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HDT 2.1 > Kidney diseases and functions > Flashcards

Kidney diseases and functions Flashcards

1
Q

Name the function of the kidneys

A
  • Homeostasis; regulates and maintains the the body states at various-different parameters
  • > elimination of waste
  • > water homeostasis
  • > acid base homeostasis; need to pass enough enough H+ ions to prevent acidosis
  • > electrolyte homeostasis
  • > blood pressure control
  • Excretion of drugs and drug metabolites
  • Metabolic/ Endocrine
  • > synthesis of hormones; Vitamin D, Erythipoietin, Renin
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2
Q

How would you measure kidney function?

A

the serum creatinine which is the traditional measure

- influenced by gender, ethnicity, age, body mass, diet

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3
Q

What does the graph for GFR vs plasma creatinine look like?

A
  • as kidney function declines, the creatinine levels increase (GFR decreases)
  • not sensitive to small changes
  • non-linear relationship to kidney function
  • doesn’t take long-term changes into account
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4
Q

How would you estimate the GFR?

A
  • calculate from creatinine, age, gender, ethnicity
  • better reflection of kidney function
  • best measure for use in stable renal function
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5
Q

Is CKD irreversible or reversible?

A

irreversible and tends to progress

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6
Q

How many stages of CKD are there?

A

CKD 1-5
stage 5 is the worst it shows kidney failure of levels of 0-15 eGFR
CKD 4- Severe decrease in GFR ; 15-29; feeling tired and insulin doses and drug tablets
CKD 3- moderate CKD; 30-59
CKD2- kidney damage but mild; 60-89
CKD 1- kidney damage but normal GFR; >90

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7
Q

What occurs with CKD 5?

A
  • end stage renal failure
  • insufficient renal function to sustain life/health
  • > haemodialysis
  • > peritoneal dialysis
  • > kidney transplantation

death
- there are renal replacement therapies are essential to prevent progression of kidney failure7

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8
Q

Who has CKD?

A
  • common
  • most of it unrecognised
  • diabetes and renovascular disease lead to CKD and most common
  • more common with older age
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9
Q

What are the risk factors for CKD?

A
  • increased age
  • hypertension (highest risk)
  • diabetes
  • smoking
  • poor education
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10
Q

Causes of CKD

A
  • systemic diseases; diabetes, hypertension, atherosclerotic disease
  • immune mediated diseases; IPA nephropathy
  • infectious diseases; HIV, HBV, HCV, TB
  • genetic diseases; polycystic kidneys
  • arterial disease; atherosclerosis
  • obstruction; tumours, stones, fibrosis
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11
Q

With chronic glomerulonephritis, what happens to the glomeruli and tubules?

A

sclerosed glomeruli and atrophied tubules

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12
Q

What is the pathology of CKD?

A
  • thickening of basement membrane; capillary walls become weak and bleed and leak protein; slow blood flow
  • mesangial expansion
  • > hyperglycaemia stimulates increased matrix production by mesengial cells
  • > stimulation of TGF-beta release
  • glomerulosclerosis
  • > due to intraglomerular hypertension or ischaemic damage
  • high levels of sugarcane also make vessels to become narrow and clogged
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13
Q

Explain the vascular disease- renal artery stenosis

A
  • low blood flow
  • consequence of poor diet and diabetes
  • both or one of the arteries leading to the kidneys becomes narrowed
  • cant use an ACE inhibitor
  • we want to constrict the afferent arterial to maintain BP and glomerular pressure
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14
Q

List the complications of CKD

A
  • anaemia
  • hypertension
  • disturbed calcium
  • CVD
  • Bone disease
  • immune suppression
  • bleeding tendency
  • treatment complications
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15
Q

What does the failure of fluid homeostasis lead to?

A
  • inability to concentrate urine
  • > loss of diurnal rhythm of urine excretion
  • > limited rate of water excretion
  • inability to excrete water load
  • > oedema
  • > hypertension
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16
Q

What is the treatment for fluid overload?

A
  1. diuretics
  2. salt restriction
  3. fluid restriction

if doesnt work then dialysis and transplant

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17
Q

What do electrolytes such as sodium do and cause?

A
  • major cause of hypertension and fluid overload; damage to vessels and blood flow
  • sodium must be within normal range
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18
Q

What do electrolytes such as potassium do and cause?

A
  • enormous functional reserve to excrete potassium
  • severe hyperkalaemia when GFR <10ml/min
  • due to:
  • > excessive load
  • > interference with potassium excretion; acidosis with volume contraction and diabetic nephropathy
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19
Q

What ECG changes are seen with hyperkalaemia?

