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kidney pathophysiology Flashcards

1
Q

what is CKD?

A

chronic kidney disease - broad term for any abnormality of kidney structure and associated health implications

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2
Q

what eGFR is seen in CKD?

A
  • eGFR <60ml/min
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3
Q

what are the most common cause of CKD?

A

DM and hypertension

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4
Q

what does CKD increases the risk of?

A
  • increases risk of CVD, ESRF (end stage renal failure) , anaemia, metabolic bone disease
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5
Q

how do you measure kidney function?

A
  • blood test for eGFR
  • urine test for albumin, creatinine
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6
Q

what does eGFR calculation include?

A
  • uses serum Cr, age, gender – no longer using race
  • includes muscle mass, age and pregnancy within calculation
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7
Q

what advice is given to someone undergoing a eGFR test?

A
  • advise associated with test: no meat (or protein supplements) for 12 hrs prior
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8
Q

what is serum cystatin C test?

A

more accurate eGFR test

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9
Q

why is serum cystatin C not used as often?

A
  • more expensive and not used as often as eGFR
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10
Q

when would serum cystatin C be used?

A
  • used in patients with extremes in muscle mass – body builders
  • used if uncertainty within eGFR and ACR (albumin: creatinine ratio)
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11
Q

what does albumin creatinine ration show?

A
  • independent risk factor for CKD progression
  • increases glomerular permeability
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12
Q

what is the most common protein secreted in urine?

A

albumin

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13
Q

when would you measure ACR in those at risk of CKD?

A

annually

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14
Q

apart from CKD when would you see proteinuria?

A
  • proteinuria may be present with UTI, prolonged exercise, menstruation, sepsis
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15
Q

when would you want to retrieve an ACR sample?

A
  • want an early morning urine sample – first wee of day
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16
Q

what result suggests a normal to mild ACR?

A
  • <3mg/mmol
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17
Q

what result indicated moderate increase of ACR?

A
  • 3-30mg/mmol
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18
Q

what result indicates severely increased ACR?

A
  • > 30mg/mol
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19
Q

what is stage 1 CKD?

A

Stage 1: Kidney damage with normal kidney function
- GFR >90

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20
Q

what is stage 2 CKD?

A

Stage 2: kidney damage with mild loss of kidney function
- GFR 89-60

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21
Q

what is stage 3a CKD?

A

Stage 3a: mild to moderate loss of kidney function
- 59-45 GFR

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22
Q

what is stage 3b CKD?

A

Stage 3b: moderate to severe kidney function
- GFR 44-30

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23
Q

what is stage 4 CKD?

A

Stage 4: severe loss of kidney function
- GFR 29-15

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24
Q

what is stage 5 CKD?

A

Stage 5: kidney failure
- GFR <15

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25
Q

what would you do with a persistent haematuria?

A
  • Persistent haematuria – 2 week wait referral (suspect malignancy  bladder, pelvis, prostate, kidney, sometimes cervical), ultra sound sonograph needed
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26
Q

what is a CKD patient more likely to die from?

A
  • 20x more likely to die from CVD than progress to ESRF
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27
Q

what lifestyle advice would you give to someone with CKD?

A

Lifestyle: no direct link between lifestyle and CKD risk
- Address to reduce CVD risk
- Weight reduction
- Diet, exercise
- Smoking: CVD risk

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28
Q

what is a target BP in non DM with CKD?

A
  • Target BP in non DM - <140/90
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29
Q

what is a target BP for a DM patient with CKD?

A

<130/80

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30
Q

what is the benefit of ACEi in CKD patients?

A
  • Lower BP and urinary protein excretion
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31
Q

what medication is given as CVD prophylaxis?

A
  • 20mg atorvastatin TO ALL for prophylaxis of CVD
  • Aim: reduce LDL cholesterol
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32
Q

what meds are no longer advised for primary prevetion within CKD?

A

anticoags
but CKD does increase risk of thrombotic and bleeding tendancy

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33
Q

what are risk factors for diabetic nephropathy?

A
  • Risk factors: poor glycaemic control, uncontrolled HTN, smoking, abnormal lipids
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34
Q

how can diabetes lead to glomerulosis?

A
  • Associated to glomerulosclerosis  hyperglycaemia causes damage to small blood vessels and can cause leaks. High blood pressure can also exacerbate this. Abnormal amounts of protein gets through and excreted in urine
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35
Q

what anaemia is seen with CKD?

A

Anaemia: normocytic, normochromic anaemia> increased CVD and mortality

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36
Q

what is the consequence of anaemia within CKD?

