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Urinary system > Chronic kidney disease > Flashcards

Chronic kidney disease Flashcards

1
Q

List the functions of the kidneys

A
  • Control of BP
  • Excretion of nitrogenous waste
  • Drug metabolism and disposal
  • Maintenance of acid and electrolyte balance
  • Activation of vitamin D
  • Production of erythropoetin
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2
Q

What was the traditional definition of chronic kidney disease?

A

Irreversible and significant loss of renal function, and thus problems with the various roles of the kidneys

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3
Q

How do we assess kidney function?

A

Filtration (excrete out) function – use estimates of GFR (eGFR) from creatinine blood test

Filtration (keep in) function – check for presence of blood or protein in urine

Anatomy – histology, radiography

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4
Q

What problems arise when using creatinine to assess GFR?

A 
o	Muscle mass
•	Age
•	Ethnicity
•	Gender
•	Weight
o	Other sources
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5
Q

What ethnic group have higher creatinine levels?

A

African Americans will have a higher serum creatinine level at any level of creatinine clearance because they have a higher muscle mass.

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6
Q

What formulae are used to estimate GFR from serum creatinine?

A
  • Cockcroft Gault
  • MDRD 4 variable equation
  • CKD-EPI equation
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7
Q

What crosses the glomerular basement membrane but is not necessarily reabsorbed?

A

– Water
– Electrolytes
– Urea
– Creatinine

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8
Q

What is the current definition of chronic kidney disease?

A

Chronic kidney disease (CKD) is defined by either the presence of kidney damage (abnormal blood, urine or x-ray findings) or GFR<60 ml/min/1.73m2 that is present for ≥3 months

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9
Q

What complications are associated with chronic kidney disease?

A
  • Acidosis
  • Anaemia
  • Bone disease
  • Cardiovascular
  • Death & Dialysis
  • Electrolytes
  • Fluid overload
  • Gout
  • Hypertension
  • Iatrogenic issues
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10
Q

List some causes of CKD

A

o Diabetes
o Polycystic kidney disease
o Glomerulonephritis and all causes of this
o Hypertension
o Renovascular disease - renal artery stenosis from atherosclerosis or fibromuscular dysplasia leads to ischaemic nephropathy
o Persistently decreased renal perfusion - on-going heart failure or cirrhosis
o Myeloma
o IgA nephropathy
o Nephrocalcinosis
o Sarcoidosis
o Chronic exposure to nephrotoxins (NSAIDs, lithium, lead, certain herbs)
o Reflux nephropathy and scarring
o Chronic obstructive nephropathy (prostatic disease, metastatic cancer, retroperitoneal fibrosis, PUJ obstruction)

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11
Q

What is the general clinical approach to CKD?

A

Detection of the underlying aetiology
– Treatment for specific disease

Slowing the rate of renal decline
– Generic therapies

Assessment of complications related to reduced GFR
– Prevention and Treatment

Preparation for Renal Replacement Therapy

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12
Q

List some symptoms and signs of CKD

A 
Pallor - anaemia
Hypertension 
Shortness of breath - oedema, anaemia, CV risk
Kidney - shape on imaging, palpable?
Itch and cramps
Cognitive changes
GI symptoms e.g. vomiting, anorexia, uraemic odour
Change in urine output
Haematuria
Proteinuria
Peripheral oedema
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13
Q

What would be asked during history to see if there is any previous history of renal disease?

A 
o	Raised urea/creatinine
o	Proteinuria/haematuria
o	Hypertension
o	Lower urinary tract symptoms
o	Family history (PKD/Alports)
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14
Q

What systemic diseases are linked to CKD?

A 
o	Diabetes mellitus
o	Collagen vascular diseases
o	SLE, scleroderma, vasculitis
o	Malignancy
o	Myeloma, breast, lung, lymphoma
o	Hypertension
o	Sickle cell disease
o	Amyloidosis
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15
Q

What drugs are linked to CKD development?

A 
o	NSAIDs
o	Penicillins/aminoglycosides
o	Chemotherapeutic drugs
o	Narcotic abuse
o	ACE inhibitor / ARBs

Also antibiotics, morphine, digoxin, metformin and contrast agents

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16
Q

List some uraemic symptoms seen in CKD

A

o Nausea, anorexia, vomiting
o Pruritis
o Weight loss
o Weakness, fatigue, drowsiness

17
Q

What are the advantages and disadvantages of using USS for CKD?

