ux)
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60
Q

How is secretion calculated?

A 
Secretion = excreted - filtered
Secretion = (V * Ux) - (GFR * Px)
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61
Q

Is glucose freely filtered, reabsorbed, or secreted in the kidney?

A

at a normal plasma level, glucose is completely reabsorbed in the proximal tubule by Na+/glucose cotransport

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62
Q

What is the threshold for glucosuria?

A

160 mg/dL

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63
Q

At what glucose level are all Na+/glucose transporters saturated?

A

Tm is at 350 mg/dL

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64
Q

How does pregnancy cause glucosuria?

A

normal pregnancy reduces reaborption of glucose and amino acids in the proximal tubule –> glucosuria and aminoaciduria

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65
Q

What reabsorbs amino acids?

A

sodium-dependent transporters in the proximal tubule

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66
Q

What is Hartnup’s disease?

A

a deficiency of neutral amino acid (tryptophan) transporter –> pellagra

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67
Q

What is the presentation of pellagra?

A

dermatitis
dementia
diarrhea

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68
Q

What is the cause of pellagra, normally?

A

niacin (B3) deficiency

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69
Q

In what section of the nephron is the brush border found?

A

early proximal tubule

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70
Q

What occurs at the early proximal tubule?

A

ISOTONIC reaborption of nearly all glucose and amino acids; most bicarbonate, sodium, chloride, phosphate, and water.
generation and secretion of ammonia (acts as buffer for secreted H+)

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71
Q

What effect does PTH have in the early proximal tubule?

A

inhibition of the Na+/phosphate cotransport –> phosphate excretion

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72
Q

What effect does ATII have in the early proximal tubule?

A

stimulation of Na+/H+ exchange –> increased Na+, H2O, and HCO3- reabsortion –> permission of contraction alkalosis

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73
Q

How much sodium is reabsorbed in the early proximal tubule?

A

65-80%

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74
Q

Where is urine made hypertonic?

A

thin descending loop of Henle

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75
Q

What is the concentrating segment of the nephron?

A

thin descending loop of Henle

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76
Q

Is the reabsorption of water in the thin descending loop of Henle a passive or active process?

A

passive

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77
Q

What occurs in the thick ascending loop of Henle?

A

active reabsorption of Na+, K+, and Cl-
resultant K+ backleak –> generation of a positive lumen potentional –> (indirect induction of) paracellular reabsorption of Mg2+ and Ca2+

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78
Q

How much sodium is reabsorbed in the thick ascending loop of Henle?

A

10-20%

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79
Q

Which areas of the nephron are impermeable to water?

A

thick ascending loop of Henle

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80
Q

Which areas of the nephron are impermeable to sodium?

A

thin descending loop of Henle

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81
Q

Do the thick ascending loop of Henle make urine less concentrated or more concentrated?

A

less

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82
Q

What happens in the early distal convoluted tubule?

A

active reabsorption of Na+, Cl-

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83
Q

How much sodium is reabsorbed in the early DCT?

A

5-10%

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84
Q

Does the early DCT make urine isotonic, hypotonic, or hypertonic?

A

hypotonic

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85
Q

What affect does PTH have in the early DCT?

A

increases Ca2+/Na+ exchange –> Ca2+ reabsorption

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86
Q

Where do thiazide diuretics act?

A

early DCT

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87
Q

Where do carbonic anhydrase inhibitors act in the nephron?

A

early proximal tubule

carbonic anhydrase catalyzes the reactions that form carbonic acid from CO2 and H2O (and vice versa)

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88
Q

What happens in the collecting tubules?

A

reabsorption of Na+ in exchange for secretion of K+ and H+

This is regulated by aldosterone.

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89
Q

Where does aldosterone act?

A

at the mineralocorticoid receptor of the collecting tubules

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90
Q

What effect does aldosterone have?

A

activation of mineralocorticoid receptor –> insertion of Na+ channel on luminal side –> increased Na+ reaborption; increased K+ and H+ secretion

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91
Q

Where in the nephron does ADH act?

A

V2 receptor on the principal cells of the collecting tubules

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92
Q

What effects does ADH have?

A

activation of V2 receptor –> insertion of aquaporin H2O channels on luminal side –> increased H2O reaborption

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93
Q

How much sodium is reabsorbed in the collecting tubules?

A

3-5%

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94
Q

Why does tubular inulin increase in concentration along the proximal tubule?

A

water is reabsorbed

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95
Q

In the proximal third of the proximal tubule, does Cl- reaborption match Na+ reabsorption?

A

No; it is slower

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96
Q

In the proximal third of the proximal tubule, does Cl- reaborption match Na+ reabsorption?

A

Yes

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97
Q

What effect do the changes in Cl- reabsorption rate have upon its relative concentration curve?

A

the relative concentration curve increases before it plateaus

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98
Q

When the TF/P ([tubular fluid]/[plasma]) is <1, what is occurring?

A

solute is reabsorbed more quickly than water

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99
Q

When the TF/P ([tubular fluid]/[plasma]) is =1, what is occurring?

A

solute and water are reabsorbed at the same rate

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100
Q

When the TF/P ([tubular fluid]/[plasma]) is >1, what is occurring?

A

solute is reabsorbed less quickly than water

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101
Q

What effect does ATII have upon the vascular smooth muscle?

A

AT1 receptors on vascular smooth muscles –> vasoconstriction –> increased BP

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102
Q

What effect does ATII have upon the arteriole of the glomerulus?