A
  • tall T waves
  • long QRS interval
  • long PR interval
  • cardiac arrest

-> alterations in membrane excitability

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20
Q

what is the treatment to prevent hyperkalaemia and hypernatraemia?

A
  • salt restriction
  • K+restriction
  • dialysis and transplants if all else fails; drugs that act as K+ binders
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21
Q

State the equation for the carbonic acid buffer system and how this system works

A

CO2 + H20 H2CO3 H+ + HCO3-

  • increasing H+ due to failure to excrete acid leads to increase in HCO3- and so increase in CO2 and H20
    the CO2 is removed by lungs to maintain pH
    there is an accumulation of hydrogen acid
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22
Q

What are the effects of acidosis?

A
  • increased respiratory drive; breathless
  • chest pain
  • confusion
  • bone pain
  • demineralisation of bone
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23
Q

What is the treatment for metabolic acidosis?

A
  • sodium bicarbonate
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24
Q

What does Vitamin D, renin and erythropoietin control?

A

Vitamin D- calcium metabolism
Erythropoietin- haemoglobin production
Renin- control of blood production

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25
Q

what is hypertension? and what mechanisms occur?

A
  • high BP
  • accelerates decline of kidney function
  • contributes to CV risk

mechanisms:

  • sodium retention
  • volume expansion
  • RAS activation
  • sympathetic nervous system activity
  • endothelial dysfunction
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26
Q

What is the treatment for hypertension?

A
  • salt restriction
  • diuretics
  • RAS blockade
  • other antihypertensive med
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27
Q

What happens when excretory function reaches failure?

A
  • accumulation of toxic waste products
  • > creatinine rises only after significant renal damage
  • > nitrogenous waste retention occurs
  • > urate retention then occurs
  • > phosphate retention then will occur
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28
Q

what is the treatment for uraemia?

A
  • dialysis or transplantation
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29
Q

why is protein restriction not used as treatment for uraemia?

A

due to it causing malnutrition which weakens the individual further

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30
Q

what happens when drugs fail to be excreted?

A
  • many drugs are usually excreted by the kidney but the metabolism of these drugs will be impaired by renal failure
  • toxicity due to accumulation of the drug will lead to:
    insulin-> hypoglycaemia
    opiates-> narcosis
    anitbiotics-> encephalopathy
    sedatives-> respiratory arrest
    digoxin-> cardiac arrythmias
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31
Q

explain the purpose of dialysis?

A

dialysis removes the waste products and excess body fluids from the individual when the kidneys are failing to excrete these substances

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32
Q

explain what is narcosis

A

it is when a patient is in a state of unconsciousness or arrested activity due to narcotics or chemicals in the body

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33
Q

how can you prevent drug toxicity?

A

you can modify the prescription according to the renal function

  • adjust the dose when needed
  • adjust the frequency when and if needed
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34
Q

What three diseases show the greatest risk of harm when a patient has all of them?

A

CKD, CVD, diabetes

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35
Q

Why does CKD progress?

A
  • major modifiable risk factors
  • > uncontrolled underlying disease
  • > hypertension
  • > proteinuria
  • > smoking
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36
Q

What is the treatment for the CKD?

A
  • control underlying diseases
  • treat hypertension
  • ACEi/ARB
  • stop smoking
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37
Q

what is acute kidney injury?

A

a rapid decline in kidney function and kidneys stop working properly

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38
Q

how can AKI be detemined?

A

Stage 1- >26umol/L increase
Stage 2- 100-200% increase
Stage 3- >200% increase or >354umol/L or needs dialysis

urine output
S1- <0.5ml/kg/hour for 6 hours
S2- <0.5ml/kg/hour for 12 hours
S3- <0.3ml/kg/hour for 24 hours or anuria for 12 hour or needs dialysis

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39
Q

Who is at risk of AKI?

A
  • older age
  • diabetes mellitus people
  • people with hypertension
  • heart disease
  • liver disease
  • CKD
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40
Q

what medication Is needed for AKI?

A
  • ACEi/ARB
  • Gentamicin
  • Vancomycin
  • Chemotherapy
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41
Q

Name the causes of AKI?

A
  • pre-renal; perfusion failure
  • renal; intrinsic disease of the kidney
  • post-renal; obstruction of the urinary system
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42
Q

What is the purpose of renal auto regulation?

A

maintain constant eGFR/BP across diff blood pressure

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43
Q

What worsens perfusion failure?

