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Case 22 CKD > CKD > Flashcards

CKD Flashcards

1
Q

What is end-stage renal disease?

A

The point at which renal disease is so severe that RRT is required

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2
Q

What is renal replacement therapy?

A

Haemodialysis (HD), peritoneal dialysis (PD) and renal transplantation

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3
Q

How is proteinuria assessed?

A

using urine Protein:Creatinine (uPCR) or urine albumin:creatinine ratio (uACR)

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4
Q

How is renal function assessed?

A

GFR and eGFR

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5
Q

What could protein on urine dipstick suggest? (2)

A

Dipstick proteinuria may suggest glomerular or tubulointerstitial disease.

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6
Q

What are white cell casts a sign of? (2)

A

interstitial nephritis (especially if eosinophils are present in the urine) or urinary tract infection (UTI).

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7
Q

What do you look at in 24-hour urine collection?

A

Albumin:creatinine ratio (ACR)

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8
Q

If microscopic haematuria is present, what is the next test to be performed on the urine?

A

Sent for a culture to exclude a UTI

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9
Q

What do you do if non-visible haematuria persists?

A

refer for Urological review

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10
Q

What is the most important factor that can be addressed that reduces risk of cardiovascular disease?

A

Blood Pressure

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11
Q

How is CKD staged?

A

Based on eGFR and ACR - Look it up!

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12
Q

How can CKD progression be slowed? (5)

A

1) Diabetes control
2) Cholesterol control
3) Lifestyle advice - weight loss, reducing cholesterol and salt in diet
4) Smoking cessation
5) BP CONTROL!!

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13
Q

What is the most abundant protein in urine?

A

Tamm-Horsfall glycoprotein (THP), also known as uromodulin, is a glycoprotein that is secreted by the renal tubules.

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14
Q

What is abnormal proteinuria?

A

> 150mg/day

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15
Q

What is an early feature of severe renal disease?

A

Microalbuminuria (30-300mg/day) is an early feature of several renal diseases

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16
Q

Which BP tablet is recommended in CKD and why?

A

ACE-I/ARBs. They are reno-protective.

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17
Q

What is the mechanism of damage in diabetic nephropathy? (3)

A

1) Increased glomerular pressure leading to hyperfiltration
2) Barotrauma of mesangial cells
3) Nephron ischaemia

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18
Q

What are the clinical findings in diabetic nephropathy? (3)

A

Increased GFR, detectable proteinuria, microhaematuria kidney failure (decreased urine output)

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19
Q

What investigations are carried out in diabetic nephropathy?

A

Urinanalysis

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20
Q

What is treatment of diabetic nephropathy? (2)

A

Anti-diabetic medication + ACE-I - stop RAS activation

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21
Q

What is CKD?

A

Evidence of damaged renal parenchyma as demonstrated by active urinary sediment and/or structural abnormality (this must be present for stages 1 and 2 CKD) and/or evidence of decreased kidney function as demonstrated by a reduced glomerular filtration rate (GFR) and chronicity to distinguish it from acute kidney injury (AKI).’

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22
Q

What is chronicity in terms of kidney disease?

A

confirmed by the presence of abnormal kidney function by eGFR or proteinuria for >3 months

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23
Q

What are the major causes of mild-to-moderate CKD? (2)

A

Diabetes and HTN

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24
Q

What are the most prevalent causes of severe CKD? (2)

A

younger patients with glomerulonephritis and genetic causes of CKD

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25
Q

What are the side effects of ACE-I? (4)

A

dry cough, angioedema, hyperkalaemia, hypotension

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26
Q

When must ACE-I and ARBs be stopped?

A

AKI

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27
Q

What is a commonly accepted increase in creatinine with ACEIs?

A

25-30% rise

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28
Q

What are the grounds for referral to nephrology? (6)

A

CKD stage 3-5, AKI, urine PCR >100, malignant hypertension, hyperkalaemia, macroscopic haematuria but urological tests (i.e. cystoscopy) negative

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29
Q

What are uACR stages?

A

A1 - <30mg/g
A2 - 30-300mg/g
A3 - >300 mg/g

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30
Q

What the stages of eGFR in CKD?

A 
G1 - >90 - damage with normal 
G2 - 60-89 - damage with mild decrease
G3 - 30-59 - moderate
G4 - 15-29 - severe
G5 - <15 - renal failure
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31
Q

What is Azoteamia?

A

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

32
Q

What is uraemia?

A

Clinical syndrome resulting from failing kidneys and progressive azotaemia

33
Q

What is the target BP in CKD?

A

130/80 or less

34
Q

When do you stop ACE-I/ARBs in a CKD patient? (3)

A

Stop if K+>6mmol/L, reduced eGFR >25% or reduced creatinine >30%

35
Q

What is the HbA1c target in CKD?

A

53mmol/mol (7.0%),

36
Q

At what stage of CKD does anaemia occur?

A

usually in stage 3

37
Q

What is treatment for Anaemia in CKD?

A

IV iron + EPO injections

38
Q

What causes CKD bone-mineral disorders (BMD)?

A

Failure of hydroxylation of vitamin D by kidneys. This leads to lack of calcium absorption and hypocalcaemia which drives secondary hyperparathyroidism.