A

 Reduced EPO production, increased RBC fragility, ureamia induced reduced erythropoiesis

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37
Q

how would you monitor bone disease within CKD?

A

Bone disease: monitor Ca2+, phosphate, vitD, PTH and ALP

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38
Q

when does bone disease become more apparent among CKD?

A

later stages

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39
Q

define AKI?

A

Acute kidney injury: abrupt deterioration in renal function over days and weeks

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40
Q

what clinical signs would diagnose AKI?

A
  • Rise in serum creatinine of 26 micromol/ or greater within 48hrs
  • It may be increased for a few days if someone is generally unwell
  • NICE: 50% increase in serum creatinine if baseline was known from previous 7 days. A fall in urine output to less than 0.5ml/kg/hr for more than 6hrs
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41
Q

what blood urea would indicate pre renal?

A
  • Pre renal failure: >100;1 – more urea than creatinine
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42
Q

what blood urea: creatinine ratio would indicate intrinsic?

A
  • Intrinsic: <40:1 – creatinine more raised than urea
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43
Q

what blood ure: creatinine ratio indicates a post-renal failure?

A
  • Post renal: 40-100 – normal
44
Q

what can cause pre-renal failure?

A

reduced perfusion to kidney
hypovolaemia
anatomical
drug induced

45
Q

what would cause reduced perfusion causing pre-renal aetiology?

A
  • Reduced perfusion to kidney – hypovolaemic, euvolemic and hypervolemic states
46
Q

what would cause hypovolaemia in pre renal?

A
  • Absolute hypovolemia: haemorrhage, over- diuresis, vomiting and nausea
47
Q

what low wffective arterial blood volume causes?

A

heart failure, cirrhosis, sepsis, third spacing fluid

48
Q

what drugs would cause pre renal failure?

A

NSAIDs, ACEi, diuretics

49
Q

what would is intra-renal failures?

A

structural or functional changes at the level of nephron

50
Q

what can cause a intra renal failure?

A
  • Acute tubular necrosis (ATN): most common cause of AKI which occurs due to ischaemic or toxic injury to cells of PCT
  • Acute intestinal nephritis (AIN): most often eosinophilic nephritis that can be drug induced (NSAIDs, penicillin), infection – induced (TB, legionella) or immune mediated (sarcoidosis, SLE or igG-related disease)
  • Glomerular disease: included nephrotic and nephritis syndromes which may be primary renal disease (anti-glomerular basement membrane, or part of systemic disease with immune complex deposition
  • Intra-tubular obstruction: multiple myeloma with paraprotein, pigment (rhabdomyolysis)
  • Other: scleroderma renal crisis, malignant hypertension
51
Q

what can cause post renal obstructive pathology?

A
  • Ureters: nephrolithiasis, retroperitoneal fibrosis
  • Bladder: bladder cancer
  • Prostate: benign prostatic hyperplasia (BPH), prostate
  • Urethra: urethral structure
  • External: retroperitoneal mass, ovarian tumours
52
Q

name some risk factors for AKI

A
  • Chronic kidney disease, history of AKI
  • Heart failure, liver failure
  • Diabetes
  • Oliguria
  • Neurological or cognitive impairment or disability – which may mean limited access to fluids because of reliance on a carer
  • Hypovolaemia
  • Use of drugs that can cause exacerbate kidney injury
  • Symptoms or history or urological obstruction or conditions that may lead to obstruction
  • Sepsis
  • Deteriorating warning scores
  • Age 65yrs +
53
Q

what would ACEi
ARB
Cyclosporin
NSAIDs
Tacrolimus
do to the kidneys?

A

GFR alteration
Affect the vascular tone of afferent and efferent arterioles, altering interglomerular blood flow

54
Q

what would Aminoglycosides
Amphotericin B
cisplatin
do to the kidneys?

A

tubular cell toxicity
direct toxicity to epithelial cells of PCT

55
Q

what do NSAIDs and rifampin do to the kidneys?

A

interstitial nephritis
inflam reaction within iterstitial of kidney

56
Q

what would acyclovir and ampicillin do?

A

crystal nephropathy
can result in precipitates of insoluble crystals

57
Q

how can NSAIDs contribute to pre-renal failure?

A

NSAIDs block prostaglandin mediated vasodilation of the afferent arteriole – limits kidneys ability to regulate local blood flow

58
Q

how can NSAIDs contribute to intra-renal failure?

A

NSAIDs can cause acute interstitial nephritis (AIN)

59
Q

how can NSAIDs contribute to post-renal?

A

long term NSAID can cause renal papillary necrosis where the medullary papilla sloughs off, causing obstruction to urine flow

60
Q

why is history important to AKI?

