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VF1 - Block 3 > Week 8 > Flashcards

Week 8 Flashcards

1
Q

Proximal tubule function

A
  • 2/3 of water and sodium get reabsorbed here
  • Permeable to sodium and water
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2
Q

Descending limb of the loop of henle does what with sodium and what with water?

A
  • No sodium reabsorption
  • Water is passively reabsorbed
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3
Q

Thick ascending limb of the loop of henle does what with sodium and what with water?

A
  • Permeable to sodium. It is pumped out of ascending limb (reabsorbed).
  • Impermeable to water.
  • Urine is diluted here. Sodium leaves and water stays in.
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4
Q

Site of most dilute urine

A
  • Distal convoluted tubule
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5
Q

Collecting duct does what with water and what with sodium?

A
  • Water is reabsorbed depending on ADH levels
  • Sodium is reabsorbed depending on aldosterone
    • Aldosterone opens sodium channels in collecting duct for reabsorption
    • Potassium is exchanged for sodium
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6
Q

What molecule is the most important regulator of water balance?

A

ADH

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7
Q

Maximal urine concentration

A
  • 1200 mOsm/kg water
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8
Q

Maximal urine concentration occurs under high/low ADH levels?

A

High

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9
Q

Minimal urine concentration

A

50 mOsm/kg water

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10
Q

Sodium regulation is governed primarily by _______ signaling

A

Volume

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11
Q

Water regulation is governed primarily by ______ signaling

A

Osmolality

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12
Q

Response of Kidneys to volume overload

A
  • Atrial Natiuretic Peptide is released from cardiac atria
  • Results in afferent arteriole dilation and efferent constriction
    • Increased GFR
  • Decreased sodium and water reabsorption in collecting duct
    • Increased excretion
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13
Q

Atrial Natiuretic Peptide

A
  • Released from cardiac atria in response to increased mechanical stretch from volume overload
  • Causes afferent arterioles to dilate, efferent arterioles to dilate
    • Increased GFR
  • Causes decreased sodium and water reabsorption in the collecting duct
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14
Q

B-Type Natiuretic Peptide

A
  • Volume sensor in clinical setting
  • Released from cardiac ventricles in response to increased mechanical stretch (volume overload)
  • Elevated levels tell us the patient is volume overloaded
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15
Q

Volume sensors for kidney regulation

A
  • Cardiac atria cells
  • Sympathetic Nervous system baroreceptors
    • low-pressure receptors: pulmonary vessels, cardiac atria
    • high-pressure receptors: carotid sinus, aortic arch
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16
Q

low-pressure sympathetic baroreceptors are located where?

A
  • pulmonary vessels
  • cardiac atria
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17
Q

high-pressure sympathetic baroreceptors are located where?

A
  • carotid sinus
  • aortic arch
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18
Q

Sympathetic response to low volume state

A
  • Afferent > efferent constriction –> decreased GFR
  • Renin released from juxtaglomerular cells –> increased sodium and water reabsorption
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19
Q

juxtaglomerular cells

A
  • Located in afferent arterioles
  • Release renin in response to low-volume or low-sodium states
  • Activation of RAAS –> sodium and water retention
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20
Q

Macula Densa cells

A
  • Located in distal tubule
  • Monitor the urine
  • Signal JG cells to release renin when sodium concentration in urine is too low
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21
Q

Renin

A
  • Produced by juxtaglomerular cells in afferent arteriole
  • Kicks off RAAS to increase volume

•Stimuli for release:

  • Low perfusion pressure (afferent arteriole)
  • Sympathetic nerve activity
  • Macula densa (low tubular NaCl delivery)
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22
Q

Angiotensin II

A
  • Activated by renin release
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23
Q

Angiotensin II effects

A

Systemic effects:

  • Systemic vasoconstriction
  • Stimulates aldosterone release from adrenal
  • Stimulates ADH release

Renal effects:

  • Increased NaCl reabsorption
  • Preferential constriction of efferent over afferent arteriole –> increase (maintain) GFR
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24
Q

If angiotensin II is released in response to a low sodium/low volume state (due to renin), why would the renal effect be to constrict efferent more than afferent arteriole?

A
  • In a low flow state, you constrict efferent arteriole more than afferent, which seems counterintuitive if you’re trying to hold onto water. But the issue is that you still need to be getting rid of waste products, so your body wants to maintain some degree of GFR and this is how it does so. This happens under the early low-flow state. Under a later low-flow state, the afferent arteriole also gets clamped down quite a bit, which does then reduce GFR.
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25
Q

Aldosterone regulators

A
  • Angiotensin II
  • Potassium levels
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26
Q

Aldosterone effects

A
  • Opens sodium channels (ENaC) in collecting duct to stimulate sodium reabsorption
  • To balance charge of sodium coming in, potassium and hydrogen are excreted
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27
Q

ADH release is stimulated by

A
  • Hypothalamic osmolality receptors
    • these are sensitive and maintain the set point)
  • Aortic arch baroreceptors
    • these are insensitive and can override the osmolality receptors if necessary)
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28
Q

ADH actions

A
  1. Increase permeability to water in collecting duct –> water reabsorption
  2. “Vasopressin” = Acts on vascular smooth muscle cells to vasoconstrict –> increased BP
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29
Q

The most important measure of ADH effect is ____

A

urine osmolality

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30
Q

Effective circulating volume

A
  • The idea that you may have plenty of total body volume, but if your organs are sensing inadequate perfusion and/or your volume/pressure receptors are sensing low blood flow, then your “effective circulating volume” (what is sensed by receptors) is low
  • This is why you get edema with low cardiac output/heart failure
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31
Q

Oliguria definition

A
  • the minimal required urine output to excrete the daily obligate solute load (eg. Na ingestion, protein metabolism)
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32
Q

What is the average obligate waste solute load?

A

600 mOsm/day

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33
Q

If the kidney’s maximal urine concentration is 1200 mOsm/kg water and the obligate solute excretion is 600 mOsm/day, what is the minimum amount of water that needs to be peed in a day?

A
  • Excretion = urine volume x [waste]
  • 600 mOsm/day = urine volume x 1200 mOsm/kg water
  • urine volume = 0.5 kg water/day
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34
Q

Role of thirst in maintaining water balance

A
  • Thirst sensation is regulated by the hypothalamus
    • Stimulated by osmolality, hemodynamic sensors, and angiotensin II
  • When you drink, there are receptors in the oropharynx and upper GI tract to sense water. So you get relief before the correction of osmolality.
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35
Q

Summary of responses to low effective circulating volume

A
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36
Q

Summary of volume vs. osmoregulation

A
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37
Q

Summary of responses to volume expansion

A
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38
Q

Two pressures that determine glomerular filtration

A
  • Hydraulic (hydrostatic) pressure
  • Oncotic pressure
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39
Q

Net filtration occurs when hydrostatic pressure > oncotic pressure

A
  • hydrostatic pressure = pushing pressure out of glomerular capillaries
  • oncotic pressure = pulling pressure back into capillary due to albumin
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40
Q

How is renal blood flow controlled?

A
  1. Myogenic Regulation
  2. Tubuloglomerular Feedback
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41
Q

Myogenic Regulation

A
  • Incresed renal blood flow –> reflex response to resist the increase
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42
Q

Tubuloglomerular Feedback Mechanism

A
  • Controls renal blood flow
  • Macula densa senses urine flow in distal tubule
  • Macula densa sends signals to JG cells in afferent arteriole to contract and/or secrete renin
  • Mesangial cells are actual contractile cells
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43
Q

Main effectors of (renal) arterial tone

A
  • alpha-1 receptors on afferent arterioles
    • Activation –> decreased GFR
  • Antiotensin II impacts efferent arterioles
    • Always reduces renal blood flow
    • Low levels increases GFR
    • High levels decreases GFR
  • Natiuretic peptides
    • Dilates afferent and constricts efferent –> increased GFR
  • Prostaglandins
    • Vasodilators that counteract alpha-1 and angiotensin II effects
  • Dopamine
    • Vasodilator
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44
Q

How do we measure GFR across the entire kidney?

A
  • Inulin = exogenous measure of GFR
    • This is filtered in glomerulus and none is reabsorbed
  • Creatinine = endogenous measure of GFR = compromise when you do not want to inject inulin
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45
Q

How do we measure renal blood flow?

A
  • GFR is about 20% of renal blood flow
  • We use PAH, which is completely cleared with 1 pass through the kidney
    • All of it is either filtered or secreted, none goes back to systemic blood flow
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46
Q

Autoregulation of GFR

A
  • Process whereby kidney keeps GFR relatively constant across a wide range of renal perfusion pressures
    • Myogenic regulation
    • Tubuloglomerular feedback
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47
Q

Proximal Tubule Cells

A
  • Have a brush border (whereas distal tubule does not)
  • Lots of mitochondria to power the pumping of sodium
  • Sodium is kept low inside the epithelial cell via the ATPase pump
  • This provides driving force for the cotransport of sodium and other molecules (like glucose) across the cell
  • Substances that cross proximal tubule epithelial cells go into peritubular capillaries to get reabsorbed into systemic circulation
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48
Q

Main substances that are reabsorbed in proximal tubule

A
  • glucose
  • bicarb
  • urea
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49
Q

Tmax

A
  • Transporters in renal tubules can be saturated
  • Ex: glucose
  • Tmax is the maximum amount of glucose that can be reabsorbed.
  • Tmax is considered a measurement of the rate of reabsorption.
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50
Q

How is bicarb reabsorbed?

