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Renal Flashcards

1
Q

State some prerenal causes of AKI due to volume depletion

A

diarrhoea, vomiting
burns
diuresis
haemorrhage

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2
Q

State some prerenal causes of AKI due to hypoperfusion

A 
embolus
renal artery stenosis
NSAIDs
ACEi
AAA
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3
Q

State some prerenal causes of AKI due to hyotension

A

sepsis
anaphylaxis
cardiogenic shock

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4
Q

State some prerenal causes of AKI due to oedema

A

cardiac failure
cirrhosis
nephrotic syndrome

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5
Q

What are some renal causes of AKI

A

glomerular disease
tubular injury
acue interstitial nephritis
vascular disease

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6
Q

What drugs are nephrotoxins causing acute tubular necrosis

A

aminoglycosides, amphotericin and ciclosporin

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7
Q

What drugs are nephrotoxins causing glomerulonephritis

A 
penicillamine, 
gold, 
captopril, 
phenytoin  
some antibiotics, including penicillins, sulfonamides and rifampicin
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8
Q

What drugs are nephrotoxins causing interstitial nephritis

A

penicillins, cephalosporins, sulfonamides, thiazide diuretics, furosemide, NSAIDs and rifampicin.

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9
Q

What are some causes of post-renal AKI

A 
pelvic mass
bladder cancer
BPH
stricture of ureters
calculi
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10
Q

What are the key findings to diagose AKI

A

raise in creatinine
fall in eGFR
decreased urine output

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11
Q

Who is at increased risk of AKI

A 
post surgical
>65y
past AKI
dehydrated
diabetes
CKD
heart failure
nephrotoxic drugs
liver disease
use of iodinated contrast in 7/7
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12
Q

What is the definition of oliguria?

A

<0.5ml/kg/hr

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13
Q

Define stage 1 AKI

A

Creatinine rise of 26 micromol or more within 48 hours

Creatinine rise of 50–99% from baseline within 7 days* (1.50–1.99 x baseline)

Urine output < 0.5 mL/kg/h for more than 6 hours

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14
Q

Define stage 2 AKI

A

100–199% creatinine rise from baseline within 7 days* (2.00–2.99 x baseline)

Urine output** < 0.5 mL/kg/hour for more than 12 hours

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15
Q

Define stage 3 AKI

A

200% or more creatinine rise from baseline within 7 days* (3.00 or more x baseline)

Creatinine rise to 354 micromol/L or more with acute rise of 26 micromol/L or more within 48 hours or 50% or more rise within 7 days

Urine output < 0.3 mL/kg/hour for 24 hours or anuria for 12 hours

Any requirement for renal replacement therapy

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16
Q

How should i check the volume status of a patient with AKI

A

Core temperature.
Peripheral perfusion.
Heart rate/blood pressure (and any postural changes).
Jugular venous pressure.
Moistness of mucous membranes, skin turgor.

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17
Q

What signs should i look for on examination of patient with AKI

A

Signs of infection or sepsis.
Signs of acute or chronic heart failure.
Fluid status (dehydration or fluid overload).
Palpable bladder or abdominal/pelvic mass.
Features of underlying systemic disease (rashes, arthralgia).

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18
Q

What investigations should i do for a patient with AKI?

A

Bedside: urinalysis, ECG
Bloods: FBC, U+E, Cr, CRP, LFT, CK, ESR, coag, ANA, serum Ig. ABG if
Micro: blood culture, culture infection sources
Imaging: USS bladder, CXR (pulmoary oedema), AXR (renal calculi), CTKUB if obstruction persists after catheter

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19
Q

What are the indications for RRT in AKI?

A 
uraemic pericarditis
uraemic encephalopathy
refractory hyperkaleamia
refractory pulmonary oedema
severe metabolic acidosis <7.2pH
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20
Q

When should a patient with AKI be referred to a nephrologist?