A

AKI can occur over hours to days: presenting history will provide clues to the likely cause of AKI
- AKI can present as asymptomatic or non-specific symptoms of fatigue, nausea and confusion

61
Q

what on the clinical exam indicate AKI?

A
  • Oliguria or anuria
  • Signs of hypovolaemia – dry mucous, reduced skin turgor, tachycardiac, hypotension
  • Signs of volume overload: hypertension, pulmonary oedema, peripheral oedema, elevated JVP
  • signs of uraemia: ecchymosis due to platelet dysfunction, uraemic encephalopathy eg asterixis, confusion, seizures
  • signs of post-renal obstruction: palpable or tender to distended bladder
62
Q

what labs must be done for AKI and why?

A
  • U&Es: creatinine, blood urea nitrogen, calcium, phosphate, potassium, sodium
  • FBC: anaemia, leukocytopenia, thrombocytopenia
  • Liver function tests (LFT): serum albumin
  • Venous blood gas: assess for acidaemia
63
Q

what urine studies should be done for AKI?

A
  • Urine analysis: proteinuria, albuminuria, haemoglobinuria, haematuria, WBC, glucose
  • Urine volume measurement: oliguria, anuria
  • Urinary microscopy and sediment: casts, crystals
  • Urine osmolarity and specific gravity: dehydration, less commonly use din clinical practice
  • Urinary eosinophil count: useful in evaluation of AIN (rare), less commonly used in clinical practice
64
Q

what imaging can be done to diagnose AKI?

A
  • Post void residual volume: can be assessed rapidly using a bedside bladder scanner
  • Ultrasound of kidneys, ureters and bladder (KUB): assess kidney size, hydroephrosis, post renal obstruction, renal lesions
  • CT non contrast: radiopaque and non-radiopaque calculi, uretic obstruction
  • CT urogram: investigate for urinary tract bleeding
  • CT triphasic kidneys: dedicated cross sectional imaging for renal lesions – often used to clarify masses on ultrasound
65
Q

what is the general management for AKI?

A

SICK DAY: stop any nephrotoxic drugs, adjust drug doses to prevent drug toxicity
- Fluid resuscitation can rapidly improve renal function in hypovolaemia/ hypotension
- Urinary catheterisation can be used where there is difficulty in measuring urine output to do relieve urinary obstruction
- Assess for evidence of sepsis and initiate six care bundle

66
Q

what is the ABCDE approach to AKI?

A
  • ABCDE – address drugs, Boost blood pressure, calculate fluid balance, Dip urine, Exclude obstruction
67
Q

when would renal replacement be indicated?

A
  • Metabolic acidosis
  • Refractory electrolyte abnormalities (hyperkalaemia .6.5mmol)
  • Presence of dialysable toxins – toxic alcohols, aspirin, lithium
  • Refractory fluid overload – diuretic resistant fluid overload in setting of AKI
  • End-organ uraemic complications: pericarditis, encephalopathy, uraemic bleeding
  • AEIOU are indications of renal replacement: Acidosis, Electrolyte imbalance, Ingested toxins, fluid Overload, Uraemia
68
Q

what complications of AKI are concerning?

A
  • Fluid overload – leg oedema, pulmonary oedema, plueral effusions
  • Electrolyte derangement – hyperphosphatemia, hyperkalaemia
  • Acid-base complications of uraemia
  • CKD, end-stage renal disease, death
69
Q

what is an AKI?

A

rapid drop in kidney function - seen in rise in serum creatinine

70
Q

describe the changes in creatinine used to diagnose AKI?

A

rise of 25mmol/L in 48hrs
rise of 50% in 7days
<0.5ml/kg/hr for 6hrs

71
Q

define CKD

A

reduction in kidney function sustained over 3mths
permanent and progressive

72
Q

how would you assess obstruction causes in AKI and CKD?

A

ultrasound

73
Q

what is classes as accelerated progression in CKD?

A

decrease in eGFR by 15ml/min/1.73 each year
or decline by 25%

74
Q

what are RF for AKI?

A

acutely unwell - post surgery, infectious
older age, CKD, HF, DM< HTN,
cognitive impairment - not drinking enough
medications, contrast

75
Q

what drugs can be nephrotoxic?

A

gentamicin
aceI
nsaids
diuretics

76
Q

how would you investigate ckd and why?

A

U&E - egfr and ACR for staging
ultrasound - obstructive
urine dip/MC&S: protein and haematuria
BP- hypertension
HbA1c: DM
lipid proflie: hypercholesterolemia

77
Q

what are risk factors for CKD?

