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FERGU > Week 1- Glomerular disease > Flashcards

Week 1- Glomerular disease Flashcards

1
Q

What are the characteristics of a proper urine specimen for urinalysis? What order to perform a urinanalysis?

A
  • collected first thing in the morning (more concentrated)
  • fresh (<1 hr since collection, otherwise refrigerated)
  • midstream catch
  1. Physical characteristics (concentration (surrogate: specific gravity), colour (foods, drugs, normal or abnormal metabolites), turbidity (should be clear, if not: crystals or cells)
  2. Chemical characteristic (diptick)
  3. Microscopic (usually reserved for samples that are abnormal in #1 or #2)
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2
Q

What are the 8 most common components of chemical urine analysis?

A

pH
Protein
Glucose
Ketones
Blood
Nitrite
Leukocyte esterase
Specific gravity

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3
Q

Where do these renal casts come from/what do they mean:

  • RBC
  • hyaline
  • coarse granular
  • fine granular
A

RBC casts:

  • glomerular hematuria, possible underlying proliferative glomerulonephritis

Hyaline

  • Hyaline casts may be observed with small volumes of concentrated urine or with diuretic therapy and are generally nonspecific.Exercise, dehydration, fever.

Coarse and fine granular

  • cell degeneration, proteinuria
  • nonspecific
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4
Q

What factors contribute to cast formation?

A

Acid pH, high salt, reduced urine flow and protein all contribute to formation.

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5
Q

What kind of cast is this?

A
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6
Q

What kind of cast is this?

A
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7
Q

What kind of cast is this?

A
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8
Q

What kind of cast is this?

A
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9
Q

Why do crystals form? What is their diagnostic significance?

A

They usualy form after voiding in concentrated urine and the type of crystal depends on the pH of the urine. The urine is supersaturated with chemical constituents.

Not usually diagnostic.

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10
Q

What is the clinical significance of this type of crystal?

A

Cystinuria (a cause of chronic kidney stones)

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11
Q

What is the clinical significance of these crystals?

A

Clockwise from top left:

  • Calcium oxalate (common)
  • Uric acid (acid urine, gout, other conditions)
  • Triple phosphate (indicator of UTI) (common)
  • Cystine (cystinuria–>a cause of chronic kidney stones) (pathologic!)
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12
Q

What is the clinical significance of RBCs and WBCs in the urine?

A

RBCs imply some kind of uriniary tract disorder. Dysmorphic RBCs imply glomerular disease, eumorphic RBCs imply extraglomerular disease

WBCs imply urinary tract inflammation

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13
Q

Define glomerulonephritis

A

Inflammation of the glomeruli

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14
Q

What is march hemoglobinuria?

A

Hemoglobin in the urine resulting from the destruction of red blood cells during continous mechanical trauma (e.g. running).

Also called march hematuria when RBCs are also present in the urine.

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15
Q

What is renal glycosuria?

A

When the kidney excretes glucose, despite normal blood sugar levels. Thought to be autosomal recessive defect in the tubular reabsorption of glucose.

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16
Q

What does glucosuria with ketouria mean? What does glucouria without ketouria mean? What does keoturia mean?

A

Glucosuria +ketouria= poorly controlled/decompensated diabetes mellitus (diabetic ketoacidosis)

Glucosuria - ketouria= controlled DM, renal glucosuria

ketouria= alcoholic ketoacidosis, starvation

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17
Q

Define pyelonephritis. What urinalysis findings would you expect to see?

A

Acute infection of the renal pelvis or parenchyma

WBCs, WBC casts, bacteria on microscopy

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18
Q

What are two urinalysis findings are normal in fever?

A

Proteinuria, hyaline casts

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19
Q

What does nitrites in the urine indicate? What does leukocyte esterase indicate?

A

The presence of nitrate (endogenous product) reducing bacteria–> bacteriuria.

Leukocyte esterase is a marker of WBC –> inflammation

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20
Q

What is the clinical significance of proteinuria?

A
  • Signifies renal parenchymal disease:
  • glomerular disease (increased protein filtration) or tubular disease (decreased protein reabsorption- Fanconi syndrome- rare)
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21
Q

What does hematuria without proteinuria signify? With proteinuria?

A

Hematuria without proteinuria usually means the bleeding is extra-glomerular (outside the glomerulus and nephron)

Hematuria with proteinuria suggests glomerular disease.

22
Q

What are the body fluid compartments, how much volume is in each?

A
23
Q

What is the Starling equation? According to the starling equation, what are the possible mechanisms of edema, and give an example of each?

A

fluid flux= permeability*surface area (hydrostatice pressure- s*oncotic pressure)

where s is the reflection coefficient for proteins

Mechanisms of edema:

  • reduced capillary oncotic pressure (hypoalbunemia)
  • increased capillary hydrostatic pressure (venous back-up, loss of arteriolar resistance)
  • reduced interstitial hydrostatic pressure (no example….maybe not clinically significant)
  • increased intersitial oncotic pressure (lymphatic blockage)
  • increased permeability (sepsis)
24
Q

What is the distribution of solutes in the cell, the interstitium and the vascular space?

