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Yr3 Medicine- Renal > CKD > Flashcards

CKD Flashcards

1
Q

What is CKD?

A
  • Progressive irreversible kidney damage that persists for 3 months or more.
  • Abnormalities of kidney structure or function, present for ≥3 months, with implications for health
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2
Q

State some risk factors for CKD

A
  • Older age
  • Hypertension
  • Diabetes
  • Smoking
  • Use of nephrotoxic medications
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3
Q

State some common causes of CKD

A
  • Diabetes
  • Hypertension
  • Glomerulonephritis
    • IgA
    • MCGN
    • SLE
  • Polycystic kidney disease
  • Renovasuclar disease
  • Obstructive nephropathy
  • Chronic recurrent pyelonephritis
  • Age-related decline
  • Medications such as NSAIDs, PPIs, lithium
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4
Q

Discuss the typical presentation of someone with CKD

A

Pts often asymptomatic and diagnnosis found on routine testing; however, signs & symptoms may include:

  • Pruritis
  • Anorexia
  • Nausea
  • Oedema
  • Muscle cramps
  • Peripheral neuropathy
  • Pallor
  • Hypertension
  • Restless legs
  • Fatigue
  • Impotence
  • Bone pain
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5
Q

Discuss what you might find on clinical examination of someone with CKD

A
  • Periphery: oedema, vasculitic rash, gouty tophi, uraemic flap
  • Face: anaemia, xanthelasma, jaundice
  • Neck: JVP raised
  • Cardiovascular: hypertension
  • Respiratory: bibasal crepitations of pulmonary oedema
  • Abdo: ballotable polycystic kidneys, palpable liver

*Findings depend on stage of CKD and underlying cause

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6
Q

State what investigations you would want to do if you suspect CKD, include:

  • Bedside
  • Bloods
  • Imaging

*For each, justify why you would do it

A

Bedside

  • Urine dipstick: look for haematuria, proteinuria
  • Urinen albumin:creatinine ratio
  • Urine protein:creatinine ratio

Bloods

  • eGFR: not a blood test in itself but used U&Es results
  • FBC: anaemia
  • U&Es: high urea, high creatinine
  • LFTs: albumin
  • CRP
  • Glucose & HbA1c: diabetes
  • Calcium: CKD mineral & bone disease
  • Phophate:CKD mineral & bone disease
  • PTH: CKD mineral & bone disease
  • Coagulation: nephrotic syndrome is pro-coagulable state

Imaging

  • USS kidneys: look for evidence of CKD
  • USS doppler: look for evidence of vascular cause of CKD
  • CT KUB: look for stones
  • ?Renal biopsy
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7
Q

How many eGFR tests are required to confirm diagnosis of CKD?

A

Two tests 3 months apart

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8
Q

Discuss how we stage CKD

A

We use two scores:

  • G score: based on eGFr
  • A score: based on albumin:creatinine ratio

*NOTE: a pt does not have CKD if they have score of A1 combined with G1 or G2. They need an eGFR of at least <60 or proteinuria

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9
Q

What are the 5 main aims of management in CKD?

A
  • Treat underlying disease
  • Reduce progression of CKD
  • Reduce risk of cardiovascular disease
  • Prevent or treat complications
  • Plan for future
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10
Q

Managment of CKD invovles:

  • Treating underlying disease
  • Reducing cardiovascular risk
  • Reducing progression of CKD
  • Preventing or treating complications
  • Planning for future

Discuss how we treat underlying disease in CKD

A

Treat underlying disese

  • Optimise diabetic control
  • Optimise hypertensive control
  • Immunnosupression for glomerulonephritis
  • Tolvaptan for ADPKD
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11
Q

ACE inhibitors are first line treatment for hypertension in CKD; who are ACE inhibitors offered to?