A
  • RAS blockade
  • NSAID
  • diuretics
  • antihypertensives
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44
Q

how does BV and BP affect perfusion failure?

A

high BP+ high BV leads to high Renal perfusion and so normal urine production

normal levels of BP and BV lead to normal levels of renal perfusion and urine production which maintains perfusion

low BP and low BV leads to normal renal perfusion and urine production

low BP and low BV lead to low renal perfusion and low urine production; this is AKI

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45
Q

how does the afferent arterial allow perfusion?

A
  • it forces blood into the kidneys
46
Q

which way does the blood flow?

A

from the afferent to the efferent arterial

47
Q

what happens to the glomerulus and the blood flow when angiotensin I and angiotensin II act and the patient has low BP?

A
  • the angiotensin I and the angiotensin II will cause constriction and this maintains kidney perfusion
  • the vessels are narrower and so the BP will rise as a result
48
Q

what happens when prostaglandins act on the glomerulus?

A
  • they increase renal blood flow by causing vasodilation

- this increases BP in turn

49
Q

what effect does ACEi/ARB have on glomerulus and what happens when NSAIDS are taken with ARB/ACEi?

A
  • stops vasoconstriction

- NSAIDs and ACEi/ARB together combined can cause AKI

50
Q

What occurs when RAS blockade happens and leads to perfusion failure with low BP and low BV?

A
  • lower eGFR occurs

- the drugs will inhibit the process and so the BP will not increase (this is due to an angiotensin system)

51
Q

What is the treatment of perfusion failure?

A
  • treat the underlying cause
  • > fluid vol. replacement
  • > blood pressure support (inotropic drug to allow kidney perfusion)
  • > restore arterial patency
  • stop NSAID
  • stop RAS blockade
52
Q

Name the type of drugs that are directly to toxic to the kidneys

A
  • drugs that are toxic need monitoring
  • some drugs are toxic if serum levels are too high
  • > gentamicin, vancomycin
  • some drugs crystallise in the tubules
  • > indinavir
53
Q

What drugs crystallise in the tubules?

A
  1. aciclovir
  2. indinavir
  3. sulfadiazine (antiviral)
54
Q

explain what is nephrocalcinosis and how it occurs

A
  • when there is too much calcium and phosphate deposition in the kidney
  • is caused by OTC calcium antacids and large quantities
  • this impairs kidney function sufficiently
55
Q

What drugs need careful dose monitoring for AKI?

A
  • drugs with predictable effects
  • amikacin
  • vancomycin; do not give high doses as can have toxicity effect
  • gentamicin
  • > narrow therapeutic range
  • > epithelial, glomerular toxicity
56
Q

what is intersitital nephritis?

A
  • the kidneys filter waste and extra fluid from the body
  • with this the spaces between the tubules become inflamed and so the kidney cant filter properly
    common with:
  • NSAID
  • PPI
  • anti-retroviral drugs
  • other antibiotics
57
Q

How much affect does metformin have on lactic acidosis?

A
  • metformin reduces mortality in type II diabetes
  • in AKI this may result in lactic acidosis or metabolic acidosis
  • there will be a decreased gluconeogenesis, conversion of lactate to pyruvate and then glucose
  • metformin decreases glucose production in liver
  • > glucose neurogenesis which increase sensitivity and decreases glucose absorption
  • the build up of metformin in kidney causes acid build up
58
Q

what drugs are effected by reduced drug clearance caused by AKI

A
  • aminoglycosides
  • penicillins
  • opiates
  • benzodiazepines
  • insulin

excretion of these relies on kidney so in AKI when this function it reduces this affects these drugs

59
Q

What are some causes of AKI death?

A
  • underlying disease
  • sepsis
  • infection
  • acidosis
  • pulmonary oedema
  • hyperkalaemia
60
Q

What is dialysis?

A

an extracorporeal therapy where fluid and solutes are removed/added to the patient’s blood
- works by separating the blood and dialysis fluid with a semipermeable membrane

  • only has a GFR of <15mls/min
61
Q

what are semipermeable membranes?

A
  • permeable to some solutes but not all

- permeability is determined by size and charge

62
Q

how are drugs in dialysis cleared?

A

by diffusion

63
Q

What is peritoneal dialysis?

A
  • out the solution into the peritoneal cavity and allow it to drain after a period of time
  • it removes what kidney filters out of blood
  • it does it several times a day
64
Q

how do patients do peritoneal dialysis?