A
25
Q

What will the following IV fluids do to intracellular volume:

  • 0.9% saline (~290 mOsm)
  • 0.45% saline (~145 mOsm)
  • 3% saline (~1000 mOsm)
A
  1. 9% saline (~290 mOsm)
    * since it is isotonic, it will distribute between the IVF (1/4) and ISF (3/4) and not change the ICF
  2. 45% saline (~145 mOsm)
    * this is hypotonic, so water will be drawn into the ICF

3% saline (1000 mOsm)

  • this is hypertonic, so water will leave the ICF
26
Q

How to replenish a depleted intravascular volume?

How to replenish extracellular fluid?

How to rectify a hyperosmotic state?

A
  • infuse with albumin 5% to replenish IVF only
  • infuse with 0.9% saline to replenish IVF and ISF
  • infuse with hypotonic saline (0.45%) or 5% dextrose (D5W)
27
Q

What forces govern the movement of fluid out of cells? What forces govern the movement of fluid between the vasculature and the interstitial space?

A

Fluid movement out/into cells is governed by osmolality, fluid movement between the interstitial and vasculature is governed by Starling forces (hydrostatic pressure and oncotic pressure)

28
Q

What is volume contraction? What parameters change with it?

A

Volume contraction is a decrease in the effective circulating volume. As a result BP and CO also fall.

The opposite is volume expansion.

29
Q

What are the two most important secratagogues for aldosterone?

A

Angiotensin II

Hyperkalemia

30
Q

What are the three types of transport used in the kidney? Provide examples of each.

A

Active transport:

  • Primary: Na/KATPase
  • Secondary: symporters (NCC, NKCC), antiporters (NHE3)
  • Endocytosis (proteins at the PCT)

Facilitated diffusion:

  • channel mediated (e.g. ENaC, ROMK)
  • carrier mediated (Glucose (GLUT-2) and urea)

Passive transport (diffusion)

  • osmotic movement of water (solvent drag accounts for much of the reabsorption in the PCT)
  • paracellular movement of Ca and Mg (arguably secondary active transport though)
31
Q

What does the proximal convoluted tubule do? What is the reabsorption coupled to?

A

Bulk reabsorption : isoosmotic process, virtually all coupled to Na reabsorption:

  • 67% water (AQP)
  • 67% sodium (symports and antiports)
  • proteins (endocytosis)
  • glucose

Secretion

  • organic anions and cations (drugs and endogenous)
32
Q

What does the loop of Henle do? Where is it permeable/impermeable to water/salt? What drives reabsorption? How does each solute get transported?

A

The loop of Henle reabsorbs water (15%), Na (25%), bicarbonate, Mg and Ca.

The descending limb is permeable to water and not salt, and concentrates the filtrate.

The ascending limb is permeable to salt and not water (no AQP) and dilutes (or desalinates) the filtrate.

Sodium reabsorption:

  • In tAL, passive reabsorptin of NaCl
  • In TAL, Na/KATPase sets up gradient
  • Na comes in with NKCC, moves out the basolateral side while K is recycled into lumen through ROMK to be used again.
  • Na comes in on NHE3, H+ moves into the lumen, HCO3- is reabsorbed
  • Na (50%) moves paracellulary via electric gradient

Bicarbonate reabsorption

  • Na comes in on NHE3, H+ moves into the lumen, HCO3- is reabsorbed

Mg and Ca

  • Paracellular diffusion via electrical gradient

Descending limb

  • impermeable to salt, permeable to water

Ascending limb (AKA diluting segment AKA desalination segment

  • permeable to salt, impermeable to water (no AQP)
33
Q

What does the distal tubule do? What is the difference between the early and late distal tubule? Which channels/transporters are involved?

A

The distal tubule reabsorbs NaCl (8%), water (late only), HCO3-, secretes K+ and H+, HCO3-.

Early segment:

  • impermeable to water
  • NCC (NaCl symport) reabsorbs Na and Cl
  • Ca is reabsorbed

Distal tubule:

  • Principal cells
    • reabsorbs Na (ENaC) and water (AQP)
    • secretes K (ROMK)
  • alpha-intercalated cells
    • secretes H+
    • reabsorbs HCO3- and K+ (H+/K+ ATPase in apical side)
  • beta-intercalated cells
    • secretes HCO3-
    • reabsorbs H+ and Cl-
34
Q

How is renal sodium handling modulated? (4 direct and 2 indirect mechanisms)

A

Direct effects

  • ATII: increased Na reabs. at the PCT
  • Aldosterone: increased Na reabs at distal tubule/collecting duct, exchange for K+
  • Uroguanylin/guanylin: from neuroendocrine cells in the intestine in response to a salty meal. decreases salt and water reabsorption.
  • Catecholamines/SNS: stimulate NaCl reabs. in the PCT

Indirect effects

  • ANP/BNP: increase renal plasma flow and GFR –> increase Na and H20 excretion
  • Prostaglandin I2: in low ECFV, dilates afferent arteriole to maintain perfusion pressure
35
Q

How is renal water handling modulated?