A

Advantages
o Non-invasive
o No ionising radiation
o May provide information about chronicity of renal disease and can be used to show progression of diseases e.g. assessing increase in hydronephrosis

Disadvantages
o No functional data
o Operator dependent

18
Q

How can renal decline be slowed in CKD patients?

A

BP control - high BP is associated with faster decline in GFR, so treating this slows progression, particularly where they have proteinuria

Control proteinuria (particularly ACE inhibitors / ARBs)

Reverse other contributing factors – treat causes

Others
o	Allopurinol
o	Dietary protein restriction
o	Fish oils
o	Lipid lowering
o	Control acidosis
19
Q

What investigations are used to identify signs of complications associated with CKD?

A

Acidosis - Bicarbonate, pH

Anaemia - Blood count, film, haematinics

Bone disease – Calcium, Phosphate, Albumin, PTH

CV risk - History of chest pain, BP, cholesterol levels

Death and dialysis - Renal function e.g. urea, creatinine

Electrolytes - including Potassium

Fluid overload - exam include BP, oedema, JVP, CXR

Gout - History and exam

Hypertension - BP +/- 24 hour tape

Iatrogenic issues - Ask about medication

20
Q

At what severity of CKD is metabolic acidosis usually seen?

A

Not usually seen until GFR<20mls/min

21
Q

How is metabolic acidosis in CKD treated?

A

• Treated with oral Na Bicarbonate

– (Care with volume overload)

22
Q

At what severity of CKD is anaemia usually seen?

A

• Usually manifest when GFR < 20mls/min

23
Q

How is anaemia in CKD treated?

A
  • Usually treat if < 10g/dl or symptomatic
  • ? Survival advantage

Treated with
• Iron replacement (Oral vs Intravenous)
• Erythropoietin-stimulating agent (ESA) therapy

24
Q

What causes bone disease in CKD?

A

Reduced GFR leads to hyperphosphataemia
Loss of renal tissue leads to lack of activated Vitamin D
Low Calcium and Raised Phosphate in the blood
Secondary Hyperparathyroidism (elevated PTH) results
May progress to tertiary hyperparathyroidism with prolonged hypersecretion becoming uncontrolled
This can result in abnormal bone deposits, fractures and CV events

25
Q

How is renal bone disease managed?

A

Control phosphate
• Diet
• Phosphate binders
• (CaCO3 Ca Acetate, sevelamer, lanthanum)

Normalise calcium and PTH
• Active Vitamin D Analogues (Calcitriol)

Tertiary disease
• Parathyroidectomy & Calcimetics (Cinacalcet)

26
Q

Why does CKD cause hyperkalaemia?

A
  • Normally excreted by exchange with Na + in distal tubule
  • Reduced delivery of Na+ to distal tubule as GFR falls
  • Other factors include underlying disease, drugs (ACE inhibitors/ARBs) and diet
27
Q

At what level is hyperkalaemia dangerous to life?

A

K+ > 7mmol/l (NR 3.5-4.5) may induce a fatal cardiac arrhythmia

28
Q

How is jyperkalaemia treated?

A

Acute
o Stabilise with Calcium Gluconate
o Shift - Salbutamol, Insulin-Dextrose
o Remove - Dialysis, Calcium resonium

Chronic
o Diet
o Drug modifications

29
Q

When does fluid overload become evident in CVD?

A
  • Usually problematic when GFR < 20mls/min
  • Unable to excrete an excess Na+ load
  • Na+ and Water retention
  • Oedema & hypertension associated with it
30
Q

How is fluid overload treated in CVD?

A
  • Na+ restriction
  • Fluid restriction
  • Loop diuretics
31
Q

What blood pressure level is optimal in CKD patients?

A

Aim <125/75 in CKD with significant proteinuria, 130/80 no proteinuria

32
Q

Summarise how complications associated with CKD are managed

A
  • Acidosis – bicarbonate
  • Anaemia – EPO and iron
  • Bone disease – diet and phosphate binders
  • CV risk – BP, aspirin, cholesterol, exercise, weight
  • Death & Dialysis – counsel and prepare
  • Electrolytes – diet and consider drugs
  • Fluid overload – salt and fluid restriction, diuretics
  • Gout – optimise +/- meds
  • Hypertension – weight, diet, fluid balance, drugs
  • Iatrogenic issues – be aware!

Urinary system (22 decks)

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