A
  • Diabetic + ACR >3mg/mmol
  • Hypertension + ACR >30mg/mmol
  • All pts with ACR >70mg/mmol
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12
Q

Managment of CKD invovles:

  • Treating underlying disease
  • Reducing cardiovascular risk
  • Reducing progression of CKD
  • Preventing or treating complications
  • Planning for future

Discuss how we reduce cardiovascular risk in CKD

A
  • Statin: atorvastatin 20mg daily for primary prevention
  • Stop smoking
  • Advise weight loss
  • Advise exercise
  • (hypertension control as mentioned previously)
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13
Q

Managment of CKD invovles:

  • Treating underlying disease
  • Reducing cardiovascular risk
  • Reducing progression of CKD
  • Preventing or treating complications
  • Planning for future

Discuss how we reduce progression of CKD

A
  • Reduce protein uria: ACEinhibitor or ARB
  • Monitor blood tests
  • (control BP)
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14
Q

State some potential complications of CKD

A
  • Anaemia of chronic disease
  • Renal mineral & bone disease
  • Secondary & tertiary hyperparathyroidism
  • Hypertension
  • Cardiovascular disease
  • Malnutrition/sarcopenia (muscle loss due to ageing or immobility)
  • Dyslipidaemia
  • As CKD progresses:
    • Electrolyte disturbances e.g. hyperkalaemia
    • Fluid overload
    • Metabolic acidosis
    • Hyperuricaemia
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15
Q

Describe the pathophysiology of anaemia of chronic kidney disease

A
  • Decreased EPO production, decreased RBC production
  • Decreased renal clearance of hepcidin, decreased release of Fe from enterocytes (functional Fe deficiency)
  • Uraemia suppresses bone marrrow production of cells
  • Shortened RBC surviaval

Also…

  • Absolute Fe deficiency (poor absorption & malnutrition)
  • Vit B12 & folate deficiency
  • Blood loss
  • Medication induced
  • S
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16
Q

Discuss the mangement of anaemia of chronic renal disease

A
  • Measure haematinics first and replace any deficiencies:
    • ​Ferritin, TIBC, transferrin saturation
    • Vit B12
    • Folate
  • Erythropoeitin injection
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17
Q

If a pt with aneamia of chronic kidney disease requires Fe, what form do we usually give it to them in?

A

IV usually better tolerated than oral

18
Q

What is the target Hb when treating aneamia of chronic kidney disease?

A

100-120g/L

19
Q

Discuss the pathophysiology of CKD mineral & bone disease

A
  • Decreased phosphate excretion leads to high serum phosphate
  • Phosphate binds to calcium causing low serum calcium
  • Secondary hyperparathyroidism occurs in response to low serum calcium- increase PTH
  • PTH causes increased osteclastic activity
  • Increased bone resorption leads to increased FBF-23 which inhibits activation of vit D
  • Kidneys are responsible for activating vitamin D, hence in CKD body’s ability to activate vitamin D is reduced leading to decreased calcium absorption
20
Q

CKD mineral bone disease can be diagnosed if pt has evidence of one or more of what 3 things?

A
  • Abnormalities of calcium, phosphate, alkaline phosphatase, PTH or vit D
  • Vascular and/or soft tissue calcification
  • Abnormalities in bone turnover, metabolism, volume, linear growth or strength
21
Q

CKD mineral and bone disease causes increased osteoclast activity; this can lead to low turnover states or high turnover states. State some conditions caused by a low turnover and high turnover response

A

Low turnover

  • Osteomalacia
  • Osteoporosis

High turnover:

  • Osteitis fibrosa (replace bone with fibrous tissue)
22
Q

What would the results of the following be in someone in with CKD mineral & bone disease:

  • Fibroblast growth factor-23
  • Alkaline phosphatase (ALP)
  • PTH
  • Phosphate
  • Calcium
  • 1,25- Vit D
A
  • FGF-23 = high
  • ALP = high
  • PTH = high
  • Phosphate = high
  • Calcium= low
  • 1,25- Vit D= low
23
Q

In advanced CKD, tertiary hyperparathyroidism can occur; explain why this occurs

NOTE: Tertiary hyperparathyroidism is a state of excessive secretion of parathyroid hormone (PTH) after a long period of secondary hyperparathyroidism

A

Occurs when PTH release continues depsite raised serum calcium levles as a result of parathyroid gland nodular hyperplasia

24
Q

Elevated serum PTH, phosphate and calcium can increase cardiovascular morbidity & mortality; true or false?