A

constriction of EFFERENT arteriole of glomerulus –> increase FF to preserve renal function (thus, increase GFR) in low-volume states (when RBF decreases)

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103
Q

What effect does ATII have upon the adrenal gland?

A

aldosterone release -> increased Na+ channel and Na+/K+ pump insertion in principal cells; enhances K+ and H+ excretion (upregulates principal cell K+ channels and intercalated cell H+ channels) –> creates favorable Na+ gradient for Na+ and H2O reabsorption (1 Na+ : 8 H2O)

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104
Q

What effect does ATII have upon the posterior pituitary?

A

ADH release –> increased H2O channel insertion in principal cells –> H2O reabsorption

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105
Q

What effect does ATII have upon the proximal tubule?

A

increased Na+/H+ activity –> Na+, HCO3-, and H2O reabsorption

This can permit contraction alkalosis.

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106
Q

What effect does ATII have upon the hypothalamus?

A

thirst

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107
Q

What effect does ATII have upon catecholamines?

A

SAS releases NE –> increased venous resistance

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108
Q

What effect does ATII have upon baroreceptors?

A

limitation of reflex bradycardia –> maintenance of blood volume and pressure

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109
Q

What three cell types are responsible for stimulating renin release?

A

JGA CELL senses decreased BP
MD CELL senses decreased Na+ delivery
B1 RECEPTORS increase sympathetic tone

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110
Q

From where is ANP released?

A

atria

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111
Q

What stimulates release of ANP?

A

increased volume / pressure in the atria

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112
Q

What effect does ANP have?

A

cGMP release –> relaxation of vascular smooth muscle –> increased GFR, decreased renin, increased Na+ filtration

NET EFFECT Na+ loss, volume loss

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113
Q

ADH regulates both low blood volume and osmolarity. Which takes precedence?

A

low blood volume

NOTE in low volume states, both ADH and aldosterone regulate low blood volume

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114
Q

What is the composition of the JGA?

A

JG CELLS modified smooth muscle of afferent arteriole

MACULA DENSA CELLS NaCl sensors, part of the distal convoluted tubule

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115
Q

How do beta-blockers affect the JGA?

A

inhibit B1 receptors –> decreased renin release –> decreased BP

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116
Q

From where is erythropoietin released?

A

interstitial cells in the peritubular capillary bed

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117
Q

What triggers the release of erythropoietin?

A

hypoxia

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118
Q

What effect does the kidney have upon vitamin D?

A

25-OH vitamin D is converted to 1,25-(OH)2 vitamin D (the active form) by 1 alpha hydroxylase

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119
Q

What positively modifies the conversion of inactive vitamin D to active vitamin D?

A

PTH

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120
Q

What effect do prostaglandins have upon the kidney?

A

vasodilation of the afferent arterioles –> increased GFR

121
Q

What effect do NSAIDs have on the kidney?

A

inhibit renal production of prostaglandins –> no afferent arteriole dilation –> decreased GFR –> acute renal failure

122
Q

What stimulates PTH secretion?

A

decreased plasma [Ca2+]
increased plasma [PO43-]
decreased plasma 1,25-(OH)2 vitamin D

123
Q

What are the total effects of PTH?

A

increased [Ca2+] reabsorption in the DCT
increased Ca2+ absorption from gut
–> increased plasma [Ca2+]

decreased PO43- reabsorption in the PCT
increased PO43- absorption from gut
–> increased plasma [PO43-]

increased 1,25-(OH)2 vitamin D production –> increased plasma 1,25-(OH)2 vitamin D

124
Q

Do the actions of ANP lead to compensatory Na+ reabsorption in the distal nephron?

A

No

Remember that the net effect of ANP on the kidney is Na+ AND volume loss.

125
Q

Do the actions of ATII lead to compensatory Na+ reabsorption in the distal nephron?

A

yes; ATII will lead to compensatory Na+ reabsorption in BOTH the proximal AND distal nephron

126
Q

What is the net effect of ATII in the kidney?

A

preservation of renal function in low-volume state (increased FF) with simultaneous Na+ reabsorption (both proximal and distal) to DECREASE additional volume loss

127
Q

What stimulates release of aldosterone?

A

low blood volume, mediated by ATII

increased plasma [K+]

128
Q

What stimulates release of ADH/vasopressin?

A

increased plasma osmolarity

decreased blood volume

129
Q

What modifications to the body lead to K+ shift out of cells, thus causing hyperkalemia?

A 
Digitalis and other cardiac glycosides
hyperOsmolarity
INSULIN deficiency
Lysis of cells
Acidosis
Beta adrenergic antagonists

–patient with hyperkalemia? DO INSULIN LAB–

130
Q

How can cardiac glycosides cause hyperkalemia?

A

inhibition of the Na+/K+ pump

131
Q

How can beta-adrenergic antagonists cause hyperkalemia?

A

blockage of K+ uptake in cells

132
Q

How can ACE inhibitors and ARBs cause hyperkalemia?

A

blockage of aldosterone secretion

133
Q

How can K+ sparing diuretics cause hyperkalemia?

A

blockage of aldosterone receptors

134
Q

How can NSAIDs cause hyperkalemia?

A

inhibition of COX –> inhibition of prostaglandin formation –> blockage of aldosterone secretion

135
Q

What are the symptoms of low Na+ serum concentration?

