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drugs used in renal disease Flashcards

1
Q

what must be considered to ensure prescribing the right drug for the patient

A
  1. does the drug work (efficacy)
  2. can the patient tolerate drug ( safety)
  3. how does the drug fit with the lifestyle of the patient
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2
Q

how is a patents renal function monitored?

A
  1. patients clinical condition
  2. biochemical data
  3. other biochemical abnormalities
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3
Q

what is the importance of diagnosing chronic kidney disease

A
  1. early diagnosis allows:
    - prevention/slowing of progression to renal failure
    - adequate time to prepare patient for dialysis/treatment
    - better and earlier management of complications
    - better medicines management
  2. Chronic kidney disease is a marker for increased cardiovascular risk
    - target patients for cardiovascular risk reduction interventions
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4
Q

what is the importance of early referral to nephrology

A
  1. late referral increases risk of morbidity, mortality and cost
  2. appropriately timed early referral gives:
    - patient choice as to modality of ESRF treatment
    - time to prepare patient for dialysis/transplantation
    - avoidance of venous catheters and associated bacteraemia
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5
Q

what patients are at risk of developing renal failure

A
  1. extremes of age- neonates and elderly
  2. polypharmacy
  3. specific disease states ( hypertension, diabetes, heart failure, renal disease, recurrent UTIs)
  4. patients receiving large amounts/long term analgesia
  5. transplant patients
  6. drug therapy- nephrotic drugs (dose adjustments)
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6
Q

define prevelance

A

total number of cases of a disease in a given population at a specific time

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7
Q

give examples of uses of bedside clinical data

A
  1. weight charts
  2. fluid balance charts
  3. degree of oedema
  4. results of dipsticks (protein, blood and glucose testing)
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8
Q

what is biochemical data useful for

A
  1. to identify renal impairment

2. to modify dosages of drugs which are really cleared

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9
Q

what would the ideal marker of kidney function

A
  1. naturally occurring
  2. not metabolised
  3. specific to kidney
  4. filtered, not secreted/reabsorbed by kidney
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10
Q

describe the relationship of plasma creatinine to true GFR

A
  1. non linear relationship with GFR

2. minor elevation of plasma creatinine can represent significant renal impairment

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11
Q

what is plasma creatinine determined by

A

determined by muscle mass, as well as renal function

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12
Q

give the calculation for the estimated glomerular filtration rate

A

eGFR= 175 x (creatine(plasma))^-1.154 x (age)^-0.203
x 0.742 if female
x 1.21 if afro caribbean

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13
Q

what is the estimated GFR

A
  1. only requires age, sex and blood creatinine level
  2. can be automatically generated by pathology labs, online, or by using reference tables
  3. allows direct lab reporting to clinicians of eGFR
    - true GFR>60ml/min (good correlation)
    - true GFR<60ml/min (inaccurate, don’t use)
  4. not for use with acute renal impairment, pregnancy, children
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14
Q

how is serum creatinine increased

A
  1. large muscle mass, dietary intake
  2. drugs: interfere with analysis (eg. levodopa, cephalosporins)
    - inhibit tubular secretion (eg. cimetidine, trimethoprim, aspirin)
  3. ketoacidosis
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15
Q

how is serum creatinine decreased

A
  1. reduced muscle mass
  2. cachexia/starvation
  3. immobility
  4. pregnancy
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16
Q

what are endotoxins

A

part of the outer membrane of the cell wall of gram negative bacteria

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17
Q

what defines acute kidney injury severity

A 
RIFLE
R- risk
I- injury 
F- failure
L- loss of kidney function
E- end stage kidney disease
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18
Q

describe the pathophysiology of AKI

A
  1. triggers (ischaemia, nephrotoxins, bacterial endotoxins) induce the release of inflammatory mediators (cytokines and chemokine) from both endothelial and tubular cells in the kidney
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19
Q

describe the role of neutrophils and leucocytes in the pathophysiology of AKI

A

Migrate to the site of inflammation and marginate along the peritubular capillary wall very early after the insult

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20
Q

what is endothelial inflammatory injury followed by

A

followed by increased vascular permeability which, within 24 hours, facilitates migration of neutrophils into the kidney interstitial and tubular lumen

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21
Q

what do neutrophils release in the pathophysiology of AKI

A

release pro inflammatory cytokines that further aggravate the tubular injury

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22
Q

what is the tubular response to AKI characterised by

A

characterised by a loss of cytoskeletal integrity leading to desquamation of viable cells and also apoptosis and necrosis