A
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51
Q

Inhibition of carbonic anhydrase has what effect on bicarb excretion?

A

More bicarb is excreted

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52
Q

Aspirin inhibits secretion of what?

A
  • Uric Acid
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53
Q

Fanconi Syndrome

A
  • Condition that causes reduced function of proximal tubule
  • Bicarb in the urine
  • Phosphate in the urine
  • Glucose in the urine
  • Amino acids in the urine
  • Uric acid in the urine
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54
Q

Counter current gradient

A
  • A gradient of osmolarity in the renal medulla that drives movement of water from the collecting duct
  • Loop of Henle generates counter current gradient
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55
Q

Thick ascending limb of the loop of Henle

A
  • Pumps sodium out of the Loop of Henle and into the interstitium
  • Impermeable to water
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56
Q

Thiazide diuretics act on what part of the nephron

A
  • distal tubule
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57
Q

Sodium and calcium reabsorption happens in what part of the nephron?

A

distal tubule

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58
Q

What part of the nephron does aldosterone act on?

A

collecting duct

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59
Q

Cell types in collecting duct

A
  • Principal cells
    • Sodium reabsorption/potassium excretion driven by aldosterone
  • Intercalated cells
    • Responsible for secretion of H+ ions
    • Acid-base function of the kidney
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60
Q

Acid-base function of the kidney is driven primarily by what part of the nephron?

A

Intercalated cells in the collecting duct

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61
Q

What determines GFR?

A
  • Number of nephrons
  • How well the nephrons are working
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62
Q

Normal GFR

A

100 mL/min/1.73 m2

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63
Q

Temporary changes in GFR result from…

A
  • REALLY low blood pressure
    • decreased GFR
  • Pregnancy
    • Increased GFR
  • Medications
    • NSAIDS
    • ACE inhibitors
    • Calcineurin inhibitors
    • IV contrast
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64
Q

Methods to estimate GFR

A
  • Urine collection
    • Urea - slight understimate of GFR b/c a little gets reabsorbed
    • Creatinine - slight overestimate of GFR b/c a little gets secreted
    • Average urea and creatinine to get close estimate of GFR
  • Blood Tests
    • Serum creatinine
      • Less serum creatinine means higher GFR
      • Problem: hard to estimate b/c When creatinine in blood increases by two-fold, your GFR has gone down by half.
      • Problem: Serum creatinine levels vary w/ age, gender, and esp. muscle mass
    • Serum cystatin C
      • ​Freely filtered and then metabolized by the kidney
      • Pros: not affected by age, muscle mass, etc
      • Cons: Like serum creatinine, there’s not a linear relationship b/w GFR and serum cystatin C
    • Blood Urea Nitrogen
      • Not that useful b/c many things alter this aside from GFR
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65
Q

Use of measuring Urea in the urine

A
  • Estimate of GFR
  • A little gets reabsorbed so this is a slight underestimate of GFR
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66
Q

Use of measuring creatinine in the urine

A
  • Estimate of GFR
  • A slight underestimate b/c some creatinine gets secreted
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67
Q

Clearance Formula

A

(UxV)/P

U = urine concentration of the molecule

V = urine Volume

P = plasma concentration of the molecule

**Include the unit time - usually expressed as mL/minute and the collection is done for 24 hours

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68
Q

Serum creatinine

A
  • Used to measure GFR
  • Low serum creatinine = high GFR b/c a lot of it is ending up in the urine
  • Problems: 1. Not a linear relationship b/w serum creatinine and GFR. 2. Serum creatinine levels vary with age, gender, and especially muscle mass
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69
Q

Relationship b/w serum creatinine and GFR

A

For a two-fold increase in serum creatinine level, the GFR has gone down by half

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70
Q

Serum cystatin C

A
  • Blood draw to measure GFR
  • This molecule is freely filtered and is then metabolized by the kidney
  • Pros: Not affected by age, muscle mass, etc the way serum creatinine is
  • Cons: Like serum creatinine, there’s not a linear relationship b/w GFR and serum cystatin C
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71
Q

Cockroft-Gault Formula

A
  • Equation attempts ot estimate GFR based on creatinine clearance
  • But b/c using creatinine clearance, it’s a slight underestimate of GFR
  • Not used much anymore but some older drug dosing recs are based on this formula
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72
Q

MDRD Formula

A
  • Used to estimate GFR
  • Limitations: based on a study done on people who already had kidney disease. Study participants were predominantly white, middle-aged, and male w/ almost no diabetes.
  • Very good estimate of GFR when GFR is low (i.e. low kidney function)
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73
Q

When is MDRD formula erroneous?

A
  • When creatinine levels in blood are not constant - i.e. during acute renal failure
  • All the scenarios that don’t match initial study participants
    • Pediatric or geriatric populations
    • Advanced liver disease
    • Good kidney function
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74
Q

CKD-Epi Formula

A
  • Used to estimate GFR
  • Bigger and more representative study sample than MDRD
  • Much better estimate of GFR than the MDRD for people with good kidney function
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75
Q

Bedside Schwartz

A
  • Most common pediatric formula to estimate GFR
  • Often the pediatric formulas rely on cystatin C, which does not depend on muscle mass the way creatinine does
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76
Q

Nephrin

A
  • Important protein found in the slit diaphragms of the glomerular capillary
  • Dysfunction –> problems with filtration –> proteinuria
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77
Q

Normal serum albumin concentration

A

3.5 - 4.9 gm/dL

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78
Q

Normal serum protein concentration

A

6 - 8.3 gm/dL

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79
Q

Normal urine protein levels

A

150 mg/day

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80
Q

Normal albumin levels in urine

A

30 mg/day

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81
Q

Types of protein in normal healthy subjects found in the urine

A
  • B2 microglobulin - filtered but not reabsorbed
  • Uromodulin – secreted by epithelial cells in the Loop of Henle
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82
Q

Abnormal Glomerular Filtration sees what change with the podocytes

A

foot process effacement

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83
Q

Loss of charge barrier of the glomerular filter is called

A

selective proteinuria

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84
Q

Key findings with selective proteinuria

A
  • Elevated levels of albumin in the urine
  • do NOT see IgG or other large molecules in the urine (size barrier of glomerular filter is still intact)
  • Foot process effacement
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85
Q

Minimal Change Disease is associated with…

A

Hodgkins lymphoma

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86
Q

Loss of size and charge barrier of glomerular filter is called…

A

non-selective proteinuria

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87
Q

Key findings of non-selective proteinuria

A
  • See elevated levels of albumin AND other large molecules in the urine, like IgG
  • Foot process effacement
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88
Q

Key findings of proximal tubular dysfunction proteinuria

A
  • Usually less than 3g/24 hours of protein in the urine
  • Proteins in urine that are filtered at the glomerulus but not properly reabsorbed
  • Fanconi syndrome can also see bicarb, glucose, amino acids in the urine
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89
Q

Overload proteinuria pathophysiology

A
  • Overproduction of light chains –> there is too much light chain to be reabsorbed by proximal tubule –> light chain in the urine
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90
Q

Overload proteinuria is associated with….

A

multiple myeloma

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91
Q

Key findings of overload proteinuria

A
  • Light chains in the urine
  • Usually less than 3 g/24 hours
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92
Q

Benign causes of proteinuria

A
  • Orthostatic proteinuria
  • Functional proteinuria
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93
Q

Orthostatic proteinuria

A
  • Benign cause of proteinuria
  • Commonly seen in healthy teens and young adults
  • Occurs in upright position
  • Usually less than 2g/24 hours
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94
Q

How to test for orthostatic proteinuria

A
  • Compare urine from first a.m. void to later in the day
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95
Q

Functional proteinuria

A
  • Occurs with patients who have healthy kidneys but some other cause
    • High fever
    • Congestive heart failure
    • exposure to cold
  • Resolves itself when the other cause resolves
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96
Q

If you have more than 3.5 g of protein in the urine, the dysfunction must be with ______

A

the glomerulus

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97
Q

gold standard for measuring protein in the urine

A

24 hour collection

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98
Q

urine dipstick only measures…

A

albumin

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99
Q

spot urine protein/creatinine ratio measures

A
  • total protein in the urine (not just albumin the way a dipstick measures)
  • easier to perform than a 24 hour collection
  • Takes the ratio of protein/creatinine to give a unitless number
  • Normal ratio is less than 0.15
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100
Q

normal spot urine protein/creatinine ratio

A

less than 0.15

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101
Q

how do we measure the types of protein found in the urine?

A

–Urine protein electrophoresis (UPEP)

–Urine immunoelectrophoresis (UIEP)

–Urine sediment (lipid droplets)

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102
Q

2 main types of glomerular disease

A
  • Nephrotic Syndrome
  • Nephritic syndrome
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103
Q

Nephrotic syndrome is an inflammatory/noninflammatory process?