A

nausea
malaise
stupor
coma

136
Q

What are the symptoms of high Na+ serum concentration?

A

irritability
stupor
coma

137
Q

What are the symptoms of low K+ serum concentration?

A

U waves on EKG
flattened T waves
arrhythmias
muscle weakness

138
Q

What are the symptoms of high K+ serum concentration?

A

wide QRS on EKG
peaked T waves
arrhythmias
muscle weakness

139
Q

What are the symptoms of low Ca2+ serum concentration?

A

tetany

seizures

140
Q

What are the symptoms of high Ca2+ serum concentration?

A 
renal STONES
BONE pain
abdominal pain
anxiety, altered mental status
but not necessarily calciuria
--Stones, Bones, Groans, and Psychiatric Overtones--
141
Q

What are the symptoms of low Mg2+ serum concentration?

A

tetany

arrhythmias

142
Q

What are the symptoms of high Mg2+ serum concentration?

A 
decreased DTRs
lethargy
bradycardia
hypotension
cardiac arrest
hypocalcemia
143
Q

What are the symptoms of low PO43- serum concentration?

A

bone loss

osteomalacia

144
Q

What are the symptoms of high PO43- serum concentration?

A

renal stones
metastatic calcifications
hypocalcemia

145
Q

In metabolic acidosis, how are pH, PCO2, and [HCO3-] affected, and what is the compensatory response?

A

pH decreased
PCO2 decreased
[HCO3-] decreased– primary response
hyperventilation (immediate)

146
Q

In metabolic alkalosis, how are pH, PCO2, and [HCO3-] affected, and what is the compensatory response?

A

pH increased
PCO2 increased
[HCO3] increased– primary response
hypoventilation (immediate)

147
Q

In respiratory acidosis, how are pH, PCO2, and [HCO3-] affected, and what is the compensatory response?

A

pH decreased
PCO2 increased– primary response
[HCO3-] increased
increased renal [HCO3-] reabsorption (delayed)

148
Q

In respiratory alkalosis, how are pH, PCO2, and [HCO3-] affected, and what is the compensatory response?

A

pH increased
PCO2 decreased– primary response
[HCO3-] decreased
decreased renal [HCO3-] reaborption (delayed)

149
Q

What is the Henderson-Hasselbalch equation?

A

pH = 6.1 + lob ([HCO3-]/[.03 x PCO2])

150
Q

What is Winter’s formula, and for what is it used?

A

FORMULA PCO2 = 1.5(HCO3-) + 8 +/- 2
APPLICATION calculates predicted respiratory compensation for a simple metabolic acidosis

NOTE if the measured PCO2 differs significantly from that calculated using Winter’s formula, then a mixed acid-base disorder is present

151
Q

If in acidemia (pH < 7.4) the PCO2 is greater than 40 mmHg, what is the diagnosis? What are the possible causes?

A

DIAGNOSIS respiratory acidosis
CAUSES hypoventilation due to: airway obstruction, acute lung disease, chronic lung disease, opiods, sedatives, weakening of respiratory muscles

152
Q

If in acidemia (pH < 7.4) the PCO2 is less than 40 mmHg, what is the diagnosis? What should be checked next?

A

DIAGNOSIS metabolic acidosis with compensation (hyperventilation)
CHECK anion gap

153
Q

What is the equation for anion gap?

A

Na+ - (Cl- + HCO3-)

NORMAL VALUE 8-12 mEq/L

154
Q

If the anion gap is increased, what are the possible causes of metabolic acidosis with compensation by hyperventilation?

A 
Methanol (formic acid)
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets / INH
Lactic acidosis
Ethylene glycol (oxalic acid)
Salicylates (late)
--MUDPILES--
155
Q

If the anion gap is normal, what are the possible causes of metabolic acidosis with compensation (hyperventilation)?

A 
Hyperalimentation
Addison's disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
--HARDASS--
156
Q

If in alkalemia (pH > 7.4) the PCO2 is less than 40 mmHg, what is the diagnosis? What are the possible causes?

A 
DIAGNOSIS respiratory alkalosis
CAUSES hyperventilation (early high-altitude exposure); salicylates (early)
157
Q

If in alkalemia (pH > 7.4) the PCO2 is greater than 40 mmHg, what is the diagnosis? What are the possible causes?

A

DIAGNOSIS metabolic alkalosis with compensation (hypoventilation)
CAUSES loop diuretics, vomiting, antacid use, hyperaldosteronism

158
Q

With what is Type 1 renal tubular acidosis associated?

A

hypokalemia

159
Q

What occurs in Type 1 renal tubular acidosis?

A

defect in the collecting tubule’s ability to excrete H+ –> urine pH > 5.5 –> increased risk for calcium phosphate kidney stones, bone resorption

160
Q

With what is Type 2 renal tubular acidosis associated?

A

hypokalemia, Fanconi’s syndrome

161
Q

What occurs in Type 2 renal tubular acidosis?

A

defect in proximal tubular HCO3- reabsorption –> urine pH < 5.5 –> increased risk for hypophosphatemic rickets

162
Q

With what is Type 4 renal tubular acidosis associated?

A

hyperkalemia, hypoaldosteronism

163
Q

What occurs in Type 4 renal tubular acidosis?