A

TRUE- hence vital to try and control CKD mineral & bone disease

25
Q

Discuss the management of CKD mineral & bone disease

A
  • Low phosphate diet (First line management)
  • Phosphate binders
  • Activated vitamin D
  • Calcimimetics for tertiary hyperparathyroidism
  • Bisphosphonates for osteoporosis
  • Parthyroidectomy may be needed in some cases
26
Q

What x-ray changes may you find in someone with CKD mineral & bone disease?

A
  • Osteomalacia: normal bone mass but decreased mineralisation hence bones soft- appears less white
  • Osteoporosis: decreased bone mass hence bones brittle- appears less white
  • Ostesclerosis: hardening of bone- appears whiter

*On x-ray of spine may see rugger jersey spine: sclerosis at both ends of vertebrate and osteomalacia in middle

27
Q

Part of CKD management involves planning for future; what might this involve?

A
  • Discussions about dialysis
  • Discussions about transplant

*see separate deck for dialysis discussions

28
Q

Pts with CKD are much more likely to die of cardiovascular disease than the need for renal replacement therapy; true or false?

A

True

29
Q

Diabetic nephropathy is most common cause of CKD in UK hence pts with diabetes should have regular testing for diabetic nephropathy; what does this testing involve?

A
  • Urine albumin:creatinine ratio
  • U&Es
  • Evidence of other microvascular disease e.g. retinopathy, peripheral neuoropathy
30
Q

Discuss the pathophysiology, and stages, of diabetic nephropathy

A
  1. Hypefiltration & hypertrophy- increase GFR
  2. Latent stage: GBM thickening and mesangial expansion (chronic high levels of glucose passing through glomerulus cause scarring= glomerulosclerosis)
  3. Microalbuminuria: small amount of albumin detected in urine (not detected on conventional dipstick), further increase in GBM thickening and mesangial expansion, podoyte changes
  4. Overt proteinuria: lots of albumin in urine/can detect on conventional dipstick, diffuse glomerular histopathological changes, falling GFR
  5. ESRD
31
Q

Explain why hypertension can cause CKD

A

Chronic raised BP can cause nephroscerlosis

*HOWEVER, often difficult to tell if pt has advanced renal disease at presenation whether it was HTN that caused renal disease or renal impairment causing HTN

32
Q

What is polycystic kidney disease?

A

Genetic condition where kidneys develop mulitple fluid filled cysts leading to enlarged kidneys with impaired function. There are also extra-renal complications.

33
Q

Polycystic kidney disease can be autosomal dominant or autosomal recessive. For each state:

  • What age it presents
  • Any subtypes
  • Which chromosome mutated gene found on
  • Which is rarer & more severe- dominant or recessive
A

Autosomal dominat

  • Adults
  • Subtypes:
    • PKD-1: chromosome 16 (85%)
    • PKD-2: chromosome 4 (15%)

Autosomal recessive

  • Often presents in pregnancy with oligohydramnios as fetus doesn’t produce enough urine. Often require dialysis within first few days of life. Can have dysmorphic features e.g. underdeveloped ear cartilage, low set ears and a flat nasal bridge. Usually have ESRD before adulthood.
  • Chromosome 6
  • Rarer & more severe
34
Q

State some extrarenal manifestations of autosomal dominant polycystic kidney disease

A
  • Cerebral aneuryseums
  • Aortic root dilation
  • Cardiac valve disease (mitral regurg)
  • Hepatic, splenic, pancreatic, ovarian, prostatic cysts
  • Colonic diverticula
35
Q

State some symptoms, signs & complications of autosomal dominant polycystic kidney disease

A
  • Hypertension
  • Gross haematuria (cyst rupture)
  • CVD
  • Renal stones
  • ESRF
  • Chronic loin pain
36
Q

How do you diagnose adult polycystic kidney disease?

A
  • Ultrasound
  • Genetic testing/family history
37
Q

Discuss the management of autosomal dominant polycystic kidney disease

A
38
Q

State some potential complications of adult polycystic kidney disease

A
  • Chronic loin pain
  • Hypertension
  • CVD
  • Gross haematuria
  • Renal stones
  • ESRD (often by 50yrs)
39
Q

Summary from passmed about antihypertensives in CKD

A
40
Q

What may you see on x-ray of spine of patient with CKD?

A

Spine xray shows sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white). This is classically known as “rugger jersey” spine after the stripes found on a rugby shirt.

Yr3 Medicine- Renal (8 decks)

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