A 
hyperkalaemia
uraemia
glomerulonephritis
systemic disease
no obvious reversible cause
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21
Q

What information does a nephrologist want to know about a patient with AKI?

A 
history and timecourse
U+E
urine dipstick
drugs
fluid balance
current volume status
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22
Q

What is glomerulonephritis?

A

inflammation of the glomeruli and nephrons!

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23
Q

What can cause glomerulonephritis?

A 
minimal change disease
FSGS
membranous glomerulonephritis
SLE
amyloidosis
diabetes
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24
Q

What drugs should be stopped in AKI due to the fact they will worsen it?

A 
NSAIDs
• Aminoglycosides
• ACE inhibitors
• Angiotensin II receptor antagonists
• Diuretics
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25
Q

What are the features of hypokalaemia on ECG/

A

u waves
flattened t waves
prolonged QT interval

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26
Q

Name some reasons for extrarenal loss of K+

A

vomiting
diarrhoea
villous adenoma

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27
Q

Name some reasons for renal loss of K+

A 
diuretics - loop and thiazide
mineralocorticoid excess 
- Conn's
- Cushing's
- corticosteroids
- ectopic ACTH
renal tubular acidosis
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28
Q

What is the mechanism for loop and thiazide diuretics causing hypokalaemia

A

loop and thiazide diuretics increase sodium delivery to the distal segment of the distal tubule,
activation of the renin-angiotensin-aldosterone system
Increased aldosterone stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion,

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29
Q

What is the mechanism of loop diuretics?

A

inhibit the sodium-potassium-chloride cotransporter in the thick ascending limb

leads to a significant increase in the distal tubular concentration of sodium, reduced hypertonicity of the surrounding interstitium, and less water reabsorption in the collecting duct.

diuresis (increased water loss) and natriuresis (increased sodium loss)

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30
Q

What is the mechanism of thiazide diuretics

A

inhibit the sodium-chloride transporter in the distal tubule

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31
Q

Name some reasons for the shift of K+ into cells causing hypokalaemia

A

insulin
salbutamol
catecholamines

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32
Q

Name some reasons decreased intake of K+ causing hypokalaemia

A

prolonged fasting

anorexia

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33
Q

What are the clinical features of hypokalaemia?

A 
lethargy
muscle weakness
u waves on ECG
ileus
arrhythmias
cardiac arrest
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34
Q

What is the treatment for hypokalaemia

A

oral KCL
IV KCL if <2.5 or at risk of arrhythmias
correct underlying cause

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35
Q

What broad categories can be the cause of hypokalaemia

A

reduced intake
uptake into cells
renal loss
GI loss

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36
Q

What causes of hypokalaemia are associated with alkalosis?

A

vomiting
diuretics
Cushing’s syndrome
Conn’s syndrome

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37
Q

Why can diuretics cause alkalosis

A

the increase in distal tubular sodium concentration stimulates the aldosterone-sensitive sodium pump to increase sodium reabsorption in exchange for potassium and hydrogen ion, which are lost to the urine.
The increased hydrogen ion loss can lead to metabolic alkalosis.

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38
Q

What causes of hypokalaemia are associated with acidosis?

A

diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis

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39
Q

What drug can hypokalaemia increase the toxicity of?

A

digoxin

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40
Q

What is the most worrying consequence of hyperkalaemia

A

VF

cardiac arrest

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41
Q

Broadly speaking, what are the reasons that hyperkalaemia occurs

A

excess release from cells

potassium retention

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42
Q

What are the causes of potassium retention leading to hyperkalaemia

A

renal failure
decreased mineralocorticoids - Addison’s, ACEi, ARB
diuretics - K+ sparing, spironolactone

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43
Q

Describe the mechanism of action of potassium sparing diuretics

A

directly inhibit ENaC
inhibiting sodium reabsorption, so less potassium and hydrogen ions are exchanged for sodium by this transporter and therefore less potassium and hydrogen are lost to the urine.
can cause hyperkalaemia

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44
Q

Describe the mechanism of aldosterone receptor antagonists

A

antagonize the actions of aldosterone (increased Na+ excretion by ENaC, at the distal segment of the distal tubule.
causes more sodium to pass into the collecting duct and be excreted in the urine.

less potassium and hydrogen ion are exchanged for sodium by this transporter and therefore less potassium and hydrogen are lost to the urine.