A

hypoaldosteronism, no collecting tubule response to aldosterone –> hyperkalemia –> impairment of ammoniagenesis in the proximal tubule –> decreased buffering capacity, decreased urine pH

164
Q

Which type of renal tubular acidosis carries and increased risk of kidney stones?

A

Type 1 (distal) due to increased urine pH

165
Q

What does the overall presence of casts in the urine (regardless of type of cast) indicate?

A

The hematuria or pyuria is of RENAL origin, not bladder.

166
Q

What is the differential diagnosis when RBC casts are present in the urine?

A

glomerulonephritis
ischemia
malignant HTN
nephritic syndrome

167
Q

What is the differential diagnosis when WBC casts are present in the urine?

A

tubulointerstitial inflammation
acute pyelonephritis
transplant rejection

168
Q

I say “fatty casts” or “oval fat bodies” in urine, you say…?

A

nephrotic syndrome

169
Q

I say “granular casts” or “muddy brown casts” in urine, you say…?

A

acute tubular necrosis

170
Q

I say “waxy casts” in urine, you say…?

A

advanced renal disease or chronic renal failure

171
Q

I say “hyaline casts” in urine, you say…?

A

nonspecific

This can be a normal finding.

172
Q

What does “focal” indicate in the description of a glomerular disorder?

A

<50% of glomeruli are involved

173
Q

What does “diffuse” indicate when describing a glomerular disorder?

A

> 50% of the glomeruli are involved

174
Q

What does “proliferative” indicate when describing a glomerular disorder?

A

hypercellular glomeruli

175
Q

What does “membranous” indicate when describing a glomerular disorder?

A

thickening of the glomerular basement membrane

176
Q

What are the four types of proteinuria?

A

overflow
small molecular weight proteins (will not react in urine dipstick test)
tubular proteinuria (beta microglobulins)
glomerular proteinuria (non-nephrotic or nephrotic; albumin versus broad spectrum)

177
Q

What are the characteristics of nephrotic syndrome?

A
  • massive prOteinuria (>3.5 g/day; “frothy”)
  • hyperlipidemia, hypercholesteremia –> fatty casts
  • hypoalbuminemia –> pitting edema
  • hypogammaglobulinemia –> increased risk of infection
  • loss of antithrombin III –> hypercoagulable state –> thromboembolism
  • normal GFR at onset
  • NO glomerular hypercellularity
178
Q

What are the conditions required to diagnose nephrotic syndrome?

A

proteinuria (>3 g/24 hours)

PLUS TWO OF THE FOLLOWING
hypoalbuminemia (<3.5 g/L)
edema
hyperlipidemia

179
Q

What is hypoalbuminemia?

A
  • <2 g/dL (filtered protein exceeds the amount of protein in the urine)
  • first consequence of urinary losses
  • increased renal albumin catabolism
  • increased volume of distribution
  • decreased hepatic production (malnutrition, role of inflammatory cytokines)

NOTE liver synthesis of albumin is increased in nephrotic syndrome (normal liver synthesis of albumin is 12-14 g/dL).

180
Q

How is hyperlipidemia correlated to nephrotic syndrome?

A

increased hepatic synthesis or decreased catabolism –> increased LDL, VLDL, triclyceride and chylomicrons

181
Q

How do lipiduria occur?

A

degeneration of renal tubular cells –> release of cholesterol ester –> free fat and/or oval fat bodies

182
Q

What is a fatty cast?

A

maltese cross under polarized light

183
Q

What are the complications of nephrotic syndrome?

A

(1) malnutrition
(2) increased FV, FVIII, fibrinogen, platelets, and susceptibility of platelet aggregation; decreased ATIII, antiplasmin –> HYPERCOAGULABILITY –> incidence of thrombus formation in renal, pulmonary, and peripheral veins
(3) intrarenal interstitial edema –> increased intrarenal pressure –> cessation of filtration –> ACUTE RENAL FAILURE
(4) decreased renal perfusion –> acute tubular necrosis –> ACUTE RENAL FAILURE
(5) NSAID usage (drug-induced interstitial nephritis) –> inhibition of prostaglandins –> loss of vasodilation –> decreased RBF –> ACUTE RENAL FAILURE
(6) decreased immunoglobulins –> increased infection
(7) increased protein metabolism in tubules –> proximal tubule dysfunction (Fanconi syndrome)
(8) deficiency of trace metals (Fe, Cu, Zn, vitamin D) –> osteomalacia, secondary hyperparathyroidism

184
Q

How does a pure nephrotic disease cause swelling?

A

glomerular disease with podocyte injury or death –> proteinuria –> hypoalbuminemia –> decreased oncotic pressure –> transudation of fluid –> edema

185
Q

If aldosterone is involved, is edema primary or secondary?

A

secondary

186
Q

How does the kidney respond in nephrotic syndrome?

A

glomerular disease with podocyte injury or death –> proteinuria –> hypoalbuminemia –> decreased oncotic pressure –> transudation of fluid –> decreased BP, CO, delivery to macula densa, GFR –> renin release –> AI –> AII –> aldosterone –> secondary salt retention –> increased edema

187
Q

How does nephrotic syndrome impact the heart?

A

glomerular disease with podocyte injury or death –> proteinuria –> hypoalbuminemia –> decreased oncotic pressure –> transudation of fluid –> decreased BP, CO, delivery to macula densa, GFR

188
Q

If you give a diuretic in nephrotic syndrome, what happens?

