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Renal (Year 2 GM) > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What is the current definition of chronic renal failure?

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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2
Q

What are the different classifications of chronic kidney disease?

A
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3
Q

When will creatinine be raised?

A

Only until about 60% of the total kidney function is lost

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4
Q

Which demographic has a high serum creatinine?

A

African Americans - because they have a higher muscle mass

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5
Q

What factors are involved in estimating the GFR from serum creatinine?

A

Age

Weight

Female/male

Ethnicity

The vraiables used depend on which formulae you are using

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6
Q

What funtion of the kidney does eGFR measure?

A

Excretory function

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7
Q

What things cross the GBM?

A

Water

Urea

Electrolytes

Creatinine

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8
Q

What things cross the GBM but are reabsorbed in the proximal tubule?

A

Glucose

Low molecular weight proteins - a2, microglobulin

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9
Q

What things don’t cross the GBM?

A

Cells (RBC, WBC)
High molecular weight proteins - albumins, globulins

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10
Q

How do we assess the filtration (keep in function) of the kidney -

A

Check for the presence of blood or protein in the urine

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11
Q

How do we assess the anatomy of the kidney?

A

Histology

Radiography

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12
Q

What are the complications of CKD?

A

Acidosis

Anaemia

Bone Disease

CVS

Death

Dialysis

Electrolytes

Fluid Overload

Gout

Hypertension

Iatrogenic issues

More likely with worsening eGFR: Vit D deficiencym hyperphosphataemia, hypoalbuminaemia, hyperparathyroidism

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13
Q

What are the different aetiologies of CKD?

A

Diabetes

Glomerulonephritis (all causes)

Hypertension

Renovascular disease

Polycystic kidney disease

Myeloma

IgA nephropathy

Sarcoidosis

Chronic exposures to nephrotoxins (NSAIDs, lithium, lead, ceratin herbs)

Reflux nephropathy and scarring

Chronic obstructive nephropathy (prostatic disease, metastatic cancer, retroperitoneal fibrosis, PUJ obstruction

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14
Q

Give examples of renovascular disease

A

Renal artery stenosis from atherosclerosis of fibromusclular dysplasia

  • Leads to ischaemic nephropathy

Persistently decreased renal perfusion - ongoing heart failure and cirrhosis

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15
Q

What are some symptoms and signs of CKD?

A

Anaemia - pallor and SOB

SOB also caused by fluid overload

Hypertension

Itch and Cramps

Cognitive changes

GI - anorexia, vomitting, taste disturbance

Haematuria

Proteinuria

Peripheral oedema - exacerbated by hypoalbuminaemia - reduced oncotic gradient

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16
Q

What are the important parts of the history to uncover for a patient with potential CKD?

Previous evidence of renal disease

History of systemic diseases

Drug exposure

Pre/post renal factors

Uraemic symptoms

A

Previous evidence of renal disease:

  • Raised urea/creatinine
  • Proteinuria/haematuria
  • Hypertension
  • LUTs
  • Family History

History of systemic diseases:

  • Diabetes mellitus
  • Collagen vascular disease (scleroderma, SLE, vasculitis)
  • Malignancy (myeloma, breast, lung, lymphoma)
  • Hypertension
  • Amyloidosis
  • Sickle cell disease

Drug exposure

  • NSAIDs
  • Penicillins/aminoglycosides
  • Chemotherapeutic drugs
  • Narcotic abuse
  • ACE i / ARBs

Pre/post renal factors

  • Congestive cardiac failure
  • Diuretic use
  • Nausea, vomiting, diarrhoea
  • Cirrhosis
  • LUTS / pelvic disease

Uraemic symptoms - THESE ARE IN LEARINNG OUTCOMES

  • Nausea, anorexia, vomiting
  • Pruritis
  • Weight loss
  • Weakness, fatigue, drowsiness
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17
Q

What are the examinations for CKD?

A

•Vital signs

–Fever, blood pressure

•Volume status

–Deplete:

–Orthostatic BP, skin turgor/temperature

–Overload:

–Raised JVP, crepitations, ascites, oedema

•Systemic illness

–Skin

–Rash – malar (lupus), purpuric (vasculitis), macular (AIN)

–Auscultation

–Cardiac murmurs (endocarditis)

–Abdomen

–Bruits, palpable organs

–Extremities

–Livedo reticularis (vasculitis, atheroembolism),

–splinter haemorrhages (endocarditis)

–Pulses

–Absent (vascular disease)

–Bones and joints

–Tender (malignancy)

–Inflammed (lupus)

–Gouty tophi

Obstruction

  • Percussable bladder, enlarged prostate, flank masses
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18
Q

How do we detect the underlying pathology in CKD?

A

Blood tests

U and E’s

FBC

Urine Tests

Urine dip

Urine PCR or ACR

Histology - renal biopsy

Radiology

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19
Q

What are the investigations to exclude active disease?

A

CK - rhabdomyolysis

Urine Protein : Creatinine ratio - intrinsic renal disease

Serum and Urine electrophoresis - myeloma

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20
Q

How do we quantify protein in the urine?

