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Year 3 > Chronic kidney disease (URO) > Flashcards

Chronic kidney disease (URO) Flashcards

1
Q

Define chronic kidney disease.

A

CKD is defined as abnormalities of kidney structure or function (GFR<60mL/minute/1.73m^2), present for >=3 months, with implications for health

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2
Q

What are abnormalities in kidney structure and function found in chronic kidney disease?

A

GFR >60mL/minute/1.73m^2 OR the presence of one or more of the following:

  • albuminuria/proteinuria
  • urine sediment abnormalities e.g. haematuria
  • electrolyte abnormalities due to tubular disorders
  • abnormalities detected by histology
  • structural abnormalities detected by imaging
  • Hx of kidney transplantation
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3
Q

What are some causes of chronic kidney disease? (5)

A
  • diabetic nephropathy (diabetes)
  • hypertensive nephropathy (hypertension)
  • glomerulonephritis
  • polycystic kidney disease
  • heat stress nephropathy (environment/climate)
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4
Q

What are the most common causes of chronic kidney disease? (2)

A

Diabetes mellitus & hypertension

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5
Q

What is the most common genetic cause of chronic kidney disease?

A

Polycystic kidney disease

  • autosomal dominant
  • screen relatives with abdominal ultrasound
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6
Q

What are the mechanisms of damage in chronic kidney disease?
(Low-yield)

A
  • renal injury –> increased intra-glomerular pressure + glomerular hypertrophy as compensation to maintain filtration
  • glomerular permeability to TGF-beta, fatty acids, pro-inflammatory markers + protein –> mesangial matrix expansion, inflammation, fibrosis + scarring
  • increase in angiotensin II –> upregulates TGF-beta –> collagen synthesis + scarring
  • inflammation + reduced blood supply –> tubulo-atrophy + interstitial fibrosis
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7
Q

What are clinical features of CKD mainly manifestations of? (3)

A
  • uraemia - lack of excretion of toxic substances
  • anaemia - lack of EPO produced by kidney
  • hyperphosphatemia - lack of excretion of toxic substances
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8
Q

How can CKD often present?

A

Often asymptomatic - may be finding of routine blood test or urine test

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9
Q

What are the clinical features of CKD?

A
  • fatigue (uraemia/anaemia)
  • oedema (peripheral/pulmonary - due to salt and water retention + hypoalbuminemia)
  • nausea and vomiting (urea accumulation)
  • pruritus (urea accumulation)
  • restless legs (uraemia)
  • anorexia (urea accumulation)
  • foamy urine (proteinuria)
  • cola-coloured urine (haematuria)
  • dyspnoea, orthopnoea (pulmonary oedema due to reduced urine output)
  • Kussmaul’s respiration (metabolic acidosis, deep inspiratory efforts without tachypnoea)
  • seizures (advanced disease, increase in unexcreted toxins)
  • infection-related glomerular disease (hepB&C, syphilis, streptococcal pharyngitis)
  • arthralgia & rashes (concomitant autoimmune disorder)
  • enlarged prostate gland (obstructive uropathy)
  • symptoms of hypocalcaemia (due to 1-alpha-hydroxylase deficiency)
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10
Q

What are the symptoms of hypocalcaemia in CKD? (4)

A
  • Convulsions (muscle twitching)
  • Arrhythmias
  • Tetany
  • Paraesthesia

(CATs go NUMB)

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11
Q

What might you find on examination of a patient with CKD? (7)

A
  • skin pigmentation
  • uraemic frost
  • purpura
  • hypertension
  • peripheral vascular disease
  • cardiac arrhythmias: increased K+
  • asterixis in encephalopathy
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12
Q

What are the risk factors for CKD?

A
  • diabetes mellitus
  • hypertension
  • age>50
  • childhood kidney disease
  • smoking
  • obesity
  • black/Hispanic ethnicity
  • Fx of CKD
  • autoimmune disorders
  • male sex
  • long-term NSAID use
  • high uric acid levels
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13
Q

What are the 1st-line investigations for CKD?