A

decrease blood pressure without change in oncotic pressure –> blood stasis

189
Q

What is the most common cause of nephrotic syndrome in children?

A

minimal change disease (nil disease)

190
Q

What serious disease may cause minimal change disease?

A

Hodgkin lymphoma

NOTE minimal change disease is usually idiopathic, but may also be triggered by a recent infection or immune stimulus.

191
Q

What is seen on light microscopy in minimal change disease?

A

normal glomeruli; lipid may be seen in proximal tubule cells

192
Q

What is seen on electron microscopy in minimal change disease?

A

effacement of foot processes
In this disease, this process is reversible.

NOTE you cannot diagnose minimal change disease solely from this finding; most nephrotic syndromes carry it.

193
Q

What is seen on immunofluorescence in minimal change disease?

A

IF is negative as there are no immune complex deposits

194
Q

Is proteinuria selective or nonselective in minimal change disease?

A

selective: loss of albumin, not immunoglobulin; this is caused by GBM polyanion loss

195
Q

Is there a treatment for minimal change disease? Why is this effective?

A

prednisone, daily for four weeks, alternating for four more weeks, then tapering off over the course of 4-6 months
The damage of the disease is mediated by cytokines from T cells.

196
Q

What percentage of minimal change disease cases are resistant to corticosteroids, and what cytogenetic result should you expect?

A

10%

NPHS2 gene mutation

197
Q

What is the only kidney disease demonstrating selective proteinuria?

A

nephrotic syndrome, minimum change disease (MCD)

also called nil disease

198
Q

If a child with nephrotic syndrome has renal failure, what happened?

A

they were overdiuresed

199
Q

What is the epidemiology of minimal change disease (nil disease)?

A

70-90% of cases in children (peak age: 1-6)
10-15% of cases in adults
idiopathic
secondary to viral infection, pharmaceutical agents, malignancy, allergy

200
Q

What is the mortality rate for minimal change disease?

A

7-12%

201
Q

What is the most common cause of nephrotic syndrome in adults, especially Hispanic and Black patients?

A

focal segmental glomerulosclerosis

202
Q

If not idiopathic, what may cause FSGS?

A

PRIMARY genetic defect of slit pore proteins (alpha3beta1 mutation, WT-1 mutation), circulating factors

SECONDARY unilateral agenesis, heroin use, HIV/AIDS, reflex nephropathy, obesity, decreased nephron number (such as in chronic kidney disease), interferon treatment, sickle cell disease, Alport Syndrome

203
Q

What is the pathogenesis of FSGS?

A

increased TGF-beta, PDGF-beta
increased permeability factor
T cell disorder –> T cell cytokines

–> podocytes affected –> podocyte injury and death with scarring –> usually presenting with HTN and decreased GFR

outcome is generally poor (40-60% will have kidney loss)

204
Q

In addition to the characteristic symptoms of nephrotic syndromes, what additional symptoms are seen in FSGS?

A

HTN

hematuria

205
Q

What is seen upon light microscopy in FSGS?

A

segmental sclerosis

hyalinosis

206
Q

What is seen upon electron microscopy in FSGS?

A

effacement of foot processes

207
Q

In focal segmental glomerular sclerosis, is the damage to podocytes reversible or irreversible?

A

irreversible

208
Q

What is seen upon immunofluorescence in FSGS?

A

negative IF; no deposition of immune complexes

209
Q

What are the variants of FSGS?

A

HYPERCELLULAR
PERIHILAR involvement of vascular pole; more common in adults; presents with on-nephrotic range proteinuria
COLLAPSING higher incidence in HIV and Black population; heavy proteinuria, less frequently have HTN; progressing to ESKD rapidly (2-4 months
TIP LESION urinary pole; older white males; rapid onset of edema

210
Q

What are the possible treatments for FSGS?

A

prednisone (minimal response); if unresponsive, use cycloserine
plasmapheresis to remove permeability factor
ACE inhibitors > ARBs

NOTE response to corticosteroids is usually minimal; FSGS progresses to ESKD; there is a high risk of recurrence in transplant (20% in adult, 40% in children)

211
Q

Which factors indicate a poor prognosis in FSGS?

A 
nephrotic range proteinuria
remission of nephrotic syndrome --> ESKD
tubular atrophy, interstitial fibrosis
high level of serum creatinine
alpha3beta1 mutation
perihilar variant?
mesangial hypercellularity?
212
Q

What is the most common cause of nephrotic syndrome in Caucasian adults, specifically?

A

membranous nephropathy

213
Q

What is the second most common cause of primary nephrotic syndrome in all adults?

A

membranous nephropathy

214
Q

What are the common causes of membranous nephropathy?

A 
idiopathy
Hepatitis B or C
solid tumors
SLE
drugs (NSAIDs, penicillamine)
215
Q

What the presentation of membranous nephropathy?

A

older adults
may have entire nephrotic syndrome or only non-selective proteinuria (the latter carrying a better prognosis)
HTN
risk of renal failure

216
Q

What is the pathophysiology of membranous nephropathy?

A

deposition of IgG –> complex formation at PLA2 receptor (phospholipase A2) on podocyte –> membrane thickening

217
Q

What immunoglobulin is involved in membranous nephropathy?

A

IgG

218
Q

What is seen upon LM in membranous nephropathy?

A

diffuse capillary and GBM thickening

trichrome: subepithelial deposition is red

219
Q

What is seen upon EM in membranous nephropathy?