A
  • at home
  • either overnight or continous
  • lasts 8-10 years or so
  • there risk of peritonitis
  • need a permanent peritoneal catheter
65
Q

what do patients with harm-dialysis need permanent access to?

A
  • the circulation
  • AV fistula
  • central venous catheter
66
Q

what is haemodialysis?

A

purifies the blood when kidneys are not working properly

67
Q

why do patients with CKD need dialysis?

A
  • depends on the symptoms and fluid volume control

- usually when eGFR <10ml/min/1.73m2

68
Q

why do patients with AKI need dialysis?

A
  • usually creatinine >500mcmol/L or oligo/anuric

- uraemia; pericarditis and encephalopathy

69
Q

how is drug clearance affected by dialysis?

A
  • depends on the nature of the drug
  • > solubility, size and charge
  • depends on the membrane pore size and charge
  • depends on drug distribution and renal and non-renal metabolism
70
Q

What drug is Vancomycin? What is clearance time for different conditions

A
  • it is a large glycopeptide antibiotic
  • 90% excreted unchanged by kidneys
    clearance:
  • normal is 4-6 hours
  • CKD5 is 54-180 hours
  • no kidneys is 7.5 days
  • with harm-dialysis its 6 hours with high flux and 7 days standard
71
Q

what is it important to remember with vancomycin dialysis doses?

A

to allow sufficient interval times with doses

72
Q

what are the endocrine functions of the kidney?

A
  • renin production
  • erythropoietin function and production
  • Vitamin D activation and function
  • > respective control of calcium and phosphate
73
Q

what does lack of erythrocytes results in?

A

anaemia

  • fatigue
  • reduced exercise tolerance
  • reduced brain function
  • increased risk of CVD
74
Q

what is erythropoiesis?

A

red blood cell production

75
Q

what does hypoxia increase?

A

it increases red cell production

76
Q

what was the process of the transfer of “hemopoietine” between rabbits?

A
  • first make rabbit anaemic
  • then remove its plasma
  • transfer plasma into another anaemic rabbit
  • the rabbit started to produce RBC appropriately
77
Q

what is the advantage of the erythropoietin being produced in the kidney?

A
  • constant blood flow rates

- stable O2 supply to use ratio

78
Q

how is erythropoietin gene transcription increased?

A
  • low iron
  • hypoxia
  • low haemoatocrit
79
Q

what is the main site of erythropoietin production?

A

cortical fibroblasts

80
Q

where is foetal erythropoietin made?

A

in the liver

81
Q

where is erythropoietin mRNA transcribed?

A

in the hypoxic cortical peritubular fibroblasts

82
Q

with normal o2 levels, what can hydroxylation of proline lead to?

A
  • can lead to proteasomal degradation
83
Q

when there is low o2 levels, will hydroxylation occur? what will form instead?

A
  • hydroxylation doesn’t occur
  • a stable complex will form with:
  • > HIF-1beta
  • > hypoxia response elements; transcription factors
  • > leads to gene transcription
84
Q

what occurs when HIF-1alpha is degraded with normal O2?

A

HIF-1alpha is degraded by the ubiquitin-proteasome pathway. it then will bind to von hippel-lindau tumour suppressor protein to form a complex
at the same 2 oxoglutarate will undergo a process with the presence of FE2+ and O2 to form succinate and Co2

85
Q

why is it important for HIF-1alpha to be stabilised? how is it stabilised?

A

hydroxylation is inhibited with hypoxia and so HIF-1alpha is stabilised and will form a complex with HIF-1beta

  • the stable HIF-1alpha in the cytoplasm can transfer to nucleus to then bind to the HIF-1beta
86
Q

after HIF-1beta HIF-1alpha complex is formed, what happens?

A
  • it will then form a complex with the hypoxia responsive element (AHNT) and this will activate gene transcription
87
Q

what is the AHNT?

A

Aryl Hydrocarbon Nuclear Translocator

88
Q

how is erythropoietin gene transcription controlled?

A

controlled by cellular iron and o2 levels

89
Q

when p300 binds to a HIF-ARNT what is formed?

A

mRNA is formed

90
Q

where is the erythropoietin receptor expressed

A

it is expressed on red cell precursors

91
Q

what does signalling from the erythropoietin receptor lead to?

A
  • decrease in apoptosis
  • increase in proliferation
  • increase in differentiation to necessary RBC to increase oxygen carrying capabilities
92
Q

what does erythropoietin stimulate?

A

the increase production of red cells

93
Q

what is the function of erythropoietin?