A

Non-inflammatory

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104
Q

Key findings of nephrotic syndrome

A
  • Edema
  • Hypoproteinemia/hypoalbuminemia
  • Proteinuria greater than 3.5 g/24 hours
  • Hyperlipidemia
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105
Q

Mechanism of edema in nephrotic/nephritic syndromes

A
  • Low oncotic pressure due to loss of albumin –> movement of fluid into interstitial space (extravascular space)
  • PLUS kidney responds to low intravascular fluid by renin release and holding onto more fluid
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106
Q

Causes of low serum albumin

A
  • Low production
    • Liver failure
    • Malnourished
  • Increased losses
    • Loss in the urine due to glomerular problems
    • Loss in the gut
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107
Q

Mimics nephrotic syndrome due to edema

A
  • Congestive Heart Failure
  • Renal Failure
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108
Q

Complications with nephrotic syndrome

A
  • Hypercoagulability
    • B/c you are losing important anti-coagulants in the urine
  • Bacterial infection
    • In the fluid that you’re holding onto, esp. in the abdomen
  • Accelerated atherogenesis
  • INCREASED MORTALITY
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109
Q

Treatment of Nephrotic Syndrome

A
  • ARBs and ACEs
    • dilate efferent arterioles –> decreased GFR –> decreased proteinuria
  • Control systemic hypertension
  • Treat hyperlipidemia
  • Diuretics and salt restriction
    • to treat edema
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110
Q

Nephritic syndrome is an inflammatory/non-inflammatory process?

A

Inflammatory

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111
Q

Key findings of nephritic syndrome

A
  • Edema
  • Proteinuria, but doesn’t need to be greater than 3.5 g/24 hours
  • Hypertension
  • Hematuria
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112
Q

Pathonemonic for nephritic syndrome

A
  • Specific look to the RBC cast
    • RBC’s get encased in this jello-like structure b/c they get trapped in the tubule by uromodulin
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113
Q

Minimal Change Disease is more commonly seen in childrens/adults?

A

children

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114
Q

Focal segmental glomerulosclerosis (FSGS) histopathology is more commonly seen in children/adults?

A

adults

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115
Q

membranous histopathology is more frequently seen in children/adults?

A

adults

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116
Q

Histopathologic findings in minimal change disease

A
  • Normal glomeruli on H&E stain
  • Immunoflouroscopy looks normal
  • podocyte effacement on EM
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117
Q

Treatment for minimal change disease

A
  • STEROIDS
  • This is basically the only kidney disease that responds well to steroids
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118
Q

When do you perform a steroid trial (instead of a renal biopsy)?

A
  • It’s a KID with symptoms of nephrotic syndrome
    • B/c minimal change disease responds well to steroids and minimal change is most common in kids. You’d rather do a steroid trial than risk complications of a biopsy.
  • Criteria are:
    • No hypertension (nephritic syndrome)
    • No blood in the urine (nephritic syndrome)
    • Normal GFR
    • Normal C3
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119
Q

Criteria for a steroid trial

A
  • No hypertension (nephritic syndrome)
  • No blood in the urine (nephritic syndrome)
  • Normal GFR
  • Normal C3
  • **It’s a kid**
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120
Q

Focal vs. diffuse

A

Diffuse = more than 50% of glomeruli

Focal = less than 50% of glomeruli

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121
Q

segmental vs. generalized (global)

A
  • Segmental = parts of the glomerulus are involved
  • Global = all of the glomerulus is involved
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122
Q

Proliferative definition (pathology)

A
  • Too many nuclei in the glomerulus under light microscopy
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123
Q

Exudative definition (pathology)

A

Too many neutrophils in the glomerulus

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124
Q

Sclerosis vs. fibrosis

A
  • Sclerosis = too much PAS stainable material in the glomerulus
  • Fibrosis = too much stainable material AROUND the glomerulus in the interstitial space
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125
Q

Histopathologic findings of focal segmental glomerulosclerosis

A
  • Light microscopy:
    • Segmental collapse
    • Fewer podocytes than normal
    • TOO MUCH STAINABLE MATERIAL = sclerosis
  • Immunologic stain:
    • Minimal flourescence according to lecture but pathoma says negative IF. It’s not the same type of IF as with membranous or Goodpasture’s, it’s less flourescent.
  • Electron microscopy
    • foot process effacement
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126
Q

Light microscopy findings with focal segmental glomerulosclerosis

A
  • Loss of podocytes shows up as less brown stain on PAS
    • See slide 79 and 80 for comparison of normal vs. abnormal
  • Extra stainable material
  • Segmental collapse = some of the glomerulus is adherent to Bowman’s capsule
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127
Q

Immunologic stain appearance for FSGS

A
  • Flourescence = antibodies in glomerulus
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128
Q

Electron Microscopy appearance for FSGS

A

podocyte effacement

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129
Q

Etiology (cause) of FSGS

A
  • Genetic
    • Mutations in podocin protein in slit diaphragm
    • Tons of other genetic causes
  • circulating factors injure podocytes
  • ANYTHING CAUSING INCREASED GLOMERULAR PRESSURE
    • diabetes
    • hypertension
    • reduced renal mass –> existing podocytes have more work to do.
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130
Q

Critical problem that leads to FSGS

A
  • podocyte injury –> loss of podocytes
    • podocytes cannot regenerate
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131
Q

Treatment of FSGS

A
  • Most importantly: control the things causing increased glomerular pressure
    • Control diabetes
    • ACEs and ARBs dilate efferent arteriole –> reduced glomerular pressure
  • Steroids are not effective
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132
Q

Natural history of FSGS

A

end stage renal failure

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133
Q

Diabetic Glomerulosclerosis histopathology findings

A
  • Marked thickening of extracellular matrix
    • Thick basement membranes
    • Thick mesangial matrix
  • KW nodules is pathonemonic
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134
Q

Appearance of diabetic glomerulosclerosis on light microscopy

A
  • Mesangial matrix is thickened with “diffuse mesangial sclerosis”
  • Nodular glomerulosclerosis shows KW nodules
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135
Q

Electron Miscroscopy appearance of diabetic glomerulosclerosis

A
  • Massive thickening of basement membrane
  • Hard to see but there is podocyte loss (not podocyte effacement) –> you’ll see podocytes in the urine
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136
Q

Key histopathologic findings for membranous glomerulopathy

A
  • Thickened capillary loops on H&E
  • Basement membrane spikes on EM
  • Subepithelial deposits on EM
    • protein deposits b/w podocyte and basement membrane
    • These are antigen-antibody complexes
  • Granular IF
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137
Q

Appearance of basement membrane spikes for membranous glomerulopathy

A
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138
Q

Appearance of subepithelial deposits in membranous glomerulopathy

A
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139
Q

Etiology of membranous glomerulopathy

A
  • Primary cause: autoantibodies against a protein in the podocyte
    • Result is that a membrane attack complex forms, punches holes in the podocyte, then the podocyte responds by trying to wall off the damage –> thickened basement membrane appearance
  • Secondary causes exist - see slide 95
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140
Q

Edema definition

A
  1. Shift of fluids from vascular space
  2. Retention of sodium and water
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141
Q

Nephrotic Syndrome characteristics

A
  • Proteinuria (>3g/d)
  • Hypoalbuminemia
  • Hyperlipidemia
  • Edema
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142
Q

4 Mechanisms of Edema

A
  1. Increased hydrostatic pressure
  • Congestive heart failure
  • Venous thrombosis
  1. Decreased oncotic pressure
  • Nephrotic Syndrome
  • Cirrhosis
  1. Increased capillary permeability
  • angioneurotic edema
  • burns, histamine, respiratory distress
  1. Lymphatic obstruction
    * radiation, cancer, surgery
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143
Q

Common edematous syndromes

A
  • Congestive heart failure
  • Nephrotic Syndrome
  • Cirrhosis
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144
Q

Physical exam findings of volume depletion

A
  • Low BP
  • Orthostatic hypertension
  • tachycardia
  • High BUN/creatinine ratio
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145
Q

Common sources of extrarenal volume loss

A
  • GI tract: vomiting, diarrhea
  • Skin: burns
  • “Third space” = bowel obstruction, peritonitis
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146
Q

common causes of renal volume depletion

A
  • Diuretics
  • Hypoaldosteronism
  • Renal failure
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147
Q

Liddle Syndrome

A
  • Constitutive expression of ENaC in collecting duct
  • Continuous reabsorption of sodium + excretion of potassium and hydrogen
  • Hypokalemia, hypertension, hypoaldosteronism, alkalemia
  • See high sodium levels, but not high sodium concentration
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148
Q

How to calculate plasma osmolality

A
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149
Q

Most of the plasma osmolality is determined by….

A

sodium

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150
Q

osmolar gap

A
  • Measured (actual) osmolality - calculated osmolality
  • Normal osmolar gap = 10 mOsm/kg water
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151
Q

Mechanisms of hypernatremia

A
  1. Water Loss (in excess of sodium loss if losing both)
  • Burns, respiratory loss, fever
  • Diabetes Insipidus
  • Diuresis
  • Diarrhea
  1. Sodium gain (in excess of water gain)
    * Administration of a hypertonic solution - iatrogenic
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152
Q

Why would we administer a hypertonic solution in the hospital setting?