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45
Q

What are the causes of excess potassium release leading to hyperkalaemia

A

rhabdomyolysis
haemolysis
GI bleed
acidosis

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46
Q

What are the signs of hyperkalaemia on ECG

A 
tall-tented T waves,
 small P waves, 
prolonged PR interval
widened QRS - sine wave appearance
asystole
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47
Q

What are the steps in treatment of hyperkalaemia in an emergency

A

stabilise cardiac membrane - 10ml 10% calcium gluconate over 2 mins

move K+ into intracellular space - insulin + glucose (10 units actrapid in 50ml 20% glucose), nebulised salbutamol

remove K+ from body - calcium resonium

dialysis if refractory

48
Q

When is hyperkalaemia considered an emergency?

A

K+ >6.5

ECG changes seen

49
Q

What is the treatment for mild hyperkalaemia

A

restrict oral and IV potassium

50
Q

What are common causes of CKD

A 
hypertension
diabetes
nephrotoxic drugs
SLE
vasculitis
glomerulonephropathy
polycystic kidney disease
recurrent pylonephritis
obstruction
51
Q

Which drugs can cause CKD

A 
lithium
ciclosporin
aminoglycosides
tacrolimus
mesalazine
52
Q

What are the key investigations in suspected CKD

A

Bedside: urine dipstick, urine sample A:Cr, urinalysis

Bloods: FBC, U+E, Cr, glucose, autoantibodies, Ca2+, phpsphate, vit D, PTH

Micro: urine MC+S

Imaging: AXR, USS KUB, CTKUB

special tests: biopsy if kidneys normal size

53
Q

What complications does uraemia cause in CKD?

A 
pericarditis
encephalopathy
nausea
vomiting
bleeding
neuropathy
54
Q

What causes renal bone disease?

A

loss of renal function that activates vitamin D (1-alpha hydroxylation)
less absorption of dietary Ca2+
increased PTH
hyperphosphateaemia
destruction of bones by osteoclasts to raise Ca2+
osteodystrophy

55
Q

Why does anaemia develop in CKD

A

reduced EPO
bone marrow not stimulated
less red blood cells made

56
Q

How is renal bone disease treated?

A

1alpha hydroxycholecalciferol = alfacalcidol = vitamin D analogue
calcium supplements
phosphate binders - decrease phosphate absorption

57
Q

how is anaemia treated in CKD

A

EPO

58
Q

how is acidosis treated in CKD

A

sodium bicarbonate supplements

59
Q

how is oedema treated in CKD

A

loop diuretics

fluid restriction

60
Q

how is hypertension treated in CKD

A

ACEi or ARB

61
Q

How is the risk of CVD managed in CKD

A

statin

aspirin

62
Q

What can cause increase the rate of progression of CKD

A 
AKI
Heart failure - chronic, 
Peripheral arterial disease
Hypertension and/or proteinuria .
Diabetes
Smoking.
NSAIDs
Nephrotoxic drugs such as lithium, ciclosporin, and diuretics.
Untreated urinary outflow tract obstruction
Structural renal tract disease
renal calculi.
Multi-system diseases with potential kidney involvement, such as systemic lupus erythematosus (SLE).
63
Q

What is the MDRD

A

Modification of Diet in Renal Disease (MDRD) equation

used to estimate the GFR using serum creatinine

64
Q

What variables are used when calculating the MDRD

A

serum creatinine
age
gender
ethnicity

65
Q

What are the limitations of eGFR

A

may be affected after protein rich meal 12 hours before test - rasied creatinine
not validated in mild renal disease
affected by muscle mass
pregnancy

66
Q

If a patient with CKD is discovered to have proteinuria, what is the best management?

