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Patho > Topic 7.1 - Renal Dysfunction > Flashcards

Topic 7.1 - Renal Dysfunction Flashcards

1
Q

How many ml of of blood flows through the kidneys per minute? What percent of cardiac output does this account for?

A

25% of cardiac output, 1200 ml/min

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2
Q

How much of the renal blood flow goes to the cortex? Medulla?

A

90% to cortex
1-2% to medulla

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3
Q

How much of the fluid filtered by the kidneys is reabsorbed?

A

99%

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4
Q

Where are 65%of electrolytes reabsorbed?

A

In the proximal tubule

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5
Q

What is a nephron?

A

The structural functional unit of the kidney
–> Glomerulus, proximal convoluted tubule, loop of Henle, distal convoluted tubule. Empties into collecting duct.

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6
Q

What are Mesangial cells?

A

Smooth muscle like cells that can pull the whole capillary bed, changing their size and impacting GFR

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7
Q

What are podocytes?

A

Cells with foot like processes that sit on the urinary side of the capillary basement membrane.
The foot-processes form pores that water and electrolytes can pass through, but proteins like albumin cannot.

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8
Q

Why is it important the the kidneys do not filter out albumin? What happens if too much of it is lost?

A

Albumin is the most common protein in the blood and is important for maintaining the oncotic gradient.
Additionally, if too much is lost the liver will be unable to keep up and produce more. The oncotic gradient will be disrupted and edema will occur.

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9
Q

What is glomerular filtration rate?

A

The rate at which plasma moved through the glomerular capillaries in ml/min

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10
Q

At what age to children reach adults GFR proportions?

A

By two years old

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11
Q

What is the driving force for GFR?

A

Capillary hydrostatic pressure - usually ~55 mm Hg glomeruli.

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12
Q

What is the formula for GFR calculation in a hypothetical/lab setting?

A

ultrafiltration coefficient x (glomerulus capillary pressure - (tubular pressure + Colloid osmotic pressure))

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13
Q

What is the ultrafiltration coefficient? Why might it decrease?

A

A constant that takes into consideration capillary surface area an fluid permeability.
Decreases in those with damage or fibrosis.

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14
Q

Why is inulin the gold standard subject to measure GFR?

A

It is freely filtered, not reabsorbed or secreted, not synthesized or catabolized by the kidney, and does not alter GFR.

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15
Q

What is the clinical standard substance used to measure GFR?

A

Creatinine
–> Produces by skeletal muscle at a constant rate from creatine-phosphate.

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16
Q

Why might Cystatin C be used to measure GFR instead of creatinine?

A

It is produced by all nucleated cells in the body. It is used for children because their different muscle mass makes a creatinine assessment less accurate.

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17
Q

Which three substances are used to measure GFR?

A

Inulin - Gold standard
Creatinine - Clinical standard
Cystatin C - Used clinically with children

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18
Q

How is GFR calculated using inulin?

A

GFR = U(in) x V / P(in)

Urine [inulin] times volume of urine, all divided by the plasma [inulin]

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19
Q

How is GFR calculated using creatinine? What addition measures does this require clinically?

A

([Cr] Urine X Urine flow rate) / [Cr] plasma

Requires
–> 12-24 hr urine collection (timed)
–> A midpoint blood sample
–> The concentration of [Cr] in urine and plasma

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20
Q

What is the caveat to using creatinine to measure GFR?

A

It slightly overestimates GFR
–> Creatinine is also secreted by proximal tubules.

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21
Q

Under normal conditions, renal excretion of creatinine should occur at the same rate that skeletal muscles are producing it. What is the normal range of plasma creatinine concentration?

A

50-110 micro mol/L

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22
Q

What happens to creatinine concentration in plasma if GFR drops slowly, as if in chronic kidney disease?

A

Excretion < production
[Cr] increases

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23
Q

What GFR rate cannot support life (kidney failure)?

A

15 ml/min

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24
Q

Plasma [Cr] does not accurately reflect GFR in acute Kidney Injury. Why?