A
  • pull water off the brain in the case of cerebral edema
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153
Q

How do you get excessive water loss?

A
  1. impaired thirst mechanism
  2. no access to water
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154
Q

Diabetes Insipidus

A
  • A defect in the kidney’s ability to hold onto water
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155
Q

2 types of diabetes insipidus

A
  1. Central DI
    * Due to impaired secretion, storage, or transport of ADH
  2. Nephrogenic DI
    * Due to impaired renal response to ADH
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156
Q

How do diagnose DI?

A
  • Water deprivation test
  • Under states of dehydration, a person should be able to concentrate their urine. If the person cannot concentrate their urine, then they have DI.
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157
Q

How do differentiate b/w the 2 types of DI?

A
  • Give exogenous ADH
  • Central DI –> you’ll see a response to ADH (urine will be more concentrated)
  • Nephrogenic DI –> you’ll see little to no response to ADH (urine will not concentrate)
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158
Q

Management of hypernatremia

A
  • Give free water but give it SLOWLY to avoid cerebral edema
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159
Q

what happens if you try to correct hypernatremia too quickly?

A

cerebral edema (and maybe death)

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160
Q

Giving 1 L of 0.9 % normal saline is equivalent to giving how much free water?

A
  • 0 mL b/c 0.9% NS is isotonic with blood plasma
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161
Q

Most common electrolyte disturbance

A

hyponatremia

162
Q

Hyperosmolar Hyponatremia

A
  • Mechanism: Too much glucose (or some other effective osmole) –> pulls water into blood –> too much H2O in the blood
  • Common causes: High plasma glucose (diabetes), mannitol, glycine
163
Q

Is the patient hypoosmolar?

A
  • First question you ask when evaluating cause of hyponatremia
  • Look at serum osmolality. If it’s less than 280 mOsm/kg, they are hypoosmolar.
164
Q

Are the patient’s kidneys resopnding appropriately to clear free water?

A
  • Second question to ask when evaluating hyponatremia causes
  • Look at urine osmolality
  • If hypoosmolar, patient should be trying to get rid of water and the urine should be pretty dilute.
  • An appropriate urine osmolality in the case of hypoosmolar patient is less than 100 mOsm/kg
165
Q

Psychogenic polydipsia

A
  • Hypoosmolar
  • Urine should be dilute (urine osmolality) b/c patient is responding appropriately to having too much water on board
  • Treat with water restriction
166
Q

SIADH

A
  • Symptom of inappropriate ADH
  • This person is hyponatremic b/c of inappropriate ADH release, NOT due to low effective circulating volume.
  • Labs show hypoosmolar (too much water on board), concentrated urine (high urine osmolality), normal/high sodium urine levels
    • Urine SHOULD be dilute if kidneys are responding appropriately - they should be getting rid of lots of water
    • Sodium WOULD be low if patient were holding onto water due to low effective circulating volume
167
Q

Causes of SIADH

A
  • Increased ADH production
    • CNS tumor
    • HIV
    • Nausea/pain
  • Ectopic production (somewhere other than hypothalamus)
    • small cell lung cancer
  • ADH potentiation
    • drugs
    • psychosis
168
Q

Management of SIADH

A
  • Treat underlying cause
  • Free water restriction
  • V2 receptor antagonist
    • V2 is the ADH receptor in the collecting duct that opens aquaporin channel
  • Hypertonic saline
169
Q

Causes of hyponatremia from impaired water excretion

A
  • Could be due to low effective circulating volume OR SIADH
170
Q

congestive heart failure, cirrhosis typical presentation of hyponatremia

A
  • hypoosmolar
  • high urine osmolality (not responding appropriately to hypoosmolality)
  • Low urine sodium (trying to hold onto sodium due to low effective circulating volume)
171
Q

histologic differences b/w nephritic and nephrotic syndromes

A
  • Nephritic = normal cellularity
  • Nephrotic = enlarged glomerulus, hypercellular
172
Q

Nephritic Syndrome findings

A

–edema

–proteinuria

–hematuria

–hypertension

173
Q

Crescent formation

A
  • Can be seen with any of the mechanisms of nephritic syndrome. Indicative of significant glomerular injury.
  • Histologic finding of:
    • Macrophages in bowman’s space
    • fibrin in bowman’s space
174
Q

Rapidly Progressive Glomerular nephritis

A
  • Can be seen with any of the mechanisms of glomerular injury
  • This is a medical emergency, it can result in renal failure
  • Characterized by a rapid rise in serum creatinine and crescent formation
175
Q

Goodpasture disease mechanism

A
  • Mechanism: Auto-antibody mediated nephritic syndrome
  • Antibody, NOT immune complexes, against a protein in basement membrane –> linear IF
  • We don’t know why this happens
176
Q

Goodpasture syndrome histologic findings

A
  • Linear deposition of IgG on immunoflourescent stain (i.e. the whole glomerulus lights up)
  • Electron microscopy does NOT show electron dense deposits in basement membrane (which would be characteristic of immune complex mediated disease)
177
Q

Goodpasture disease clinical findings

A
  • Hemoptysis and hematuria
  • rapidly progressing glomerular nephritis
  • *You see hemoptysis b/c the auto-antibody binds the same protein in the kidney as it does in the lung
178
Q

Tx for Goodpasture’s Disease

A
  • Remove circulating antibodies (phoresis)
  • Immunosuppression to keep B-cells from making more antibodies - Rituximab
  • High dose of corticosteroids to knock down inflammation
179
Q

Post-Streptococcal Glomerulonephritis clinical presentation

A
  • 21 days post infection
  • Can see RPGN
180
Q

Biopsy results of post-strep glomerulonephritis

A
  • Hypercellular, inflamed glomerulus on H&E
  • Immune-complex depositions –> granular IF
  • Subepithelial humps on EM
181
Q

subepithelial humps on EM

A
  • electron microscopy results of post-streptococcal GN
182
Q

Tx of post-streptococcal GN

A
  • Supportive therapy
  • Usually resolves itself
183
Q

IgA nephrophathy clinical presentation

A
  • Often following mucosal infections (upper respiratory infections)
    • B/c that’s when IgA is produced
  • Episodic hematuria
  • May slowly progress to renal failure
184
Q

Biopsy results of IgA nephropathy

A
  • This is the only thing that shows IgA deposits in the kidney
  • IgA and C3 deposits in the mesangium
185
Q

Things that cause depressed C3 levels

A
  • Lupus
  • post-infectious glomerular nephritis
  • cryglobulinemia
  • membranoproliferative glomerulonephritis
186
Q

giant subepithelial humps on EM

A

post-streptococcal GN

187
Q

IgA Nephropathy clinical presentation

A
  • Intermittent gross hematuria
  • often after an upper respiratory infection
  • Edema
  • Slowly progressive rather than rapid
188
Q

IgA nephropathy light microscopy results

A
  • Mesangial hypercellularity
  • May have crescents
189
Q

IgA nephropathy immunoflourescent results

A
  • IgA and C3 deposits in MESANGIUM, not in capillary loops
190
Q

Henoch-Schoenlein Purpura (HSP)

A
  • A variant of IgA nephropathy
191
Q

Clinical presentation of henoch-schoenlein purpura

A
  • systemic vasculitis
  • a rash below the waste
  • abdominal pain (colitis)
  • arthritis
192
Q

Tx for IgA nephropathy (and Henoch-Schoenlein Purpura)

A

No effective tx

193
Q

Pauci-Immune Glomerulonephritis clinical presentation

A
  • Systemic vasculitis
  • ANY TISSUE can be involved. Often these people have had multiple instances of pulmonary infiltrates b/c the lungs have been involved before anyone thinks to check the urine
194
Q

mechanism of pauci-immune glomerulonephritis

A
  • ANCA = anti-neutrophilic cytoplasmic antibody
  • The body’s own B-cells produce an antibody against a protein in the cytoplasm of the neutrophils
195
Q

Light microscopy for pauci-immune glomerulonephritis

A
  • Focal crescents
  • Segmental necrosis
196
Q

Immunoflourescence for pauci-immune glomerulonephritis

A
  • Shows NO IgG or C3. It’s dark.
  • This is why it’s called Pauci-Immune b/c there is no immune depositions
197
Q

electron microscopy for pauci-immune glomerulonephritis

A

No immune complex deposits

198
Q

Tx and prognosis for pauci-immune glomerulonephritis

A
  • Tx: Immunosuppression (Rituximab). Untreated it’s fatal. Treated, 95% remission but with frequent relapses.
199
Q

Alport syndrome causes

A
  • Shows blood and protein in the urine but this is NOT INFLAMMATORY
  • Most commonly X-linked, but can be autosomal recessive, or autosomal dominant
200
Q

clinical presentation of alport syndrome

A
  • Nephritis (microscopic hematuria, proteinuria, renal failure)
  • Sensorineural deafness
  • Ocular abnormalities
201
Q

Biopsy results for Alport Syndrome

A
  • EM shows
    • “basket woven” appearance of basement membrane
    • Some variants show a really thin basement membrane
  • Light and IF are unremarkable
202
Q

