Chronic Kidney Disease Flashcards

1
Q

what is orthostatic proteinuria

A

benign condition, high urinary protein excretion during the day associated with activity and upright posture

due to compression of LRV between aorta and SMA

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2
Q

what causes proteinuria

A
CKD 
after physical exercse
fever 
pregnancy 
UTI 
nephrotic syndrome
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3
Q

how do you measure 24h urinary protein excretion and what does it show?

A

spot test for protein:creatinine ratio, shows rate of progression of kidney disease

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4
Q

how do you measure albumin:creatinine ratio and what else is measured alongside?

A

creatinine clearance
24hour urine collection

albumin is most common protein in urine

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5
Q

why is proteinuria considered pathological?

A

bc LMW proteins are normally filtered and reabsorbed by glomeruli
= high glomerular permeability

30-300mg albuminuria is pathological

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6
Q

what does azotaemia mean

A

elevation of nitrogenous metabolic waste in blood due to failure of clearance in the kidneys

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7
Q

what is uraemia

A

clinical syndrome resulting from failing kidneys and progressive azotaemia

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8
Q

what parts of kidney absorb what?

A

REFER TO CASE notes

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9
Q

what is CKD?

A

reduction in kidney function for > 3 months
eGFR of <60 on 2 seperate occasions, with 90 days between them both
evidence of kidney damage in urine, biopsy or renal tract

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10
Q

what direct causes are there for kidney disease?

A
diabetes 
hypertension uncontrolled
glomerulonephritis 
polycystic kidney disease 
medications such as NSAID's, proton pumps and lithium 
UTIs 
auto immune disease
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11
Q

what are other RF for CKD?

A

older age, smoking, family history, low birth weight, reduced kidney mass

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12
Q

how does CKD present?

A

usually asymptomatic

or pruritus, loss of appetite, nausea, oedema, muscle cramps, peripheral neuropathy

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13
Q

what is the eGFR

A

capillaries have a high UF coefficient
pressure of blood through the glomerulus is the hydrostatic pressure
acting oppositely is the negative oncotic pressure: keeps fluid not leaving circulation
capillaries allow fluid to leak out through fenestrations = gfr

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14
Q

what functions does the kidney have?

A
  • ultrafiltration/reabsorptive functions
    -urine dilution
    excretory functions of H+, K+, creatinine
  • activation of vitamin D
  • renin production
    -EPO production
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15
Q

what investigations would you do for CKD?

A
  • eGFR (creatinine based estimate)
  • ACR
  • urine dip for haematuria
  • renal USS
  • blood tests (mentioned later)
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16
Q

what does a high blood creatinine mean?

A

poor clearance of creatinine by kidneys (this is a product of wear and tear of muscles)

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17
Q

when do you refer to renal specialists?

A

eGFR <30 urgent
30-59 routine referral if other signs eg ACR, haematuria, fall in GFR > 5ml in 1 year

immediate: malignant hypertension, hyperkalemia
urgent: proteinuria with oedema and low serum albumin

routine referral for proteinuria and urine PCR/ACR, haematuria

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18
Q

what blood tests would you do for CKD?

A
  • FBC for Hb, WCC (immunosuppressed)
  • calcium and phosphate
  • HbA1c
  • PTH can cause itch, hypercalcaemia
  • immunosuppression level
  • sodium bicarbonate: low indicates metabolic acidosis
  • serum potassium bc CKD and ACE-I = hyperkalaemia
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19
Q

how do you stage CKD?

A
G score: based on eGFR 
1 >90
2: 60-98
3a 45-59
3b 30-44
4: 15-29
5: <15

A score is based on ACR ratio
A1: <3
2: 3-30
3: >30

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20
Q

what are the complications of CKD?

A
anaemia 
renal bone disease
CV disease
peripheral neuropathy 
dialysis related problems
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21
Q

what is the management of CKD initially?

A
  • slow progression, reduce risk of complications
  • hence optimise hypertensive control and optimise diabetic control
  • treat glomerulonephritis
  • lifestyle changes
  • low phosphate,
  • atorvastatin 20mg
22
Q

how to treat complications of CKD?

A
  • oral sodium bicarbonate to treat MA
  • iron supplementation and EPO to treat anaemia (may need IV bc renal patients may not absorb it properly)
  • vit D to treat renal bone disease
  • RRT if ESRD
23
Q

how do you treat hypertension in CKD?

A
  • ACE-I
  • offered to all patients with comorbidities and ACR>30
  • everyone with ACR>70
24
Q

why do you get anaemia in CKD?

A
  • kidney cells produce EPO so damage to them = reduced RBC

- IV iron, then offer EPO replacement

25
Q

what is renal bone disease?

A

CKD mineral and bone disorder

osteomalcia, osteoporosis and osteosclerosis

26
Q

what is the pathophysiology of RBD?