A

when iron levels are low erythropoietin will enter kidney to stimulate bone marrow to produce RBC to increase oxygen carrying capacity

94
Q

what occurs from the interaction between erythropoietin and Angiotensin II?

A

Angiotensin II increases erythropoietin production

however ACEi and ARB will reduce the production

95
Q

how can erythropoietin be a drug of abuse?

A

can increase haematocrit and so increased endurance and exercise capacity
can have risk of clots and some potentially dangerous

96
Q

what can the consequences of failed erythropoietin production be?

A
  1. this means less oxygen delivery to tissues
  2. impaired quality of life and so impaired cognition and reduced exercise capacity
  3. becomes sensitive to blood types and so transfusion required; iron overload can occur which is hard to get rid out of the body
  4. there’s an increased risk of left ventricular hypertrophy
  5. increase CV disease in patients with CKD and anaemia
97
Q

what should be monitored with the endocrine functions of the kidney?

A
  • Hb target 100-200g/L; done at unit and monthly checks for EPO
  • BP; 180 over 90 and anything over should reduce dose and increase dose intervals
  • thrombosis; inflammation
  • anaemia teams
98
Q

what can EPO cause and where should it be avoided?

A
  • can cause endothelial damage and so should be avoided with CV stent
99
Q

what is calcium and phosphate vital for?

A 
calcium
- cardiac and muscle function
- nerve function 
- blood clotting and bone metabolism 
phosphate
- muscle and cardiac function
- bone metabolism 
- cellular functions; energy metabolism and cell signalling
  • both ions are tightly controlled serum conc.
100
Q

where is calcium and phosphate widely distributed?

A

in the tissues with huge reservoir in bone

101
Q

what key hormones are involved in the control of Ca and phosphate?

A

Vitamin D and parathyroid hormone

102
Q

what organs are involved in the homeostasis of calcium and phosphate?

A

bones and heart- exchange with the bone pool
kidneys- filtration and reabsorption; can remove/absorb when necessary and allow it to be maintained in the blood to maintain the serum conc of both
kidneys are also involved in their excretion

103
Q

what is the molecule 1,25 dihydroxycholecalceiferol important for?

A

important in the regulation of

  • serum calcium
  • serum phosphate
  • bon turnover
  • other CV, immunological and cell proliferation functions
104
Q

where is VD activated? how is this done

A
  • activated in proximal tubule epithelial cells
  • occurs in the cells mitochondria
  • activated by two protein hydroxylation steps
    1. hydroxylated in the liver to form 25-OHD from D3 (cholecalcerifol) which is catalysed by the enzyme vitamin D 25-hydroxylase and then expressed by hepatocytes. this is released into the plasma to then bind to the DBP
    2. then transported to the kidneys where its metabolised at the 1-alpha position to form 1,25(OH)2D3
105
Q

how can 25(OH)2D3 transported around the body?

A

when this molecules binds to the DBP it can be transported to the kidneys intestines bones

106
Q

how does the inactivation of Vitamin D occur?

A
  • occurs when 1,25 (OH)2D3 undergoes hydroxylation with a catalyst of 24-hyroxylase enzyme into calcitroic acid which is soluble and inactive
107
Q

what is the role of vitamin D?

A
  • promotes Ca and Phosphate uptake from intestinal lumen
  • vital for osteoblast and osteoclasts activity
  • increases calcium re-absorption from tubule
  • maintains normal serum calcium
  • induces calcium sensor expression on parathyroid glands
  • suppresses 1alpha-hydroxylase and promotes 24-hydroxylase in the kidney
108
Q

what is the role of Vitamin D, Calcium and parathyroid hormone in renal failure?

A

when there is low calcium this is detected and a signal is sent to the parathyroid and so PTH is released into kidney and bone; this stops 1,25 Vit D being produced and increased bone resorption occurs which leads to increased serum Ca2+ to stop PTH release

109
Q

what risks are there with ectopic calcification?

A
  • risk of CV
  • risk of calcification of vessels
  • cause mortality
110
Q

what treatments prevent bone disease and ectopic calcification?

A
  • 1alpha-hydroxylated vitamin D replacement
  • phosphate restriction
  • phosphate binders
  • calcimimetics

if all this fails

  • parathyroidectomy
  • > remove parathyroid glands to stop negative feedback failure
111
Q

what interactions does vitamin d have?

A

has interactions with parathyroid hormone which increases Calcium ion uptake from the gut

112
Q

what type of hormone is vitamin D?

A

a steroid hormone

HDT 2.1 (11 decks)

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