Definition of diabetes

A
  • Chronic disorder of carbohydrate metabolism
203
Q

Major characteristics of diabetes

A
  1. Chronic hyperglycemia
  2. Insufficient Insulin
  3. Three P’s: Polyuria, Polydypsia, Polyphagia
  4. Macro- and microvascular complications
204
Q

Hallmarks of diabetic ketoacidosis

A
  1. high blood glucose
  2. metabolic acidosis (with an anion gap)
  3. high serum ketones
205
Q

Pathophysiology of ketoacidosis

A
  • Low cellular glucose –> breakdown of muscle –> free fatty acids in the blood
  • Liver responds to free fatty acids by producing ketone bodies, which are acidic
  • Metabolic acidosis –> compensatory respiratory alkalosis
  • Hyperglycemia –> polyuria –> pulls H2O and sodium out of the blood –> fluid and electrolyte depletion
206
Q

Hyperglycemic hyperosmolar state

A
  • Occurs WITHOUT ketoacidosis
  • Life-threatening metabolic complication of diabetes
207
Q

pathophysiology of hyperglycemic hyperosmolar state

A
  • Hyperglycemia –> polyuria –> volume depletion –> blood more concentrated –> worsening hyperglycemia etc etc
208
Q

Microcascular complications of diabetes

A
  1. diabetic retinopathy
  2. diabetic nephropathy
  3. diabetic neuropathy
209
Q

Risk factors for debveloping diabetic nephropathy

A
  • Age (older)
  • Genetics
  • Race (african american)
  • Increased GFR (hyperfiltration)
  • Poor glycemic control
  • Obesity
  • Smoking
210
Q

leading cause of end stage renal disease in the U.S.

A

diabetes

211
Q

APOL1

A
  • Gene risk allele common in african americans that is a strong predictor for chronic kidney disease
212
Q

what is the natural history of GFR in diabetes

A
  • First increases - you see hyperfiltration at first, which keeps albuminuria low
  • Eventually, decreased GFR and increased albuminuria
213
Q

albumin levels for microalbuminuria

A
  • diabetes lecture
  • 30 - 300 mg albumin/24 hours
214
Q

urine albumin to creatinine ratio for microalbuminuria

A

30 - 300 mg/gm

215
Q

macroalbuminuria definition (levels)

A
  • greater than 300 mg albumin/24 hours
  • UACR greater than 300 mg/gm
216
Q

Screening recommendations for diabetic nephropathy

A
  • Measure urine albumin-creatinine ratio
  • Measure eGFR
  • **1 time per year
  • In Type 1 diabetes for 5 years or more; in all type 2 diabetics regardless of duration
217
Q

Histopathologic findings in diabetic nephropathy

A
  • Mesangial sclerosis
  • KW nodules in advanced diabetes
  • Hyaline arteriosclerosis
218
Q

key pathologic findings in diabetes

A
  • Enlarged glomerulus
    • Due to hyperfiltration and increased GFR
  • Thickened basement membrane
  • Podocyte damage and loss
    • Occurs due to enlarged glomerulus
    • Correlates to progression of diabetic nephropathy
  • Increased metabolism of glucose –> more glycosylated molecules within cells –>
    • Inflammation
    • Reactive oxygen species
    • Expanded mesangial matrix
219
Q

3 important therapeutic interventions to slow progression of diabetic nephropathy

A
  1. Control glucose
  2. Control hypertension
  3. ACE inhibitors and ARBs
220
Q

Calculating pH

A

pH = -log[H+]

pH of 5 has a hydrogen ion concentration of 1 x 10-5

221
Q

Major buffer system of extracellular fluid

A
  • carbonic acid/bicarbonate
  • This has a pKa of 6.1, but b/c you can so closely change CO2 levels with respiration, carbonic acid/bicarb is an extremely effective buffer. (You can blow off CO2 to pull Hydrogen ions to the right)
222
Q

Major buffer system intracellularly

A
  • Proteins
223
Q

Major buffer system(s) in the urine

A
  • Phosphate
  • Ammonia
224
Q

Normal physiologic bicarb levels

A

22-30 mmol/L

225
Q

Normal physiologic pCO2 levels

A

38-42 mm Hg

226
Q

Relationship of pCO2, bicarb, [H+], and pH

A
227
Q

How would the body respond if we dumped hydrochloric acid in to the blood?

A
  • Acidosis –> H+ combines with bicarb –> generates CO2 –> chemoreceptors read this and increase respiratory rate to blow it off.
228
Q

How does the kidney respond to metabolic acidosis?

A
  • It needs to generate bicarb and it does so in 2 ways:
    • Reabsorption of bicarb in the proximal tubule
    • Synthesis of bicarb in the collecting duct
229
Q

Mechanism of bicarb reabsorption in proximal tubule

A
230
Q

Carbonic anhydrase

A

Catalyzes H2CO3 H2O + CO2

231
Q

Mechanism of collecting duct excretion of H+

A
232
Q

Amount of H+ that must be excreted daily simply from protein metabolism

A

100 mmol

233
Q

Phosphate buffer

A
  • Found in collecting duct tubule
  • One of two urinary buffers that keeps the pH above 4.5 so that the hydrogen pump in the collecting duct can continue pumping hydrogen ions into the urine
234
Q

Ammonia buffer

A
  • Urinary buffer in collecting duct tubule
  • The largest contributer to urine pH maintenance
235
Q

Physiologic responses to metabolic acidosis

A
236
Q

Winters Formula

A
  • Used to predict expected pCO2 as a compensatory response to acidosis
237
Q

Anion gap

A
  • Helps to differentiate the causes of acidosis
238
Q

Abnormal anion gap

A
  • Due to addition of anions OTHER than chloride or bicarb
  • Most commonly this is due to lactate
239
Q

Common causes of non-anion gap metabolic acidosis

A
  • Diarrhea (loss of bicarb in the stool)
  • Addition of HCl (why would this happen?)
240
Q

Common causes of anion gap metabolic acidosis

A
  • Lactic acidosis
    • Cancer
    • Hypoperfusion of the tissues (shock)
  • Ketoacidosis
    • Diabetes
  • Ingestion of various substances
    • Ethylene glycol
241
Q

MUDPILES

A
  • Differential diagnosis for anion gap metabolic acidosis
  • Methanol
  • Uremia
  • Diabetic ketoacidosis
  • propylene glycol
  • isoniazad
  • lactic acidosis
  • ethylene glycol
  • salicylates
242
Q

Common causes of lactic acidosis

A
  • Hypoperfusion/shock
  • Liver failure
  • Cancer
243
Q

Major causes of respiratory acidosis

A
  • Diseases of the airways (such as asthma and chronic obstructive lung disease)
  • Drugs that suppress breathing (Pain Medicines)
  • Severe obesity, which restricts lung expansion
  • Obstructive sleep apnea
  • Nerve or muscle diseases that “signal” the lungs
244
Q

physiologic responses to respiratory acidosis

A
  • when respiration is impaired, you lose two large mechanisms for maintaining the pH
  • Must rely on kidneys and intracellular buffering system
245
Q

Major causes of metabolic alkalosis

A
  • Vomiting (loss of H+ ions)
  • Diuretics (volume contracture-reabsorb sodium bicarbonate as you are depleted of sodium chloride)
  • Alkali administration
  • Recovery from Respiratory Acidosis
246
Q

Relationship b/w pH and potassium

A
  • When you are alkalotic, hydrogen leaves your cells to counteract alkalosis
  • Potassium comes into the cells in exchange for hydrogen
  • Alkalosis shows high intracellular potassium and low serum potassium
  • Acidosis shows the reverse
247
Q

Common causes of respiratory alkalosis

A
  • Anxiety
  • Hypoxemia
  • Central Nervous System Diseases
  • Pregnancy
  • Plus others
248
Q

Physiologic responses to respiratory alkalosis

A
  1. hydrogen comes out of cells (and potassium goes in to balance charge)
  2. proximal tubule rejects bicarb reabsorption
249
Q

physiologic response to metabolic alkalosis

A
  1. reduce ventilation rate to increase pCO2
  2. Release hydrogen from intracellular stores
250
Q

How is potassium excreted?

A
  • 10 - 15% in the stool
  • 85 - 90% by the kidney
251
Q

Relationship between sodium, hydrogen, and potassium

A
  • Na+/H+ antiport brings sodium into the cell in exchange for potassium
  • Na+/K+ ATPase pump sends sodium out of the cell in exchange for potassium in
  • **When hydrogen leaves, potassium comes in, and vice versa**
252
Q

What regulates the Na+/K+ ATPase pump?