A

subepithelial deposits with “spike and dome” appearance

effacement of foot processes

220
Q

What is seen upon IF in membranous nephropathy?

A

granular deposition of IgG and C3

221
Q

How do you treat membranous nephropathy?

A

low risk: diuretics and ACE inhibitors to bring down proteinuria
high risk: immunosuppressives and steroids (aggressive therapy); cyclophosphide + prednisone, not prednisone alone
second line: cyclosporine
NOTE little response to steroids

Make sure to test for Hepatitis B

RESEARCH rituximab as a treatment. This has not reached clinical application yet.

222
Q

What is the presentation of amyloidosis due to Familial Mediterranean Fever?

A

large kidneys
low BP
possible impairment of renal function

223
Q

What is seen upon LM in amyloidosis?

A

Congo red stain shows apple-green birefringence under polarized light
amyloid deposition in mesangium

224
Q

What is the most commonly involved kidney in systemic amyloidosis?

A

kidney

225
Q

With what is amyloidosis associated?

A

chronic conditions: multiple myeloma, TB, RA

226
Q

What are the other terms for membranoproliferative glomerulonephritis (MPGN)?

A

mesangiocapillary glomerulonephritis

MCGN

227
Q

What is MPGN, Type II also called?

A

dense deposit disease

228
Q

What is the presentation of MPGN?

A

nephrotic AND/OR nephritic syndrome: RBCs, WBCs, casts, broad spectrum proteinuria, increased BUN and serum creatinine
HTN

Type I: associated with Hep B and C; no inflammation
Type II: overactivation of complement, lipid abnormalities –> inflammation, low levels of circulating C3

229
Q

What is seen upon LM in MPGN?

A 
lobular glomerulonephritis
proliferative changes (hypercellularity) in mesangium causing closure of the capillary loops

May be able to see:
TYPE I “tram tracks,” no evidence of inflammation
TYPE II “dense deposits,” some evidence of inflammation

DIFFERENTIAL FOR LM lupus nephritis, HIVAN

230
Q

What is seen upon EM in MPGN?

A

effacement of the podocytes
TYPE I “tram tracks,” splitting of the GBM, mesangial and subendothelial interposition of IgG AND C3
TYPE II “dense deposits,” intramembranous C3 deposition (NO IgG)

231
Q

In MPGN, what happens to the podocytes?

A

they are a direct or indirect target of antibodies

232
Q

What is seen upon IF in MPGN?

A

TYPE I granular deposits of IgG, IgM, C3, C4,
properdin and fibrin in mesangium and
peripheral capillary loops
TYPE II granular deposition of C3 alone

DIFFERENTIAL PSGN

233
Q

Which type of MPGN is associated with Hep B and C?

A

Type I

234
Q

Which type of MPGN is associated with C3 nephritic factor?

A

Type II

235
Q

How should you decrease protein losses in MPGN?

A

ACE inhibitors > ARBs

NSAIDS

236
Q

What drugs do not work in adults with MPGN?

A

steroids, immunosuppressive drugs

Patients normally progress to ESKD.

237
Q

If the patient undergoes a transplant, will MPGN be cured?

A

No; MPGN recurs

238
Q

What is the leading cause of ESKD in the US?

A

diabetic nephropathy

239
Q

What are the associations of diabetic nephropathy?

A 
DM > 8 years
bland urinalysis
HTN
retinopathy, 85%
kidneys normal or larger
nodular sclerosis or diffuse thickening
ESKD in three years after onset of nephrotic syndrome
240
Q

What is the pathogenesis of diabetic nephropathy?

A

hyperglycemia –> nonenzymatic glycosylation of structural and circulating proteins –> advanced, IRREVERSIBLE glycosylation products –> accumulation –>

  1. nonenzymatic glycosylation of vascular basement membrane –> hyaline arteriolosclerosis –> expansion of mesangial matrix and GBM thickening
  2. glomerular efferent arteriole more affected than afferent arteriole –> high glomerular filtration pressure –> macrophage receptors engaged by glycosylated proteins –> secretion of PDGF, TNF, IL –> increased permeability –> hyperfiltration injury –> increased transglomerular passage of glycosylated albumin –> microalbuminuria –> proteinuria
241
Q

What is the presentation of diabetic nephropathy?

A 
retinopathy
peripheral neuropathy
polyuria
microalbuminemia at Stage III
albuminemia >200 mg/min at Stage IV
242
Q

What is seen upon LM in diabetic nephropathy?

A
  • mesangial expansion
  • GBM thickening
  • lipid droplets
  • diffuse glomerulosclerosis
  • Kimmelstiel-Wilson lesions (eosinophilic nodular glomerulosclerosis, aka nodular sclerosis)
  • capsular drop lesions (homogenous, waxy, eosinophilic material in Bowman’s capsule)
  • exudative / fibrin cap lesions (eosinophilic waxy structures located on the inner surface of the capillary wall or within the lumens of the capillary loops)
243
Q

What is the treatment for diabetic nephropathy?

A

control BP and glucose
ACE inhibitor or ARB
Maintain urine / creatine <2 or at least half of value upon presentation

244
Q

How, specifically, do ACE inhibitors affect diabetic nephropathy?

A

slow progression of hyperfiltration-induced damage

245
Q

Which nephrotic syndromes have the best prognoses?

A

minimal change and membranous glomerulonephritis&raquo_space;» FSGS and MPGN

246
Q

What are the symptoms of nephritic syndrome?