A

high serum phosphate
low active vitamin D bc kidney is meant to do this
vit D important in calcium absorption
PT glands react to low calcium and high phosphate = excrete PTH to remove phosphate
= increased osteoclast activity
= osteomalacia occurs due to increased turnover of bones without adequate calcium supply
= osteoscleorisis bc new tissue is created but not mineralised due to low calcium

27
Q

how do you manage RBD?

A

alfacalcidol and calcitriol = active forms of vitamin D
low phosphate diet
bisphosphonates can be used to treat osteoporosis

28
Q

what are the indications of renal failure?

A
  • increasing acidosis
  • increasing potassium urea and creatinine
  • partial respiratory compensation
  • renal failure is <15ml / min
29
Q

what are the indications for dialysis?

A
pH <7.25
K+ >7
fluid overload 
creatinine >400
toxins SLIME 
uraemic pericarditis
30
Q

haemodialysis?

A

filtration of blood through dialsysi machine
AV fistula created / use neck for IV line
blood passes through dialyser
fluid restriction and diet changes

31
Q

what are the disadvantages of haemodialysis?

A
  • infection, IE, stenosis at site, air embolus etc

- CI: low BP, dementia, severe HF, bleeding disorders

32
Q

what is peritoneal dialysis?

A
  • dialysis solution injected into abdominal cavity through permanent catheter
    -draws waste products from blood
    leave to dwell: exchange
33
Q

what are the disadvantages of having peritoneal dialysis?

A
  • constipation
  • peritonitis, infection, catheter blockage
  • fluid retention
  • hernias
34
Q

what are the contraindications of peritoneal dialysis?

A
  • IBD, diverticulitis, abdominal abcess, pregnancy, hernias, obesity, blindness
35
Q

what are the 2 types of peritoneal dialysis?

A

CAPD: exchange is 30 mins, dwell time is 4-8 hours

APD: dialysis machine fills and drains abdomen while patient is sleeping, 3-5 exchanges over 8 hours

36
Q

how does a kidnet transplant work?

A

donor is transplanted into groin, renal vessels from donor connected to iliac vessels of recipient
- ureter and recipients bladder joined together

37
Q

what medications do you have to take after transplantation?

A

cyclosporin or tacrolimus which act on t-lymphocytes and puts them to “sleep”
MMF or azathioprine
= risk of infection

38
Q

what are the complications of a renal transplant?

A

infections: UTI and chest most common, cholecystitis etc all lifethreatening
- malignancy of kidney

39
Q

what are clinical features of a failing renal transplant?

A

anaemic, pale, skin lesions

pulm oedema, tachypnoeic due to MA, pleural effusion

hypertension, pericardial rub

ascites

neuro: restless leg syndrome, uraemic flapping tremor, myoclonic jerks

40
Q

what is the relationship between ACEI-/ARBs and CKD?

A

= renoprotective in CKD, including diabetics

AVOID IN AKI

ARBs reduce proteinuria

contra indicated in pregnancy

41
Q

why are ACE-I contraindicated in AKI?

A
  • angiotensin 2 inhibits efferent arteriole
    but in AKI, body wants to maintain the pressure and vasoconstricts it
    hence if patient is on ACE-I it cannot do this
42
Q

what drugs should you avoid in renal failure?

A
  • antibiotics
  • NSAIDs
  • lithium
  • metformin
43
Q

what is the pathophysiology of diabetic nephropathy

A

hyperglycaemia results in constant activation of renin, as does poor blood flow to kidney (due to hypertension etc)

efferent arteriole is vasoconstricted so increase in pressure

barotrauma = affects mesangial cells = expansion = leaky capillaries

44
Q

what are the clinical findings of diabetic nephropathy

A

initially, increased eGFR
detectable proteinuria
microhaematuria
eventually low eGFR and decreased urine output

45
Q

how do you treat diabetic nephropathy

A

control BP

ACE-I and diabetic meds prevent constant activation of RAAS

46
Q

what is EPO

A

growth factor stimulating production of RBC
secreted by kidney in response to cellular hypoxia

main use of exogenous EPO is to treat anaemia associated with kidney disease

47
Q

what are the side effects of EPO

A
accelerated hypertension 
bone aches
flu like symptoms 
skin rashes 
pure red cell aplasia
48
Q

how do osmotic diuretics work and give an example

A

eg mannitol

work in PCT and LOH, increase solute concentration within tubules so water retains within tubule

49
Q

how do loop diuretics work and give an example

A

eg furosemide

work at LOH and ascending limb sympotrer, prevents chloride from being reabsorbed and hence affects sodium reabsorption so water is excreted out more too

relieves stress in heart conditions bc lowers plasma volume and hence lowers BP

50
Q

How do thiazide like diuretics work and give an example

A

work on sodium and chloride symporter in DCT
increases excretion of sodium, potassium and water
increases reabsorption of urea in pCT
= SE is gout bc uric acid

eg hydrochlorithiazide

51
Q

how do potassium sparing diuretics work and give an example

A

work in DCT and CD
decrease reabsorption of sodium but prevent excretion of potassium
eg amiloride