A
  • renal chemistry (U&Es)
  • estimation of GFR (equation using serum creatinine)
  • serum cystatin C and cystatin C-based estimation of GFR (when serum creatinine inaccurate e.g. extremes of muscle mass)
  • urinalysis
  • urinary albumin (ACR)
  • renal ultrasound
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14
Q

What do U&Es (renal chemistry/profile) show for CKD?

A
  • elevated serum creatinine (may be falsely low in conditions of low muscle mass e.g. older, malnourished, liver failure)
  • electrolyte abnormalities (tubular disorders –> metabolic acidosis) e.g. hyperkalaemia, hypocalcaemia
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15
Q

What can indicate if kidney injury is chronic and not acute?

A

Hypocalcaemia
(Kidney cannot produce 1-alpha-hydroxylase)

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16
Q

What is the GFR in CKD?

A

<60mL/minute/1.73m^2

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17
Q

When is GFR not a good measurement in CKD?

A
  • reduced muscle mass –> overestimation of GFR
  • increased muscle mass –> underestimation of GFR
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18
Q

What can urinalysis show for CKD?

A

Haematuria and/or proteinuria

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19
Q

What results does ACR (urinary albumin) show for CKD?

A

To check for proteinuria
Moderately increased ACR 30-300mg/g

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20
Q

What is the 1st-line imaging modality for kidney structure and what might you see (CKD)?

A

Renal ultrasound - small kidney size; presence of obstruction/hydronephrosis; kidney stones
(Large kidneys if diabetes uncontrolled in early diabetic kidney disease)

21
Q

What might BNP be like in CKD?

A

Renal dysfunction (GFR<60) can cause a raised serum natriuretic peptides

22
Q

What might FBC show in CKD?

A

Normocytic, normochromic anaemia due to EPO deficiency

23
Q

When is kidney biopsy done for CKD?

A

For infectious causes, glomerular nephrotic and nephritic syndromes

24
Q

What calcium/phosphate/PTH levels would we see in CKD?

A
  • low calcium
  • high phosphate
  • high PTH
  • low vitamin D
25
Q

What are the stages of CKD?

A
  • G1: eGFR>90ml/min + signs of kidney damage on other tests
  • G2: eGFR 60-90ml/min + signs of kidney damage on other tests
  • G3a: eGFR 45-59ml/min, moderate reduction in kidney function
  • G3b: eGFR 30-44ml/min, moderate reduction in kidney function
  • G4: eGFR 15-29ml/min, severe reduction in kidney function
  • G5: eGFR<15ml/min, established kidney failure - dialysis or kidney transplant may be needed
26
Q

What does G1 and G2 need to be classified as CKD?

A

Markers of kidney disease e.g. proteinuria, haematuria, electrolyte abnormalities, structural abnormalities

27
Q

What can be used if eGFR is thought to be inaccurate?

A

Serum cystatin C, cystatin C-based eGFR

28
Q

What are the stages of albuminuria for CKD?

A
  • A1: <30mg/g or <3mg/mmol
  • A2: 30-300mg/g or 3-30mg/mmol (microalbuminuria)
  • A3: >300mg/g or >30mg/mmol (macroalbuminuria)
29
Q

What GxAy stages of CKD correspond to what type of risk of progression and complications?

A
  • low risk: G1A1 and G2A1
  • moderate risk: G3aA1, G1A2, G2A2
  • high risk: G3bA1, G3aA2, G1A3, G2A3
  • very high risk: G4A1, G5A1, G3bA2, G4A2, G5A2, G3aA3, G3bA3, G4A3, G5A3
30
Q

What are some differential diagnoses for CKD? (6)

A
  • diabetic kidney disease
  • hypertensive nephrosclerosis
  • ischaemic nephropathy (long-standing essential hypertension that is suddenly uncontrolled)
  • obstructive uropathy
  • nephrotic syndrome
  • glomerulonephritis
31
Q

What is the 1st line treatment for G1-G4 CKD without uraemia?