A

Plasma concentration will continually increase if GFR is suddenly 0.
It will therefor lag behind the GFR loss and underestimate it.

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25
Q

How might a GFR of 50 mml/L be interpreted?

A

Below normal range (should be higher than 90). Kidney disease present.

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26
Q

What is the normal GFR, according the the National Kidney Foundation?

A

90-120 ml/min/1.73 m^2

(Based on the prototypical body surface area for an average individual)

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27
Q

Which GFR calculating formula takes into account age, ethnicity, and sex? Which substance does it use to measure GFR.

A

The Modification of Diet in Renal Disease (MDRD) Formula.
Uses creatinine concentration.

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28
Q

Which GFR calculating formula takes into account body mass? Which substance does it use to measure GFR.

A

The Cockcroft-Gault formula.
Uses creatinine concentration.

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29
Q

How does age affect creatinine production and filtration?

A

Older adults lose muscle mass and therefore produce less creatinine.
Additionally, the amount of glomeruli decrease with age.

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30
Q

What are the three kinds of acute Kidney Injury?

A
  1. Pre-renal failure
  2. Primary renal failure
  3. Post-renal failure
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31
Q

What causes pre-renal failure?

A

Decreased perfusion due to loss of blood volume, burns, or congestive heart failure. Reperfusion might cause ischemia-reperfusion injury.

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32
Q

What is intrinsic/primary renal failure?

A

Direct kidney issue due to
–> Toxins (Mercury, iron, etc.)
–> Obstruction to blood flow (Renal embolism/thrombosis, arterial stenosis
–> Autoimmune issue

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33
Q

What is post-renal failure?

A

Obstruction to urine flow
–> Prostatic enlargement, urethra obstruction, etc.

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34
Q

What complications does acute kidney injury cause?

A

–> Less urine production
–> Damage to kidney tubules leads to necrosis and blockages
–> Loss of ability to concentrate urine

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35
Q

How common is AKI? What is its prognosis?

A

30-50% of those admitted to the ICU develop AKI, and the survival prognosis for an AKI is 50%.
If one does recover, they have an increased risk of developing chronic kidney disease later on.

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36
Q

What is renal artery stenosis? What does it cause?

A

Stenotic lesion that causes hardening of the renal artery to a kidney. This triggers activation of the RAAS, which has other downstream effects.

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37
Q

What is nephrolithiasis?

A

The formation of kidney stones

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38
Q

What kind of minerals are renal caliculi usually made of?

A

Calcium oxalate, Struvite, Uric acid, etc.

39
Q

What might cause Kidney stones?

A

Low fluid intake, or dietary sodium/protein. Acidic food can also increase risk. Major component is calcium oxalate.

40
Q

How can kidney stones be treated?

A

Chemolysis of stone through alkalinization of urine.
Diuretics to increase flow rate and inhibit stasis.
Allopurinol to lower uric acid levels.
Lithotripsy (ultrasound) to remove stone.

41
Q

What is hydronephrosis/hydroureter?

A

When fluid is blocked from exiting ureter or bladder and backs up into the kidney.

42
Q

What is vesicourethral reflux?

A

When urine moved backwards from bladder to kidneys, causes hydronephrosis.

43
Q

What are the two kinds of vesicourethral reflux?

A

1° - a congenital malformation of the ureter, usually unilateral

2° - a blockage of the urethra, usually bilateral reflux.

44
Q

How does low vitamin A affect developing kidneys?

A

Can cause dysplasia/ aplasia

45
Q

A low nephron number at birth is associated with…

A

Chronic kidney disease and hypertension.

46
Q

What is CKD

A

Chronic kidney disease is a gradual decline of GFR that progresses over a period of years. It is considered chronic is it has been progressing for over three months.

Eventually leads to End Stage Renal Disease, where renal function is insufficient to maintain homeostasis.

47
Q

A GFR of between 60-90ml/min is considered what?