A

Direct:

  • AVP (ADH): insertion of AQP-2 into collecting duct, reabs. of water

**Other hormones modulate NaCl, and this can affect H20 as well, but ultimately the amount of water reabsorbed depends on AVP**

36
Q

What is the feedback loop modulating ADH release?

A
37
Q

How is osmolality regulated in the body?

A

AVP stimulates V2 receptor to insert AQP-2 in collecting duct.

38
Q

What are some non-osmotic stimuli of AVP?

A
  • volume depletion (10% change)
  • nausea/vomiting
  • pain
  • medications
  • nicotine
39
Q

What are the two important ADH receptors? Which one is targeted pharmacologically in shock?

A

V1: found in arterioles, brain. mediates vasoconstriction. Not physioloically sitmulated by ADH, but pharmacologically stimulated by vasopressin.

V2: found in collecting ducts,mediates water reabsorption

40
Q

Where are volume receptors found?

A

Low pressure:

  • atria
  • RV
  • large pulmonary vessel

High Pressure:

  • carotid sinus
  • aortic arch
41
Q

How is volume regulated?

A

Low volume sensed by baroreceptors

  1. SNS to kidney
    • stimulated renin release (beta)
    • afferent arteriole (blocks alpha-1 vasoconstriction)
    • direct tubule input, NaCl reabsorption
  2. ANP/BNP released
  3. AVP release if change is large enough

Low volume sensed by kidneys

  1. low NaCl in macula densa –>renin release
  2. low pressure in afferent arteriole –> renin release
  3. SNS input (beta) –> renin release

RAAS effects

  1. Aldosterone stimulation –> increases Na reabs at the distal tubule in principal cells (NCC, ENac)
  2. Direct systemic vasoconstriction
  3. Stimulates AVP release and thirst
  4. ACE inactivates bradykinin (a vasodilator)

**All act to increase salt**

42
Q

What determines extracellular fluid volume?

What determines intracellular fluid volume?

What is one important exception to both of these?

A

Serum sodium content

Serum sodium concentration

Severe hyperglycemia is the exception to this. Glucose will draw fluid out of the cell and into the vascular space. This contracts cells and also dilutes the sodium in blood and becomes a determinant of ECFV.

43
Q

How is the urine concentrated? Generally speaking…

A

The filtrate arriving at the collecting duct is dilute, due to the desalination of the TAL. In the absence of AVP it will remain dilute.

In the presence of AVP, water will be pulled into the intersitium by the gradient, concentrating the urine.

N.B: the gradient MUST be present for H20 to move…it cannot be pumped, it can only flow. The NKCC in the TAL creates this gradient.

44
Q

In a healthy individual, what is the urine sodium and urine volume equal to?

A

It should equal their salt and fluid intake.

45
Q

Explain the pathophysiology of edema. What can cause edema? What is common among all the causes?

A

Edema can result from:

  • decreased capillary oncotic pressure (e.g. hypoalbuminemia from cirrhosis or nephrotic syndrome)
  • increased hydrostatic capillary pressure (e.g. venous backlog from pulmonary edema)
  • increased capillary permeability (e.g. sepsis)
  • increased intersitial oncotic pressure (e.g. lymphatic back-up

In all cases the net result is for fluid to move into the interstium, causing volume contraction. This volume contraction (dec. BP and CO) results in activation of RAAS and results in salt retention, increasing the effective circulating volume back to normal. These mechanisms are physiologic, they are meant to preserve effective circulating volume, but are pathophysiologic in edema.

46
Q

How might glomerular disease be manifested clinically?

A

proteinuria

hematuria

decreased GFR/rise in SCr (this always goes along with proteinuria +/- hematuria)

(or some combination thereof)

47
Q

What is the pathogenic classification of glomerular kidney disease (5 main categories)?

A

Immune mechanisms

  • antibody mediated (immune complexes, antiglomerular basement membrane antibody)
  • cell mediated

Hemodynamic

  • hyperperfusion/hyperfiltration (e.g. focal glomerulosclerosis)
  • ischemia

Podocyte injury (e.g. viral injury from HIV)

Polyanion loss (e.g. minimal change disease)

Metabolic

  • familial (Fabry’s disease –> lipid acculumation in podocytes)
  • acquired (e.g. diabetic glomerulosclerosis)
48
Q

What is the pathogenesis of antibody mediated glomerular disease when deposits are in the subendothelial or mesangial space?

A
  1. Deposit
  2. cell activation and C5a activation
  3. inflammatory cells infiltrate
    • procoagulation–> fibrin
    • growth factor–> increased ECM production
    • ROS/proteases–> damage
    • cytokines–> recruitment
49
Q

What is the pathogenesis of antibody mediated glomerular disease when the deposits are on urinary space side?

A
  1. complement is activated, but C5a is washed away so no inflammatory cells come
  2. the membrane attack complex (MAC) still forms
  3. podocyte damage
50
Q

What difference would you expect to see on the Ig stained renal biopsy of IC-mediated disease and AGBM disease?

A

IC stains will be granular because the deposits go everywhere. AGBM disease will be linear and smooth because the antibodies are to the basement membrane.

FERGU (7 decks)

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