A
  1. Insulin
  2. Beta-receptors

**The binding of insulin or catecholamines to their receptors causes activation of the pump, brings K+ into the cell

253
Q

Factors regulating distribution of K+ b/w intracellular and extracellular compartments

A
  1. Acid-base status
  2. Insulin
  3. Catecholamines
254
Q

Most important part of the nephron for K+ regulation

A

collecting duct (specifically the principal cells)

255
Q

principal cells

A
  • found in collecting duct
  • Most important cells for potassium regulation
256
Q

intercalated cells

A
  • found in collecting duct
  • most important for acid-base regulation
257
Q

3 major regulating mechanisms of potassium

A
  1. aldosterone
  2. plasma K+
  3. Tubular flow rate
258
Q

cellular aldosterone actions

A
  • Increases the number of Na+/K+ ATPase pumps on basolateral side
  • Increases the number of sodium channels on urinary side
  • Increases the number of mitochondria that makes ATP for pumping
  • **Reabsorption of sodium, potassium excretion
259
Q

Amiloride

A
  • blocks the sodium and potassium channels on urinary side = prevents reabsorption of sodium and excretion of potassium
  • this is a diuretic
260
Q

Relationship b/w magnesium and potassium

A
  • Magnesium controls K+ ion channels
  • Without enough magnesium, the K+ channels stay opened, which can impair recovery from hypokalemia
261
Q

Where does magnesium reabsorption occur in the nephron?

A
  • Mostly in the thick ascending limb
  • Distal tubule to a small amount
262
Q

why do loop diuretics cause magnesium wasting?

A
  • They block reabsorption of sodium at thick ascending limb, which indirectly inhibits reabsorption of magnesium as well
263
Q

Endogenous causes of hyperkalemia due to redistribution (intracellular –> extracellular movement)

A
  • Lack of insulin - i.e. diabetes
    • Insulin brings potassium into cells
  • Beta blockers
    • Beta receptor brings potassium into cells
  • Acidemia
    • Excess H+ going into cells –> K+ moves into blood
  • Hyperosmolar state - i.e. hyperglycemia
    • Hyperosmolar state pulls fluid out of cells and potassium comes with it
264
Q

Exogenous causes of hyperkalemia

A
  • Increased dietary intake
    • Lots of foods have high amounts of potassium
    • “Salt substitutes” are a high hidden source of potassium
  • Usually only causes hyperkalemia if excretion is impaired
265
Q

Hyperkalemia due to decreased potassium excretion results from:

A
  1. Decreased number of functioning nephrons
  2. Obstruction of collecting tubules
  3. Blocking channels for potassium excretion from drugs
    * Amiloride
  4. Low flow state
    * Volume depletion –> low solute delivery to collecting duct
  5. Lack of aldosterone/blocking aldosterone
  • Addison’s disease
  • ACE inhibitors
  • ARBs
  • spironolactone (aldosterone receptor blocker)
266
Q

Biggest problem with hyperkalemia

A

cardiac arrhythmias

267
Q

Tx of hyperkalemia in the short term

A
  1. Insulin to drive K+ back into cells
  2. B2 agonists (albuterol) to drive K+ back into cells
  3. Sodium bicarbonate for acidosis
  4. Calcium to restore excitability in the heart
268
Q

What do we use to restore cardiac excitability in cases of hyperkalemia?

A

give calcium

269
Q

Tx of hyperkalemia longer term

A
  • Need to cause excretion of K+
  • Kayexalate
    • Binds K+ in the gut and helps excrete more in the stool
  • Drink more water to increase urine flow
  • Furosemide
    • diuretic that causes potassium to go
  • dialysis
  • limit dietary intake of potassium
  • Mineralocorticoids (i.e. aldosterone)
  • Limit ACEI/ARB, Aldo blockers, NSAIDs, non-selective b-blockers
270
Q

causes of hypokalemia due to redistribution from extracellular –> intracellular stores

A
  • Alkalemia
    • drives H+ out of cells into serum, and K+ into cells in exchange
  • Hyperadrenergic states
    • ex: low effective circulating volume from heart failure, diuretics
  • Insulin excess
  • Drugs
    • Beta-adrenergic agonists
      • epinephrine
      • albuterol
271
Q

renal causes of excess loss of K+

A
  • Increased aldosterone
    • Can be primary due to hyperaldosteronism
      • Conn’s syndrome
      • syndrome of apparent mineralocorticoid excess
    • Can be secondary to heart failure and lower effective circulating volume
  • Tubule function abnormalities
    • Due to low magnesium
    • Type 1 renal acidosis
272
Q

Conn’s syndrome

A
  • primary hyperaldosteronism
  • causes hypokalemia
  • Characterized by hypertension
273
Q

Syndrome of apparent mineralocorticoid excess

A
  • cause of excess hypokalemia
  • dysfunction in enzyme that converts cortisol to cortisone
  • cortisol acts like aldosterone in the body
274
Q

Licorice

A
  • Inactivates the enzyme that converts cortisol to cortisone
  • Excess cortisol acts like aldosterone in the body –> hypokalemia
275
Q

Tubule function abnormalities leading to hypokalemia

A
  • Low magnesium
    • Magnesium is needed to keep tubule potassium channels closed
    • Low magnesium –> channels stay opened –> potassium loss
  • Diuretics, diarrhea
276
Q

Hypokalemia does not fully correct until…

A

potassium AND magnesium are replaced

277
Q

Secondary hyperaldosteronism causes and effects on the kidney

A
  • Causes
    • Diuretics
    • Heart failure –> low effective circulating volume –> RAAS
    • Liver disease
    • nephrotic syndrome
    • GI fluid loss
  • Effects
    • Hypokalemia
278
Q

type 1 renal tubular acidosis

A
  • Normally acidosis causes hyperkalemia due to redistribution of potassium stores from intracellular to extracellular space
  • BUT IN THIS CASE intercalated cells in collecting duct are dysfunctional and cannot pump hydrogen into the urine
  • Result is that the principal cells pump more potassium into urinary space
279
Q

Bartter’s syndrome

A
  • Causes hypokalemia
  • Due to dysfunctional sodium reabsorption in thick ascending limb
  • Result is that there’s more sodium delivered to the collecting duct, where it is reabsorbed and drives excretion of potassium
280
Q

Gittelman’s syndrome

A
  • Defect in sodium transport in the distal tubule
  • Causes more sodium to be delivered to the collecting duct, where it is reabsorbed and drives the excretion of potassium
  • Genetic cause of hypokalemia
281
Q

GI causes of hypokalemia

A
  • Vomiting
    • Loss of hydrogen –> aklalosis –> drives potassium from extracellular to intracellular
  • Diarrhea
    • Direct loss of potassium in the stool with large volume losses –> aldosterone activation –> potassium excretion
282
Q

Mechanisms by which metabolic alkalosis causes hypokalemia

A
  1. redistribution of K+ from extracellular to intracellular space
  2. hypokalemia –> H+ gets driven into the cells –> more H+ loss from intercalated cells –> further alkalosis –> further hypokalemia
283
Q

**Understand hypokalemia by the company it keeps***

A
  1. Alkalosis
  • Upper GI losses
  • Diuretics
  1. Acidosis
  • Lower GI losses
  • renal tubular acidosis
  1. Urine chloride
  • Low chloride in context of metabolic alkalosis = volume depletion as cause of hypokalemia
  • High chloride in context of metabolic alkalosis = due to mineralocorticoid excess
  1. Hypertension
  • Low BP = fluid losses as cause of hypokalemia
  • High BP = primary hyperaldosteronism as cause of hypokalemia
284
Q

why do we use urine chloride to determine cause of hypokalemia in cases of metabolic alkalosis?

A
  • Normally, low urine sodium indicates that the body is holding onto sodium to conserve volume
  • But in cases of metabolic alkalosis, you can have normal sodium levels b/c the increased bicarb in the urine can drag sodium with it due to charge conservation
  • Measure urine chloride levels instead
285
Q

Urine chloride levels as indicators of hypokalemia causes

A
  • Used in cases of metabolic alkalosis to determine underlying cause of hypokalemia
  • Low urine chloride = volume depletion
    • Hypokalemia due to vomiting/diarrhea or diuretics
  • High urine chloride
    • cause of hypokalemia is due to excess aldosterone
286
Q

Manifestations of hypokalemia

A
  1. cardiac arrhythmias
  2. decreased insulin release
    * Insulin causes uptake of K+ from serum into cells. Low serum K+ causes compensatory response of low insulin to prevent further losses of K+
  3. rhabdomyolysis
  4. renal dysfunction
    * intracellular alkalosis makes kidney think you’re overall acidodic (K+ leaves cells under states of acidosis) –> increased ammonia production –> worsening of alkalosis
287
Q

Tx of hypokalemia - how much potassium to replace?

A
  • When serum K+ goes down by 0.3 mEq/L, your intracellular potassium has gone down by about 100 mEq/L
  • This means that you when serum K+ is down by 1 mEq/L, you need to replace about 300 mEq/L of potassium
288
Q

Tx of hypokalemia

A
  • Oral K+ replacement
    • spironolactone (aldosterone antagonist) = potassium sparing diuretic
  • IV K+ replacement
    • Must be done very slowly b/c you’re infusing K+ into extracellular space –> easy to induce hyperkalemia
289
Q

hypomagnesemia causes

A
  • starvation, malnutrition
  • decreased intestinal absorption
  • diuretics
290
Q

hypomagnesemia is often seen in conjunction with…

A
  • hypokalemia
  • hypocalcemia
291
Q

Tx of hypomagnesemia often includes replacing magnesium AND…

A
  • potassium
  • calcium
292
Q

Stimuli for renin release

A
  • Low perfusion pressure (afferent arteriole)
  • Sympathetic nerve activity
  • Macula densa (low tubular NaCl delivery)
293
Q

Angiotensin II acts on….