A

Early-stage kidney disease

48
Q

A GFR between 15-60 mm/min is considered what?

A

Low, kidney disease present.

49
Q

How is kidney disease treated and managed?

A

Controlling BP
–> Target under 130-40 mmHg Systole
–> Can be done with ACEi, ARBs, Diet

Dialysis:
–> Hemodialysis, peritoneal dialysis

Transplant:
–> Rejection is always a possibility
–> Takes time to find right donor

50
Q

How does hemodialysis work?

A

Blood undergoes reverse osmosis, balances electrolytes in blood and remove toxins that build up between sessions.

51
Q

What is a downside of peritoneal dialysis?

A

Over time, the peritoneal membrane becomes less efficient at carrying out dialysis

52
Q

What are some potential causes of CKD?

A

Diabetes (leading cause)
Hypertension
FSGS
Genetic mutations
Immune disorders

53
Q

What size of molecules are not able to pass through glomerular capillaries due to molecular sieving?

A

Molecules greater than 10,000 MW

54
Q

Why does albumin not pass through glomerular capillaries?

A

Glomerular capillary basement membrane, endothelial cells, and podocytes are all negatively charged, and so is albumin. Charge repulsion contributes to low albumin permeability.

Additionally, albumin is too large to be filtered.

55
Q

What are the two physiological responses to podocyte loss?

A

Repair Response
–> Endothelial cell replaces podocyte

Scar Formation
–> Protective mechanism that prevents blood loss due to capillary ballooning
–> Causes permanent damage, increasing workload on healthy capillaries

56
Q

What is podocyte effacement?

A

When the podocyte foot processes flatten and large gaps are present between the foot processes. Gaps are large enough for albumin to pass through - proteinuria.

57
Q

What kind of molecules bind together in a slit membrane to produce a pore that prevents protein from getting through?
What codes for it?

A

NPHS1 codes for nephrin
–> Those with high incidence rate of congenital nephrotic syndrome are unable to produce and arrange these proteins correctly

58
Q

How can the stages of kidney disease be assessed clinically?

A

Albuminuria (stages A1-3) can be used to assess the degree of kidney failure.

59
Q

High protein levels in urine is a risk factor for developing…

A

Kidney failure, heart disease, and HTN.

60
Q

What are primary glomerulopathies?

A

Sources of disease that occur to the glomerulus itself (intrinsic) in the absence of a multi-system disorder

61
Q

What are nephrotic syndromes?

A

A group of symptoms including proteinuria, low blood protein levels, high cholesterol levels, high triglyceride levels, and edema.

62
Q

What is considered proteinuria?

A

> 3.5 grams per day in urine

63
Q

What are nephritic syndromes?

A

A group of disorders that cause swelling or inflammation of the glomeruli and other internal kidney structures.

64
Q

What causes hypertension in those with nephritic syndrome?

A

The inability to remove salt and water from blood.

65
Q

What kinds of conditions might cause nephrotic syndrome?

A

FSGS, congenital conditions, membranous nephropathy, diabetic kidney disease, minimal change disease

66
Q

What is FSGS?

A

Focal segmental glomerulosclerosis is when scaring is found on specific segments and a small subset of glomeruli.

67
Q

Why do sub-Saharan African populations have a higher incidence of some forms of kidney disease?

A

Because a mutation in the APOL1 gene destroys the parasite that causes ‘sleeping sickness,’ but this polymorphism predisposes individuals to kidney disease.

68
Q

What is minimal change disease? Who does it affect most often? How is it treated?

A

Podocyte effacement with no change in gross glomerular architecture - causes heavy proteinuria

Affects children most commonly and can be treated with steroids (which implies T cell invovlement)

69
Q

A larger than normal population of those with minimal change disease have circulating antibodies for….

A

Nephrin

70
Q

What is the most common cause of CKD?

A

Diabetic kidney diseases

71
Q

What occurs in diabetic kidney disease? How is it treated?

A

Functional injury causes increased GFR due to hormones.