A

DM and HTN
CVS disease
smoking obesity
black, asian ethnic minorities

78
Q

what are the pre renal causes of aki?

A

insufficient blood supply - dehydration, shock, HF

79
Q

what are the intrinsic causes of AKI?

A

ATN, glomerulonephritis, acute tubular necrosis, haemolytic uraemic syndrome, rhadomyolysis

80
Q

what are post renal - obstructive causes inAKI and CKD?

A

kidney stones
tumours, strictures to ureters, BPH, neurogenic bladder

81
Q

what is neurogenic bladder?

A

lack of bladder control due to CNS or PNS damage

82
Q

how might an AKI present?

A

non specific:
N+V,
dehydration, confusion,
abdo pain, back pain,
oedema, reduced urine output

83
Q

how might CKD [present and why?

A

might be asymptomatic until it progresses - non-specific
fatigue
pallor- anaemia (lack of EPO production)
anorexia
prurtitis: build up of toxins
oedema, HTN
peripheral neuropathy - build up of toxins

84
Q

what are the complications of AKI?

A

fluid overload
HF
pulmonary oedema
hyperkalaemia
metabolic acidosis
uraemia - encephalopathy, pericarditis

85
Q

what are the complications of CKd?

A

anaemia - reduced EPO production
renal bone disease - build up of phosphorus - as kidneys chnage vitD tpo active form
cvd, peripheral neuropathy, end stage -kidney disease, dialysis related complications

86
Q

how does vitD link to kidney disease?

A

kidneys responsible for chnaging vitD to active form
active D brings Ca into bones as well as absorbing Ca in intestines and kidneys

87
Q

how can you prevent an AKI?

A

adequate fluid intake, avoid nephrotoxic drugs, additional fluids before and after contrast

88
Q

what do you include in AKI management and why?

A
  1. IV fluids: dehydration amd hypovolemia
  2. withhold nephrotoxic meds - nsaids, aceI
  3. adjusting meds: metformin, opiates
  4. relieve obstriuction: catheter
  5. dialysis in severe cases
89
Q

when should you involve a renal specialist in ckd?

A

eGFR <30, ACR>70
accelerated progression
5yr risk >5%
uncontrolled HTN

90
Q

in CKD what BP should you aim for?

A

130/80

91
Q

what general amangemet is given to CKD patients?

A

atorvostatin 20mg
exercise, diet, smoking cessation

92
Q

what diabetic medication are beneficial in ckd?

A

SGLt: if acr >30
dapliflozin: 3-30

93
Q

when should an ACEi be initiated in CKD?

A

diabetic +ACR >3
HTN and ACR >30
anyone with ACR >70

94
Q

what needs to be monitored with ACEi esepcially in CKD?

A

hyperkalaemia - check UEs

95
Q

what is given for anaemia in CKD?

A

EPO stimulating agents eg recomb human erythopoiteins
IV iron

96
Q

what blood product should be avoided in anaemia by CKD?

A

blood transfusion - risk of sensitisation and rejection in organ donation

97
Q

what is acute tubular necrosis?

A

damage and death of epithelial cells in renal tubules
most common cause of AKI

98
Q

what causes ATN?

A

hypoperfuion - ischaemia
nephrotoxins: gentamicin, nsaids, aceI

99
Q

how would you diagnosis ATN?

A

urinalysis: muddy bronw casts

100
Q

how do you manage ATN?

A
  1. IV fluids: dehydration amd hypovolemia
  2. withhold nephrotoxic meds - nsaids, aceI
  3. adjusting meds: metformin, opiates
  4. relieve obstriuction: catheter
  5. dialysis in severe cases
    like AKI - may take 1-3 weeks to recover
101
Q

what blood results are seen in renal bone disease by CKD?

A

high phosphate
low calcium
low VIt D

102
Q

how do you manage renal bone disease in CKD?

A

low phosphate diet
phosphate binders
calcitrol
good Ca intake

103
Q

how should CKD induced osteoporosis be managed?

A

bisphosphonates

104
Q

what is osteomalacia?

A

occurs due to increased turnover of bones without adequate calcium supply.

105
Q

what is osteosclerosis?

A

occurs when the osteoblasts respond by increasing their activity to match the osteoclasts, creating new tissue in the bone. Due to the low calcium level, this new bone is not properly mineralised.

106
Q

what is rugger jersey spine?

A

is a characteristic finding on a spinal x-ray. This involves sclerosis of both ends of each vertebral body (denser white) and osteomalacia in the centre of the vertebral body (less white). The name refers to the stripes found on a rugby shirt.

107
Q
A

GI (12 decks)

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