A

blood pressure control - ACEi

67
Q

Depending on ACR result, what is the best course of action in CKD

A

An ACR of less than 3 mg/mmol does not require further action.

An ACR of 3-30 does not usually require action, though would be checked annually.

An ACR of greater than 30 suggests significant leakage of protein through the kidneys, and the higher the level the more concern, especially if it is over 100.

68
Q

What should be done before prescribing any drug in CKD?

A

check how its administration should be altered!

renal drug handbook!

69
Q

Which drugs are particularly significant in terms of dose modification in CKD

A 
aminoglycosides
cephalosporins
heparin
lithium
opiates
digoxin
70
Q

What are the indications for dialysis in CKD

A 
uraemic pericarditis
uraemic encephalopathy
hyperkalaemia
acidosis
pulmonary oedema
71
Q

What defines end stage renal failure

A

need for RRT

GFR <15

72
Q

What defines stage 1 CKD

A

GFR >90

with presence of kidney damage

73
Q

What counts as ‘presence of kidney damage’ in the CKD stages

A

proteinuria
haematuria
evidence or abnormal anatomy
evidence of systemic disease

74
Q

What defines stage 2 CKD

A

GFR 60-89

with presence of kidney damage

75
Q

What defines stage 3a CKD

A

GFR 45-59

76
Q

What defines stage 3b CKD

A

GFR 30-44

77
Q

What defines stage 4 CKD

A

GFR 15-29

78
Q

What defines stage 5 CKD

A

GFR <15

79
Q

State the basic mechanism of action of haemodialysis

A

AV fistula formed
blood and dialysis fluid separated by semipermeable membrane
flow in opposite directions
solutes move from blood to fluid

80
Q

How long does it take for an AV fistula to be usable after it has been formed

A

8 weeks

81
Q

why do the dialysis fluid and blood need to flow in opposite directions in haemodialysis

A

so the blood always meets a less concentrated solution

allows diffusion down concentration gradient from blood to fluid

82
Q

State the basic mechanism of action of peritoneal dialysis

A

uses peritoneum as semipermeable membrane
permanant catheter inserted into peritoneal cavity
isotonic/hypertonic glucose solution infused into peritoneal cavity
solutes move from blood into peritoneum
drained after several hours

83
Q

Why is hypertonic fluid used in peritoneal dialysis

A

removes excess fluid from body

84
Q

What are the key indications for renal transplant?

A 
ESRF
polycystic kidney disease
diabetes
pyelonephritis
glomerulonephritis
85
Q

What are the contraindications for renal transplant

A 
Cancer.
Active infection.
Uncontrolled ischaemic heart disease.
AIDS with opportunistic infections.
Active viral hepatitis.
Extensive peripheral vascular disease.
86
Q

What are the common problems caused by haemodialysis

A 
inconvenience - 4h 3xweek
high cost
increased risk cardiovascular disease
fluid restriction
fistula problems - thrombosis, infection
disequilibration syndrome
hypotension
87
Q

What are the common problems caused by peritoneal dialysis

A

peritonitis

exit site infection

88
Q

Which organisms commonly cause peritonitis in peritoneal dialysis patietns

A

Staphylococcus epidermidis

Staphylococcus aureus

89
Q

What are the common problems caused by renal transplant

A

immunosupression leads to infection and malignancy
graft failure
cardiovascular disease

90
Q

What cancers are more likely after immunosupression following renal transplant

A

lymphoma

skin

91
Q

Name some common drugs used for immunosupression following renal transplant

A 
tacrolimus
ciclosporin
azathioprine
prednisolone
sirolimus
monoclonal antibodies
92
Q

Name some of the infections that are likely after immunosupression following renal transplant