Structural injury:
–> Increase is glomerular basement membrane width and mesangial cell hypertrophy
–> Progressive scarring/collapse of glomeruli
–> Tubular lumen obliteration
–> Podocyte loss or damage

Treated by managing BGL and BP

72
Q

In early DKD, there is an increase in GFR. Why?

A

Due to dysregulation of afferent/afferent arteriole constriction due to vasoactive hormones like the RAS system

73
Q

What health promotional activities can treat the diabetes/DKD epidemic?

A

Education, physical activity, better eating habits.

74
Q

What to SGLT2 inhibitors do?

A

Reduces glucose reabsorption in the proximal tubule - more glucose in urine.

75
Q

What kinds of disorders cause nephritic syndrome?

A

Infection or disorders that involve the immune system.
e.g., glomerulonephritis, lupus nephritis, IgA nephropathy, hemolytic uremic syndrome, poststreptococcal GN.

76
Q

What are the symptoms of nephritic syndrome?

A

Hematuria, proteinuria, rapid reduction in GFR, hypertension

77
Q

What is IgA nephropathy?

A

An autoimmune disorder in which IgA antibodies are deposited in the kidneys, causing inflammation and capillary leakage. (Nephritic)

78
Q

What is membranous nephropathy?

A

When antibodies deposit between the glomerular capillary and podocytes - causes inflammation (Nephritic)

79
Q

What kind of autoantibodies underlie most membranous nephropathy cases?

A

sPLA2 autoantibodies

80
Q

What secondary disorders are caused by renal failure?

A

–> Hyperkalemia
–> Edema (generalized + pulmonary)
–> Hypertension
–> Metabolic acidosis
–> Uremia

Seen only in CKD:
–> Anemia
–> Bone disease
–> Failure or concentrate or dilute urine

81
Q

How does angiotensinogen become angiotensin II?

A

Angiotensinogen (from liver ) + Renin (from kidneys) –> Angiotensin I + ACE (from lungs) –> Angiotensin II + ACE2 –> Ang1-7

82
Q

What does angiotensin II do?

A

–> ADH secretin
–> Aldosterone secretion
–> Thirst centre

83
Q

What does aldosterone do?

A

increase salt and water retention

84
Q

What is the role of AngII antagonists?

A

AngII stimulation contributes to resistance of efferent arteriole (vasoconstriction)

Antagonists block this and cause efferent arteriole to dilate, and glomerular capillary pressure returns to normal - protects against damage.

85
Q

How does COVID-19 affect the kidney?

A

After a lung infection the virus might enter the blood and accumulate in the kidney and cause damage to resident renal cells.

If you have been diagnosed with AKI, your chance of surviving a COVID infection greatly decreases.

86
Q

Which receptor does SARS interact with on epithelial cells?

A

The spike proteins on COVID interact with ACE2 receptors on epithelial cells to enter the cell.

When it does this, it internalizes the receptor itself, so there is no anti-inflammatory antagonist to ACE1

87
Q

What do ACE1 receptors do?

A

Signal or vasoconstriction, inflammation, oxidative stress, and apoptosis

88
Q

What do ACE2 receptors do?

A

Signal for vasodilation, angiogenesis, anti-inflammation, anti-oxidation, anti-apoptotic

89
Q

Collapsing FGSG is a characteristic of what infection?

A

COVID-19
–> Capillaries might collapse as they are surrounded by scar tissue

90
Q

Collapsing glomerulopathy is a distinct variant of FSGS. What unique characteristics does it have?

A

–> Segmental or global glomerular turf collapse
–> Hypertrophy and hyperplasia of overlying podocytes

91
Q

Who is of higher risk for collapsing glomerulopathy?

A

Individuals of sub-Saharan African descent with APOL1 polymorphism

92
Q

What drug can be used to decrease uric acid levels?

A

Allopurinol

93
Q

What is the BP goal for Pts with CKD?

A

Systolic between 130-40 bpm.

Patho (14 decks)

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