39
Q

What is the treatment for CKD BMD?

A

Vitamin D supplements. if PTH persists, treat with activated via D analogues.

40
Q

What blood tests do you measure in for CKD BMD?

A

Ca2+, Pi, ALP, PTH and 25-OH vit D if eGFR <30.

41
Q

How do you manage fluid and electrolyte balance?

A

Restrict fluid and salt intake

42
Q

How do you manage oedema?

A

High dose loop diuretics

43
Q

How is acidosis treated?

A

HCO3- replacement

44
Q

What are the treatment for increased CVD risk?

A

Atorvastatin, BP control, aspirin (atherosclerotic events)

45
Q

When should prep for RRT begin?

A

CKD stage 4 or risk of renal failure is 10-20% within year

46
Q

What are the options for CKD stage 5?

A

PD, HD, transplant, conservative management

47
Q

What immunisations do CKD patients require?

A

pneumococcal, influenza, hep B

48
Q

How is stage 1&2 managed?

A
  • smoking cessation, exercise, cholesterol, BP, ACEI/ARB
49
Q

How is stage 3 managed?

A

As in stage 1&2 +:

Immunise
Aspirin, EPO, alfacalcidol, bicarbonate, diuretic

50
Q

How is stage 4 managed?

A

As for previous stages +:

prepare for RRT, treat any complications

51
Q

How is stage 5 managed?

A

As in earlier stages+:

HD/PD, vascular access, transplant workup, living donor

52
Q

At what eGFR should metformin be stopped?

A

Less than 30mL/minute/1.73m^2

53
Q

What is the interaction between simvastatin and amlodipine?

A

Increased risk of myopathy and rhabdomyolysis

54
Q

What are the indications for dialysis?

A
  • pH <7.25
  • K+ > 7 mmol
  • Fluid overload
  • Toxins - SLIME = salicylate, lithium, isopropanol, magnesium, ethanol glycol
  • Creatinine >400
  • Uraemic symptoms (N&V, cognitive impairment, pericarditis, pruritus)
55
Q

How do the osmotic diuretics work?

A

Act at the PCT and thick descending limb to Increase solute concentration (osmolality) prevents the reabsorption of water which will reduce plasma volume

56
Q

How do loop diuretics work?

A

Loop diuretics block the Na+/K+/2Cl- co-transporter by stopping chloride transport. Na+ reabsorption is also blocked, hence loss of countercurrent mechanism + loss of water reabsorption

57
Q

How do thiazide diuretics work?

A

Act at the Na+/Cl- cotransporter at the DCT + increase water excretion

58
Q

What is a side effect of thiazide diuretics?

A

Increases urea reabsorption at PCT –> increase plasma uric acid levels –> GOUT

59
Q

How does spironolactone work?

A

It is a K+ sparer. It blocks aldosterone which stops Na+/K+ insertion at DCT + collecting ducts. This stops Na+ and water reabsorption.

60
Q

What are the requirements for HD?

A

Creation of AV fistula or central (tesio) line, dietary changes

61
Q

What needs to done before PD can start?

A

Tenckoff catheter insertion

62
Q

What are problems with HD?

A

Access (fistula: stenosis, thrombosis, steel syndrome.

Tunnel line: infection, blockage,

Dialysis disequilibrium, hypotension, time-consuming, diet+fluid restriction, tiredness, hospital based small bleeding risk due to anti-coagulation

63
Q

What are the problems with PD

A

Catheter site infection, PD peritonitis, hernia, loss of membrane function over time (6 years), regular laxatives to keep bowels open

64
Q

What are main contraindications for HD?

A

Inability to achieve suitable vascular access

65
Q

What the main contraindications for PD?

A

IBD, ischaemic bowel, acute diverticulitis, abdominal abscess, pregnancy 3rd trimester

66
Q

What does bone biochemistry show in hyperparathyroidism?

A

1) Primary hyperparathyroidism - high PTH, low Pi, high Ca2+
2) Secondary - High PTH, low calcium, high Pi
3) Tertiary - high PTH, high Ca2+, high Pi

67
Q

What are the advantages of renal transplant?

A

Independence, significant survival advantage, no diet/fluid restriction, few symptoms, less complications

68
Q

What are the disadvantages of Renal transplant?

A

Immunosuppression SEs, infections, malignancy

69
Q

What are the advantages of HD?

A
  • 4 days a week dialysis free
  • more healthcare pro support
  • treatment can be given during dialysis
70
Q

What are the advantages of PD?

A
  • less fluid/food restrictions
  • home based
  • no blood, no needles
  • more portable
  • less time for permanent access placement
71
Q

What 4 variables are used to in the MDRD equation to calculate eGFR?

A

Creatinine, Age, Gender, Ethnicity (CAGE)

72
Q

How does acute graft rejection present? (2)

A

Acute rejection occurs within 6 months, typically presents with signs and symptoms of infection

73
Q

How is acute graft rejection managed?

A

Increased steroid dose

74
Q

What are RBCs and Red cell casts in urine suggestive off?

A

Urine sediment with red blood cells and red blood cell casts suggests proliferative glomerulonephritis.

75
Q

What is the target BP for diabetics?

A

< 140/90

Case 22 CKD (1 decks)

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