A

HSV
Candida
Pneumocystis jirovecii
CMV

93
Q

What are the side effects associated with tacrolimus and cicllosporin

A

hypertension, tremor, increased incidence of diabetes mellitus and renal impairment

94
Q

What are the side effects associated with azathioprine and mycophenolate

A

neutropenia

95
Q

Define nephrotic syndrome

A

proteinuria >4.5g in 24h
hypoalbuminaemia <30g/L
peripheral oedema

96
Q

What is the pathophysiology behind nephrotic syndrome

A

damage to podocytes leads to widening of filtration barrier
high molecular weight proteins can leak through the basement membrane and into the glomerulus
not reabsorbed, so lost in urine

97
Q

What are the causes of nephrotic syndrome

A 
glomerulonephritis - minimal change, membranous, FSGS
diabetes
amyloidosis
SLE
multiple myeloma
98
Q

Describe the key features of minimal change disease

A

affects children
mainly idiopathic
can be due to NSAIDs or Hodgkin’s lymphoma
responds well to steroids

99
Q

Describe the key features of membranous glomerulonephritis

A

can be caused by infection, rheumatoid drugs and cancer
thickened BM
IgG and C3 present

100
Q

Describe the key features of FSGS glomerulonephritis

A

mainly idiopathic

IgM and C3

101
Q

What investigations should be done in suspected nephrotic syndrome

A

urinalysis, BP, 24hr urine collection, urine P:Cr
FBC, U+E, glucose, lipid profile, ANA, Ig screen
USS KUB
renal biopsy

102
Q

What is the differential diagnosis in nephrotic syndrome

A

CCF

liver disease

103
Q

What are the compliciations of nephrotic syndrome

A

hypercoaguability - leads to DVT, renal vein thrombosis
hypercholesterolaemia
increased susceptibility to infection - esp pneumococcal

104
Q

Why does hypercoaguability occur in nephrotic syndrome

A

loss of ATIII in urine

105
Q

Why does increased susceptibility to infection occur in nephrotic syndrome

A

loss of Ig

106
Q

What is the treatment for nephrotic syndorme

A

reduce oedema - loop diuretics eg IV furosemide
prevent loss protein - ACEi
reduce complications - anticoagnulation. statins, pneumococcal vaccine
treat underlying cause

107
Q

What are the key investigations to rule out multiple myeloma?

A

plasma electrophoresis

urine electrophoresis - Bence-Jones proteins

108
Q

Define nephritic syndrome

A

haematuria
mild proteinuria
inability to excrete fluids - leading to oedema and HTN
reduced eGFR - leading to uricaemia

109
Q

What are the causes of nephritic syndrome

A

rapidly progressive glomerulonephritis
- due to Goodpasture’s, Wegener’s SLE
IgA nephropathy

110
Q

Describe the key features of Goodpasture’s syndrome

A

affects lungs and kidney
anti-GBM antibody
leads to acute renal failure and pulmoanry haemorrhage

111
Q

Describe the key features of Wegener’s granulomatosis

A

affects upper airway, lungs and kidneys
cANCA
crescents seen in glomeruli on microscopy

112
Q

Describe the key features of SLE

A

affects joints, kidneys and skin

ANA, anti dsDNA

113
Q

Describe the key features of IgA nephropathy

A

history of upper respiratory infections

mesangial IgA deposits

114
Q

What are the features of chronic GN on USS kidneys

A

small shrunken kidmeys

115
Q

What investigations should be done in suspected glomerulonephritis

A

urine dipstick, urine microscopy, urine protein
FBC, U+E, eGFR, Cr, ANA, dsDNA, antiGBM, cANCA
blood cultures
USS kidneys
renal biopsy

116
Q

What are the features of atherosclerotic renal artery stenosis

A

HTN - due to reduced blood flow to kidneys, so increased RAAS
fluid overload of bilateral
small kidney on USS

Finals (32 decks)

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