A
  • 1st line: ACEi or ARB (controlling BP, reducing proteinuria)
    • lisinopril if ACR>30mg/mmol
    • losartan
    • 2nd line: non-dihydropyridine CCB
  • consider dapagliflozin (SGLT2 inhibitor)
  • PLUS statin (+/- ezetimibe if G3-4)
  • consider additional antihypertensive therapy
  • consider glycaemic control
32
Q

When is dapagliflozin contraindicated in CKD?

A

eGFR<30ml/min/1.73m^2 (G4-5) including patients with end-stage renal disease who are on dialysis

33
Q

How do we manage anaemia in CKD?

A
  • IV iron (ferrous sulphate) to correct iron deficiency
  • EPO-stimulating agents: epoetin alfa (correct iron deficiency before starting)
  • aim for 10-11g/dl
34
Q

How do we manage secondary hypoparathyroidism (due to low calcium) in CKD?

A
  • dietary modification (reduce phosphate intake)
  • phosphate-binding drug: sevelamer
  • ergocalciferol (alfacalcidol)
  • active vitamin D analogue (calcitriol)
35
Q

How do we manage metabolic acidosis in CKD?

A

Oral sodium bicarbonate

36
Q

What is key for management of proteinuria in CKD?

A

ACEi

37
Q

What are the 1st and 2nd line treatments for CKD G5 or with uraemia?

A
  • 1st line: dialysis (haemodialysis or peritoneal dialysis)
  • 2nd line: kidney transplant
38
Q

What type of dialysis is more common?

A

Haemodialysis more common than peritoneal dialysis

39
Q

How does haemodialysis work?

A
  • patient’s blood is removed from body through an arteriovenous fistula/graft/dialysis catheter and then returned after traversing a dialysis membrane/solution
  • usually in hospital 3x a week, 4h each session
40
Q

How does peritoneal dialysis work?

A
  • catheter inserted into abdomen and dialysis fluid is instilled in order to allow for toxic waste products to be removed on a daily basis
  • done at home
  • continuous cycling peritoneal dialysis is done with a machine at night on a daily basis
  • continuous ambulatory peritoneal dialysis is done on a daily basis
41
Q

What organism is the most common cause of peritonitis in peritoneal dialysis?

A

Staphylococcus epidermidis

Diffuse tenderness + rebound tenderness and guarding on examination

42
Q

If a patient gets ill soon after a kidney transplant, what is the most likely cause?

A

Cytomegalovirus

43
Q

What condition can the immunosuppressives e.g. ciclosporin taken after kidney transplant cause?

A

Squamous cell carcinoma of skin

44
Q

What are some other principles of management of CKD? (4)

A
  • fluid and salt restrictions to maintain fluid balance
  • EPO-stimulating agents (correct iron deficiency first)
  • vitamin D supplements - alfacalcidol (does not require activation in kidneys)
  • reduce dietary intake of phosphate or phosphate binders (sevelamer or alendronic acid) - try dietary reduction first
45
Q

What type of drugs are avoided in CKD?

A

NSAIDs and other nephrotoxic drugs

46
Q

When do NICE guidelines suggest referring to a nephrologist from primary care for CKD?

A

If eGFR<30 or falls progressively by >15 in a year

47
Q

What are some complications of CKD? (7)

A
  • anaemia
  • renal osteodystrophy (due to low calcium + high PTH –> high phosphate)
  • cardiovascular disease (CKD on haemodialysis - most likely cause of death is IHD)
  • protein malnutrition (anorexia, N&V, lack of protein intake)
  • metabolic acidosis (inability to excrete acid once eGFR<50ml/min)
  • hyperkalaemia (may cause muscle weakness, ECG peaked T-waves, treat with IV calcium, insulin + dextrose, beta agonists, loop diuretics, oral potassium binders, haemodialysis)
  • pulmonary oedema (treatment of fluid overload with loop diuretic)
48
Q

Describe the prognosis of CKD.

A
  • mostly progressive and leads to end-stage renal disease and the need for renal replacement therapy
  • cannot be cured, but can be controlled and managed

Year 3 (145 decks)

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