A
  • efferent arterioles
  • Always reduces renal blood flow
  • Low levels increases GFR
    • Wants to maintain GFR to maintain some amount of waste excretion
  • High levels decreases GFR
294
Q

Most common cause of nephrotic syndrome in children

A

minimal change disease

295
Q

Most common cause of nephrotic syndrome in hispanics and african americans

A

FSGS (focal segmental glomerular sclerosis)

296
Q

Lupus is associated with what glomerular disorders

A
  • Diffuse Proliferative glomerular nephritis is most common
  • IF they present with a nephrotic syndrome, then it’s membranous nephropathy
297
Q

Glomerular Disorders

A
  • Nephrotic syndrome
  • Nephritic syndrome
298
Q

Nephrotic syndromes

A
  • Minimal Change Disease
  • FSGS
  • Membranous nephropathy
  • Diabetic Nephropathy
  • Systemic amyloidosis (not covered in lecture)
299
Q

Foot Process effacement is seen in…

A
  • Minimal Change Disease
  • FSGS
  • **Electron microscopy**
300
Q

Minimal Change Disease Key Findings

A
  • Normal glomeruli on H&E stain
  • Effacement of foot processes on EM
  • Negative IF findings
  • Selective proteinuria (loss of albumin but not IgG’s)
  • **Responds well to steroids**
301
Q

FSGS is what type of kidney problem

A
  • Glomerular disease
  • Nephrotic Syndrome
302
Q

Minimal change disease is what kind of kidney problem

A
  • Glomerular disease
  • Nephrotic syndrome
303
Q

Key findings of FSGS

A
  • Focal and segmental sclerosis on H&E stain
    • Focal = some glomeruli
    • Segmental = parts of the glomerulus
    • Sclerosis = lots of pink collagen depositions
  • Foot Process Effacement on EM
  • Negative IF
    • Lecturer says differently – you can see some small flourescence in glomerulus
  • Does NOT respond to steroids
    • This is basically the result of minimal change disease if minimal change disease did not respond to steroids
304
Q

Membranous nephropathy is what kind of kidney problem?

A
  • Glomerular disease
  • Nephrotic syndrome
305
Q

Membranous Nephropathy Key findings

A
  • Thick glomerular basement membrane on H&E (thick capillary loops)
    • Due to immune complexes that kick off podocyte from basement membrane, which stimulates the podocyte to make more basement membrane
  • Granular IF
  • Subepithelial deposits w/ spike and dome appearance on EM
306
Q

Immune deposits seen on EM in which kidney problems?

A
  • MEMBRANOUS problems
  • Membranous nephropathy
    • subepithelial
  • Type 1 membranoproliferative glomerular nephritis
    • subendothelial
  • Type 2 membranoproliferative glomerular nephritis
    • in the basement membrane
307
Q

KW nodules are pathonemonic for…

A

diabetic nephropathy

308
Q

Tx for diabetic nephropathy

A

ACE inhibitors

309
Q

Linear IF results are virtually pathonemonic for…

A

Goodpasture’s syndrome

310
Q

subendothelial immune complexes are characteristic of…

A

Diffuse proliferative glomerulonephritis

311
Q

Most common renal disease seen with lupus

A

diffuse proliferative glomerulonephritis

312
Q

Three labs we look at when evaluating hyponatremia

A
  1. Serum osmolality
  2. Urine osmolality
  3. Urine sodium levels
313
Q

Most common causes of a high osmolar gap

A

ingestion of an alcohol, including ethanol, methanol, ethylene glycol, diethylene glycol, propylene glycol, and isopropanol (isopropyl alcohol)

314
Q

why does an unmeasured anion in the blood cause an anion gap?

A
  • Na - (Cl + HCO3) = anion gap
  • If you have lots of some other anion, it will cause chloride and bicarb to go down in order to maintain proper charge
  • Results in an anion gap
315
Q

Conditions associated with a recet osmostat –> hyponatremia

A
  • Pregnancy
  • Psychosis
  • malnutrition
316
Q

Conditions associated with SIADH

A
  • Malignancies
  • CNS disorders
  • Pulmonary infections
317
Q

Primary causes of acute interstitial nephritis

A
  • drug-induced reaction
    • Bactrim
    • Omeprazole
    • Plus tons others
318
Q

Classic triad of symptoms for acute interstitial nephritis

A
  • low-grade fever
  • rash (25%)
  • eosinophilia (may be transient)
319
Q

Antibiotic notorious for causing acute interstitial nephritis

A

Bactrim

320
Q

Pathologic findings of acute interstitial nephritis

A
  • **Eosinophils
  • Interstitial edema
  • Exudate filled with other inflammatory cells - neutrophils, macrophages
321
Q

Clinical findings of acute pyelonephritis

A
  • back pain
  • fever
  • bladder/urethral irritation (dysuria, frequency, urgency)
  • pyuria
  • +/-hematuria
322
Q

Most common organism causing pyelonephritis

A

E.coli

323
Q

Two different pathogenesis of pyelonephritis

A
  • Ascending urinary tract infection
  • Hematogenous infection (from bacteremia)
324
Q

Pathologic findings of acute pyelonephritis

A
  • TONS of neutrophils in the interstitium
325
Q

Causes of papillary necrosis

A
  • **Analgesic abuse
    • Story about workers who were continuously popping pills with phenacitin-aspirin-caffeine combo (Note: phenacitin is now banned by FDA)
  • Plus others we didn’t talk much about
326
Q

Pathogenesis of papillary necrosis

A

Medullary ischemia

327
Q

What will you find in the urine with acute interstitial nephritis? And how do you differentiate from a urinary source?

A
  • WBCs/WBC casts
  • Urinary infection will present with problems peeing, whereas acute interstitial nephritis does not.
328
Q

Distinctive feature of Acute Interstitial Nephritis

A
  • Eosinophils, both in the urine and the biopsy
  • These are the little pink dots in the interstitium on biopsy
329
Q

Biopsy pic of normal renal interstitium

A
  • Tubules are right up next to each other
  • There’s very little in the interstitium, which is the space b/w the tubules
  • The tubules are surrounded by peritubular capillaries
330
Q

Distribution of infection in hematogenous vs. ascending urinary tract forms of pyelonephritis

A
  • Hematogenous - the whole kidney is infected
  • Ascending infection - The poles are infected
331
Q

Microscopic appearance of acute pyelonephritis

A
  • TONS of neutrophils
  • Not in this picture, but you can also see WBC casts
332
Q

what predisposes people to ascending urinary tract infections (pyelonephritis)

A
  • Obstructions (kidney stones, enlarged prostate)
  • Pregnancy
  • Diabetes
  • Immunosuppressed
  • Weird anatomy - strange attachment of ureter to bladder
333
Q

How is acute pyelonephritis diagnosed? What organisms are usually responsible for the infection?

A
  • You try not to biopsy b/c that can cause infection to spread
  • Diagnose with cultures, urinalysis, and clinical symptoms
  • WBC casts in the urine
  • E-coli is most common organism
334
Q

Causes of renal failure in the setting of multiple myeloma.

A
  • Light chain casts occur when this buildup of light chains gets into the tubule and then precipitates. These can obstruct the flow of urine through the tubules and give rise to renal failure.
335
Q

The kidney is derived from what embryologic source?

A
  • Intermediate mesoderm
336
Q

Development of the metanephros depends on continuous and reciprocal interactions between…

A
  • metanephric mesenchyme and the ureteric bud
337
Q

Ureteric bud gives rise to…

A
  • collecting ducts
  • minor and major calices
  • ureter
338
Q

metanephric mesenchyme gives rise to

A
  • podocytes
  • epithelial cells lining bowman’s capsule
  • proximal tubule
  • loop of henle
  • distal tubule
339
Q

pathophysiology of Potter Syndrome

A
  • Decreased amniotic fluid production due to congenital abnormalities of the kidney
  • Results in increased mechanical pressure on the developing fetus
340
Q

Clinical presentation of potter syndrome

A
  • Flattened face
  • Limb abnormalities
  • lung hypoplasia
  • GI abnormalities
341
Q

Ectopic ureter pathophysiology

A
  • Due to problem w/ induction signals during embryologic development
  • Results in a ureter that connects to the bladder in the wrong location
342
Q

Wilms Tumor/Nephroblastoma

A
  • 10 - 20% of cases are associated with deletions/mutations in WT1 gene
  • Kidney cancer that arises from mutations in developmental genes
  • Presents in childhood
343
Q

Loss of function mutations in PAX2 produce…

A

congenital urinary tract and optic abnormalities of renal colomba syndrome

344
Q

Gain of function mutations of PAX2 result in…

A

congenital abnormalities and pediatric and adult kidney tumors

345
Q

3 main drug classes used in transplant care

A
  1. calcineurin inhibitors (cyclosporin, tacrolimus)
  2. Steroids
  3. Antiproliferative agents
346
Q

Cyclosporin and Tacrolimus drug class and uses

A
  • Calcineurin inhibitors
  • Used for maintenance in post-transplant care
347
Q

Delayed Graft function

A
  • non-immune process
  • defined as need of dialysis within first week post-transplant
  • associated with acute tubular necrosis
348
Q

hyperacute rejection

A
  • antibody-mediated cause of transplant rejection
  • Rejection occurs immediately upon implantation as soon as kidney gets perfused
  • This is really rare now b/c of all the testing we do before transplantation
349
Q

Acute Rejection

A
  • Most common cause of transplant rejection, but it rarely occurs after the first year
  • Either T-cell mediated or antibody mediated
350
Q

Which is worse for the graft - T-cell mediated or antibody mediated rejection?