A
  • hematuria (>5 RBCs per high power field; RBC casts and dysmorphic RBCs)
  • limited proteinuria (<3.5; note that the protein is not GREATLY elevated and is nonselective)
  • oliguria and azotemia
  • impairment of renal function (abrupt increase of creatine, decreased GFR) –> retention of sodium and water –> HTN, edema
  • hypercellular, inflamed glomeruli
  • immune-complex deposition –> complement activation –> C5a attraction of neutrophils –> damage
247
Q

What are the causes of renal function impairment in nephritic syndrome?

A

compression of tufts by proliferative cells or crescents
glomerular thrombosis
tubular necrosis or obstruction by casts

248
Q

What are the possible causes of acute glomerulonephritis?

A

immune complex mediated glomerulonephritis
ANCA-mediated glomerulonephritis
associated with systemic disease

249
Q

What are the three types of immune complex disease?

A

(1) SUBEPITHELIAL DEPOSITS membranous nephropathy, PSGN
(2) SUBENDOTHELIAL DEPOSITS type I MPGN, class IV SLE
(3) MESANGIAL DEPOSITS IgA nephropathy, Henoch Schonlein Purpura, class II or III lupus nephritis

250
Q

If a patient has acute glomerulonephritis with low complement, what are the possible causes?

A 
SLE
subacute and acute bacterial endocarditis
visceral abscess
shunt nephritis
cryoglobulinema
post infectious glomerulonephritis
MPGN types I and II
251
Q

If a patient has acute glomerulonephritis with normal complement, what are the possible causes?

A

IgA nephropathy
antiglomerular basement membrane: Goodpasture’s
antineutrophilic cytoplasmic antibody/ANCA: Wegener’s

252
Q

What are the agents involved in post-infectious acute glomerulonephritis?

A 
viruses
Mycoplasma
gram positive and negative bacteria
spirochetes
fungi
protozoa and helminths

MOST COMMON Strep (PSGN)

253
Q

What are the factors of post-Streptococcus glomerulonephritis (PSGN), which is a type of proliferative glomerulonephritis?

A

SYMPTOMS edema, HTN, oliguria, occasionally with seizures, SEVEN TO FOURTEEN DAYS after Strep infections
LABS urine shows RBCs, WBCs, casts; urine is the color of “weak tea”

254
Q

What is the epidemiology of sporadic cases of PSGN?

A

TEMPERATE follow URI, pharyngitis, and tonsillitis; more frequent in the winter and spring (patient stay inside; infection spread more readily)
TROPICAL follow skin infection; more frequent in summer and fall

255
Q

What is the most common age range of PSGN?

A

2-12, average age of 7

256
Q

What is the concern for patients under 2 with PSGN?

A

the child’s immune system is may be too underdeveloped to fight the disease

257
Q

What is the presentation of PSGN?

A

nephritis arising after Group A beta-hemolytic
Streptococcus or other infection

decreased distal delivery and increased proximal absorption –> sodium and H2O retention –> edema
EXTRAVASCULAR EDEMA 1. Soft tissue (89%): pedal, palpebral, anasarca 2. GI: abdominal pain, nausea, vomiting 3. CNS: headache, somnolence, seizure, coma 4. Kidney: dull lumbar discomfort
INTRAVASCULAR EDEMA 1. HTN in 60-82% of cases 2. Cardiovascular congestion

Hematuria (dark colored, smoky urine) with dysmorphic RBCs and red cell casts
Oliguria
Proteinuria in 80% of cases, nephrotic syndrome occurs in 20% of patients during recovery

Elevation of BUN and serum creatinine; 1% of patients will have RPGN

ASO > 200 U in 1-3 weeks, peaking at 3-5 weeks after infection in 60-85% of cases; early antibiotic treatment decreases this amount.

As ASO titer elevation is not commonly seen in skin infection PSGN, use streptozyme test.

258
Q

Where are epidemic outbreaks of PSGN seen?

A

areas with poor hygiene conditions and densely populated dwellings
areas with high incidence of malnutrition, anemia, and intestinal parasites

259
Q

What is the virulence factor of Streptococcus that leads to PSGN?

A

M protein

260
Q

What is the pathogenesis of PSGN?

A

immune complex disease of three possible antigens

  1. M protein, bacterial cell walls cross reacting with human system
  2. Endostreptosin, intracellular
  3. Cationic proteins, secreted by the bacteria
261
Q

What is seen upon LM in PSGN?

A

glomeruli enlarged and hypercellular
neutrophils (“global proliferative change”)
“lumpy-bumpy” appearance

262
Q

What is seen upon EM in PSGN?

A

subepithelial immune complex (IC) humps

263
Q

What is seen upon IF in PSGN?

A

granular appearance due to IgG, IgM, and C3 deposition along GBM and mesangium

DIFFERENTIAL type I MPGN

264
Q

What is the treatment for PSGN?

A

supportive (low salt; diuretics, antihypertensives to decrease BP)
1% of children progress to renal failure
25% of adults develop RPGN

265
Q

What systemic disease can cause proliferative glomerulonephritis like that seen in PSGN?

A

SLE

266
Q

What is a streptozyme test?

A

ASO, streptokinase, hyaluronidase, DNase, DNase B

Positive in 89.1% of cases of skin PSGN.

267
Q

If complement is depressed after 6-8 weeks PSGN, what should you consider?