A

Protein : creatinine ration

Albumin : Creatinine ration

24 hour urine collection

Renal disease is often asymptomatic - only sign may be abnormal BP or urinalysis

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21
Q

What imaging techniques are used in detecting the aetiology of CKD?

A
  • Ultrasound - no functional date, may provide information about chronicity of renal disease
  • Plain radiology
  • CT
  • Nuclear medicine
  • MRI
22
Q

What does bilateral small kidneys with thinned cortices suggest?

A

Intrinsic disease (glomerulonephritis)

23
Q

What does unilateral small kidney indicate?

A

Renal artery disease

24
Q

What does clubbed calyces and cortical scars suggest?

A

Reflux with chronic infection or ischaemia

25
Q

What do large cystic kidneys suggest?

A

Cystic kidney disease

26
Q

How do we slow the rate of renal decline?

A

Blood pressure control (High Bp is associated with faster decline in GFR)

Control proteinuria (ACEi and ARBs)

Reverse other contributing factors - treat causes

•Others

–Allopurinol

–Dietary protein restriction

–Fish oils

–Lipid lowering

–Control acidosis

27
Q

How do we assess the complications related to reduced GFR?

Acidosis

Anaemia

Bone disease

CV risk

Death & Dialysis

Electrolytes

Fluid overload

Gout

Hypertension

Iatrogenic issues

A
28
Q

When is metabollic acidosis normally seen?

A
  • Not usually seen until GFR<20mls/min
  • Most marked in tubular-interstitial disease
29
Q

What are the effects of acidosis on potassium and bone disease?

A
  • Worsens hyperkalaemia
  • Exacerbates renal bone disease
30
Q

How is acidosis treated?

A

Treated with oral sodium bicarbonate

31
Q

What causes anaemia in CKD? When does it occur

A

Caused by reduced erythropoietin production

Caused by reduced red cell survival

Usually manifests when GFR is less than 20 mls / min

32
Q

What is the treatment for anaemia that is secondary to chronic renal disease?

A

Iron replacement therapy

ESA therapy (erythropoeitin stimulating agent)

Oral vs Intravenous

33
Q

What causes bone disease in chronic kidney disease?

A

The kidney’s function to excrete phosphate is impaired (reduced serum calcium)

The combination of low calcium and high phosphate stimulates PTH - Bone resorption

The kidney has impaired ability to hydroxylate vitamin D (low levels of 1 a hydroxylase- leads the reduced absorption of calcium) - high phosphate results in reduced 1 a hydroxylase - therefore low vitamin D

Liver + cholecalciferol = 25 hydroxycholecalciferol

+kidney = 1,25 dihydroxycholecalciferol

(high phosphate is also associated with vascular and cardiac calcification)

34
Q

What is the management of renal bone disease?

A

Control of phosphate:

  • Diet - try to reduce phosphate
  • Phosphate binders
  • Calcium carbonate, ca, Acetate, sevelamer, lanthanum)

Normalise calcium and PTH:

Active vitamin D anologues (calcitrol)

Tertiary disease (parathyroidectomy and celcimetics - cinacalcet)

35
Q

What is tertiary parathyroidism?

A

When there is prolonged hypersecretion it can become uncontrolled

36
Q

Name some cardiovascular risks

A
  • Hypertension
  • Hyperlipidemia
  • Smoking
  • Underlying disease (e.g. diabetes)
  • Renal bone disease (perhaps because increased phosphate)
  • Endothelial dysfunction
  • Uraemic pericarditis
  • Lifestyle factors

Improve above factors

37
Q

Where is potassium normally exchanged with sodium?

A

Normally excreted by exchange with sodium in the distal tubule

38
Q

How does the delivery of sodium change when GFR falls?

A

When GFR falls there is reduced delivery of sodium to the distal tubule

39
Q

How does an ACE i affect potassium levels?

A

ACE i causes the retention of potassium

40
Q

What foods are high in potassium?

A

Bananas

Avacado

Tomatos

Milk

Yoghurt

Chocolate

Seeds and nuts

41
Q

What level of potassium can induce fatal cardiac arrhythmia?

A

When potassium is greater than 7mmol/l

42
Q

What is the treatment for hyperkalaemia?

A

Acute

•Stabilise

–Calcium Gluconate

•Shift

–Salbutamol

–Insulin-Dextrose

•Remove

–Dialysis

–Calcium resonium

Chronic

  • Diet
  • Drug modifications
43
Q

When us fluid overload a problem?

A

WHen GFR is less than 20 mls/min

The kidney is unable to excrete and excess sodium load

Leads to sodium and water retention

44
Q

What are the complications of sodium and water retention?

A

Oedema and hypertension

45
Q

What is the treatment for fluid / volume overload?

A

Sodium restriction

Fluid restriction

Loop diuretics

46
Q

What is the blood pressure aim for CKD with proteinuria and withour proteinuria?

A

With - aim for less than 125/75

Without - aim for 130/80

47
Q

Which drugs cause acute kidney injury on top of CKD?

A

Contrast agents

Antibiotics

48
Q

What is the risk of the build of of urea?

A

Uraemic pericarditis

49
Q
A

Haemodialysis vs Peritoneal

50
Q
A

Renal (Year 2 GM) (28 decks)

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