A

Antibody mediated

351
Q

Chronic rejection

A
  • All transplants eventually succumb to this
  • no good treatment exists
352
Q

T-cell mediated transplant rejection mechanism

A
  • An antigen presenting cell from either host or donor must go to a secondary lymphoid organ in the recipient
  • The antigen presenting cells have to present the antigen to memory T cells
  • The T-cells have to be activated and undergo clonal expansion and differentiation
  • These signals from T-cells activate a bunch of intracellular pathways and start doing stuff
  • This results in damage
353
Q

Main drug interactions post-transplant occur with what drug class?

A
  • Calcineurin inhibitors
  • B/c they’re metabolized by p450 enzyme
354
Q

Explain the process of cross-matching in transplant prep

A
  • You combine blood from the potential recipient and one potential donor and see if they react with each other
355
Q

Explain the panel of reactive antibody

A
  • You take your recipient’s blood and test it against a bunch of POTENTIAL donors
  • This gives you a sense of how many different people, out of 100, your recipient would attack IF transplant occurred.
  • Ideal is to have a LOW number for PRA
356
Q

Blood in the urine is…

A

CANCER UNTIL PROVEN OTHERWISE

357
Q

Blood in the urine plus flank pain

A

Stone

358
Q

Blood in the urine plus tobacco use

A

bladder cancer

359
Q

blood in the urine plus fever

A

infection

360
Q

Acute kidney injury definition

A
  • Abrupt loss of renal clearance function
  • See acute increases in BUN and creatinine
361
Q

Pre-renal causes of Acute Kidney Injury

A
  • hypovolemia –> kidneys are not getting perfused
  • Decreased effective circulating volume –> kidneys not getting perfused
  • NSAIDs, ACEs, ARBs
362
Q

Fractional sodium excretion in the contex of oliguria

A
  • Look at this when trying to determine cause of acute kidney injury
  • Less than 0.01 favors a prerenal cause of oliguria
  • Greater than 0.01 favors a renal cause of oliguria
363
Q

Renal causes of acute kidney injury

A
  • glomerulonephritis
  • interstitial nephritis
  • tubular necrosis
364
Q

primary finding on urinalysis during most forms of renal causes of AKI

A

granular casts = acute tubular necrosis

365
Q

Both kidneys are the same size and a normal size in the context of renal dysfunction. Explain.

A

It’s a recent injury

366
Q

Both kidneys are small when an ultrasound is done in the context of renal dysfunction.

A
  • A disease that has affected them both
    • chronic glomerulonephritis
    • parenchymal loss
    • hypertension
367
Q

Large kidneys are ultrasound are associated with

A

diabetes

368
Q

assymetrically sized kidneys are ultrasound are associated with…

A

renal artery stenosis

369
Q

What do you first need to rule out in cases of acute kidney injury?

A
  • Obstruction
  • This is easily treatable
370
Q

Indications for dialysis in acute kidney injury

A
  • hyperkalemia
  • acidosis
  • Uremia, BUN > 80 - 100
  • Uremic complications - change in mental status
  • High rate of creatinine increase
371
Q

Thiazide diuretics mechanism

A

limit sodium reabsorption in distal convoluted tubule

372
Q

thiazide diuretics effect on other solutes

A
  • decreased calcium excretion
    • less sodium reabsorption leaves room for more calcium reabsorption
  • decreased uric acid excretion
    • Due to increased reabsorption in proximal tubule
  • Increased magnesium excretion
373
Q

Most common use for thiazide diuretics

A
  • Garden variety hypertension
  • Tx for kidney stones
    • reduce calcium in the urine
  • mild edema
  • Diabetes insipidus
374
Q

Side effects of thiazide diuretics

A
  • hypokalemia
  • Hyponatremia
  • difficulty with glycemic control
375
Q

mechanism of hypokalemia with thiazide diuretics

A
  • Increased delivery of sodium to the distal tubule, which ramps up sodium-potassium pump –> increased excretion
  • Low total body volume activates RAAS, which causes increased excretion of potassium in the collecting duct
376
Q

mechanism of hyponatremia with thiazide diuretic

A
  • Sodium is not reabsorbed in distal tubule
  • Body senses low volume –> ADH release –> body holds onto water while sodium is constantly excreted
377
Q

Loop Diuretic mechanism

A
  • Impairs sodium reabsorption in the thick ascending limb
    • This is the site of 20 - 25% of sodium reabsorption and the distal tubule has limited ability to reabsorb sodium, so this is the most powerful of the diuretics
378
Q

Loop diuretic effect on other solutes

A
  • Increased K+ excretion
  • Increased Mg excretion
379
Q

Loop diuretics most common clinical use

A
  • Severe fluid overload
  • Bad hypertension
  • To treat hyponatremia, especially if that was produced by thiazides
    • B/c loop diuretics make you lose a lot of water
  • Forced diuresis in cases of overdose
380
Q

Side effects of loop diuretics

A
  • Difficulty making concentrated urine
    • B/c impairing sodium reabsorption in thick ascending limb disrupts the osmotic gradient in the medulla –> impairs water reabsorption
381
Q

why are loop diuretics used to treat hyponatremia?

A
  • They impair sodium reabsorption in thick ascending limb, which disrupts osmotic gradient in medulla and impairs body’s ability to reabsorb water
  • Treatment effect is through increased water excretion
382
Q

________ drug class tends to produce hyponatremia while _______ drug class is used to treat hyponatremia

A

Thiazides, loop diuretics

383
Q

Hearing loss is commonly associated with which diuretic?

A

ethacrynic acid

384
Q

loop diuretic drug names

A
  • furosemide
  • bumetanide
  • torsemide
  • ethacrynic acid
385
Q

Ethacrynic acid

A
  • loop diuretic that has no allergic crossreactivity (which is why it is used), but it is also ototoxic (hearing loss)
386
Q

Potassium Sparing diuretics mechanism

A
  • Block reabsorption of sodium in the collecting duct, which also blocks excretion of potassium
387
Q

triamterene, amiloride

A

potassium sparing diuretics that block sodium channels in collecting duct

388
Q

spironoloactone

eplerenone

A
  • potassium sparing diuretics that block the aldosterone receptor
389
Q

Potassium sparing diuretics effect on other solutes

A
  • limit potassium excretion –> limited hydrogen excretion due to crosstalk b/w principal cells and intercalated cells
390
Q

Clinical uses of K+ sparing diuretics

A
  • hypertension, especially in conjunction with thiazides
  • manage hypokalemia
  • Tx of hyperaldosteronism with spironolactone and eplerenone
391
Q

Side effects of K+ sparing diuretics

A
  • Hyperkalemia
  • Metabolic acidosis
  • Gynecomastia
392
Q

Diuretic combinations

A
  • potassium-sparing diuretics combined with any of the others
  • Thiazide diuretic + loop diuretic for maximal diuresis
  • We do NOT use two diuretics that are in the same class
393
Q

Why are thiazides used to treat hypercalcuria

A
  • They decrease sodium reabsorption in the distal tubule and this leaves more room for calcium reabsorption
  • Increased calcium reabsorption –> less calcium in the urine –> fewer kidney stones
394
Q

What causes an increase in PTH?

A
  • Low serum calcium
    • This can occur due to kidney disease b/c the kidney produces calcitriol, which is necessary for reabsorbing calcium from the gut.
    • Kidney disease –> less calcium reabsorption from the gut
  • High phosphorous levels
    • Kidney disease = lower GFR –> buildup of calcium
  • Low calcitriol
    • Another manifestation of kidney disease b/c kidney is responsible for producing calcitriol
395
Q

Risk factors for uric acid stones

A
  • Low urine volume
  • Acidic urine
  • hyperuricosuria
396
Q

T/F: Uric acid stones can be seen on X-ray.

A

False

397
Q

Tx for uric acid stones

A
  • Mainstay: limit uric acid generation in the body with drugs
  • Make urine more alkaline
398
Q

Tx for calcium stones

A
  • Thiazides to increase calcium reabsorption
    • Limiting sodium reabsorption leaves more room for calcium reabsorption
  • Increased fluid intake
  • Sodium restriction
399
Q

combined hematuria and proteinuria

A

this is glomerular nephritis until proven otherwise

400
Q

Acute tx of hyperkalemia

A
  • Give calcium immediately to restore cardiac excitability
  • Insulin/glucose to drive K+ back into cells
  • Beta agonists to drive K+ back into cells
  • Bicarb to correct acidosis –> drives K+ back into cells
  • Diuresis if needed

VF1 - Block 3 (7 decks)

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