A

possible SLE or MPGN instead of PSGN

268
Q

When do complement levels return to normal in PSGN?

A

2 months later in 94% of cases

269
Q

The pathologist sees a “subepithelial hump.” What’s the likely diagnosis?

A

PSGN

270
Q

What are the causes of RPGN?

A

Goodpasture’s
Wegener’s granulomatosis
microscopic polyangiitis

271
Q

What are the indications for biopsy in PSGN?

A

prolonged oliguria
anuria
persistent hypocomplementemia
nephrotic syndrome

This is ordered to rule out crescentic glomerulonephritis and MPGN. Also note that the biopsy is fairly expensive.

272
Q

What are the causes of rapidly progressive glomerulonephritis (RPGN)?

A

Goodpasture’s
Wegener’s
microscopic polyangiitis

273
Q

What are the lab findings in RPGN?

A

daily increases in the serum creatinine levels greater than 0.5 and increases in BUN greater than 10 mg/dL

274
Q

What differentiates RPGN from other glomerulonephritis types?

A

less HTN and fluid retention
active urinary sediment
low level proteinuria

275
Q

What is seen upon LM in RPGN?

A

crescents of fibrin and plasma proteins
glomerular parietal cells, monocytes, macrophages

glomeruli free from proliferation

276
Q

What do fibrotic crescents in RPGN indicate?

A

no potential for recovery

277
Q

What is the appearance of Type I RPGN upon IF, and what is the likely cause?

A

APPEARANCE linear, “smooth”

CAUSE Goodpasture syndrome (anti-GBM)

278
Q

What is the appearance of Type II RPGN upon IF, and what is the likely cause?

A

APPEARANCE granular, “lumpy-bumpy”

CAUSE PSGN or diffuse proliferative glomerulonephritis (IC depoisition)

279
Q

What is the appearance of Type III RPGN upon IF, and what is the likely cause?

A

APPEARANCE negative, “pauci-immune”

CAUSE Wegener’s, microscopic polyangiitis, Churg-Strauss (c-ANCA and p-ANCA)

280
Q

RPGN + hematuria/hemoptysis.

Diagnosis?

A

Goodpasture’s syndrome (anti-GBM)

281
Q

RPGN + c-ANCA.

Diagnosis?

A

Wegener’s (granulomatosis with polyangiitis)

282
Q

RPGN + p-ANCA.

Diagnosis?

A

microscopic polyangiitis or possibly Churg-Strauss

TO DIFFERENTIATE Churg-Strauss has granulomatous inflammation, IgE, eosinophilia, and asthma

283
Q

What is the prognosis for RPGN, pauci-immune?

A

untreated, poor

cyclophosphamide treatment is correlated with only 15% renal loss

284
Q

What is the most common cause of death in SLE?

A

diffuse proliferative glomerulonephritis

285
Q

What are the causes of diffuse proliferative glomerulonephritis?

A

SLE

MPGN

286
Q

What is seen upon LM in diffuse proliferative glomerulonephritis?

A

“wire looping” of capillaries

287
Q

What is seen upon EM in diffuse proliferative glomerulonephritis?

A

subendothelial > intramembranous IgG based immune complexes

C3 deposition

288
Q

What is seen upon IF in diffuse proliferative glomerulonephritis?

A

granular appearance (Type II RPGN)

289
Q

What is the most common nephropathy worldwide?

A

Berger Disease (IgA nephropathy)

290
Q

What is the presentation of Berger Disease (IgA nephropathy)?

A
  • childhood
  • episodic gross or microscopic hematuria with RBC casts
  • usually follows mucosal infections (gastroenteritis, URI), as IgA production is increased during infection
  • IgA deposition in mesangium of glomeruli
291
Q

To what is Berger Disease (IgA nephropathy) related?

A

Henoch-Schonlein Purpura

292
Q

What is seen upon LM in Berger Disease (IgA nephropathy)?

A

mesangial proliferation (>4 cells), segmental proliferation

293
Q

What is seen upon EM in Berger Disease (IgA nephropathy)?

A

mesangial IC deposits

subepithelial deposition denotes advanced case

294
Q

What is seen upon IF in Berger Disease (IgA nephropathy)?

A

IgA-based IC deposits in mesangium

subepithelial deposition denotes advanced case

295
Q

What is the prognosis of Berger Disease (IgA nephropathy)?

A

70% will die due to HTN and complications thereof (PRESCRIBE ANTIHYPERTENSIVES)
30% will progress to ESKD, requiring dialysis, transplantation, or causing death in 1-40 years

Transplant normally leads to recurrence (6 months to 4 years).

296
Q

How do you differentiate Berger Disease (IgA nephropathy) from PSGN?

A

BERGER’S:
absence of latent period
normal complement
normal ASO

297
Q

Berger’s with IgG.

Diagnosis?

A

lupus nephritis

298
Q

What cytogenetic findings are associated with Berger’s Disease (IgA nephropathy)?

A

HLA-DR4

HLA-DR35

299
Q

What is Alport Syndrome?

A

X-linked defect in Type IV collagen –> thinning and splitting of GBM

300
Q

What is the presentation of Alport Syndrome?

A

isolated hematuria due to glomerulonephritis
sensory hearing loss
ocular disturbances (less often)

301
Q

What is the major complication of Alport Syndrome?

A

FSGS

From Flashcardlet (18 decks)

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