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23
Q

give examples of novel biomarkers

A

neutrophil gelatinise associated lipocalin (NGAL), KIM-1

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24
Q

what is NGAL

A
  1. A lipocalin iron carrying protein that is highly expressed in the tubular epithelium of the distal nephron and released from tubular epithelial cells following damage such as AKI
  2. expressed in multiple molecular forms in the urine- dimeric from neutrophils and monomeric from kidney tubular cells
    - this difference has the potential to improve specificity of NGAL as a renal biomarker
  3. studies detected elevated NGAL levels in both urine and plasma of adult patients with established AKI
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25
Q

what is KIM-1

A
  1. kidney injury molecule 1- a cell membrane glycoprotein
  2. plays a role in the regeneration process after injury
  3. not detectable in normal kidney but is elevated in clinical renal damage
  4. urinary KIM-1 decreases with antiproteinuric therapies
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26
Q

what is the role of the pharmacist in monitoring drug therapy

A
  1. efficacy of treatment
  2. adjust drug dosing regimens in line with renal status
  3. monitor renal function of patients receiving nephrotoxic agents
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27
Q

what are the limitations of serum urea as a marker

A
  1. it varies with the dietary protein intake
  2. reabsorbed by the tubules
  3. reabsorption varies with urine flow
    - its clearance is independent of GFR at low urine flow rates
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28
Q

what factors increase serum urea

A
  1. high protein diet
  2. hyper catabolic conditions (hyperthyroidism, burns)
  3. GI bleeding
  4. muscle injury
  5. drugs (eg. glucocorticoids)
  6. hypovalaemia
29
Q

what factors decrease serum urea

A
  1. malnutrition
  2. liver disease
  3. sickle cell anaemia
30
Q

what is the role of urea

A

it is the final degradation product of protein and amino acid metabolism

  • in protein catabolism, the proteins are broken down to amino acids and deaminated
  • the ammonia formed in this process is synthesised to urea in the liver
  • most important catabolic pathway for eliminating excess nitrogen in body
31
Q

what could increase blood urea nitrogen levels?

A

may be due to prerenal causes (cardiac decompensation, water depletion due to increased intake and excessive loss, high protein diet), renal causes (chronic nephritis, tubular necrosis) and post renal causes (all types of obstruction of the urinary tract, eg. stones, tumors, enlarged prostate gland)

32
Q

what is the significance of proteinuria

A
  1. indicative of glomerular disease
  2. proteinuria itself is nephrotoxic- causes renal tubular cell damage
  3. marker for increased risk of progression of renal disease
  4. reduced with ACE inhibitors/ARBs
33
Q

describe the process of obtaining a Protein:creatinine and albumin:creatinine ratio

A
  1. send spot urine sample for: PCR or ACR
    - no need for 24 hour urine collections
  2. PCR/ACR x 10 equates to 24 hour excretion
34
Q

what other biochemical abnormalities may be seen in renal impairment

A
  1. raised serum potassium
  2. raised serum phosphate
  3. decreased serum calcium- linked to vitamin d production
35
Q

describe the properties of the ideal drug used in renal impairment

A
  1. <25% renal excretion
  2. largely hepatic/biliary excretion
  3. not nephrotoxic
  4. wide therapeutic index
  5. pharmacodynamics unaffected by changes in renal function
  6. unaffected by protein binding or fluid balance
36
Q

what mneumonic is used to describe drug pharmacokinetics

A 
ADME
A- absorption
D- distribution 
M- metabolism
E- excretion
37
Q

describe absorption in the altered pharmacokinetics in renal impairement

A
  1. related to the consequences of:
    - pathology of renal disease (uraemia, oedema, salivary ammonia)
    - underlying disease (neuropathy, peritoneal dialysis)
    - drug interactions (phosphate binders, calcium resonium)
38
Q

describe distribution in the altered pharmacokinetics in renal impairment

A
  1. changes in functional compartment
  2. alterations in protein binding (mainly acidic drugs, configuration of albumin)
  3. tissue binding (digoxin decrease Vd- competitive binding)
39
Q

describe metabolism in altered pharmacokinetics in renal impairment

A

limited importance for kidney

  • involved in metabolism of insulin
  • insulin requirements in diabetics reduced in renal impairment
40
Q

describe elimination in altered pharmacokinetics in renal impairment

A

highly significant for drugs where renal function is the main organ of clearance
- many antibiotics (pencillin, aminoglycosides), digoxin, ciclosporin

41
Q

what are the characteristic of nephrotic syndrome

A

proteinuria, hypoalbuminaemia, generalised oedema, hyperlipidaemia, weight gain, fatigue, loss of appetite

42
Q

how can nephrotic syndrome be treated

A
  1. treatment of causative disorder (manage infections, allergic desensitisation, stopping drugs)
  2. angiotensin inhibition
  3. Na restriction
  4. diuretics for excessive fluid overload
  5. statins versus hyperlipidaemia
  6. rarely, nephrectomy
43
Q

how is nephrotic syndrome caused

A

antibodies produced which attack glomerular basement membrane

  • glomerulus leaks protein
  • results in oedema
44
Q

what are the different classifications of drug induced renal failure

A
  1. pre renal
  2. direct toxicity (intra renal)
  3. immunological damage (intra renal)
  4. obstructive uropathy (post renal)
45
Q

how is drug induced renal failure diagnosed (causation)

A
  1. establish a full drug history
  2. when were the drugs prescribed
  3. modifications to doses?
  4. appearance of symptoms?
46
Q

what is the likely diagnosis of a urinalysis of red blood cells or proteinuria

A

glomerular disease

47
Q

what is the likely diagnosis of a urinalysis of white blood cells/pus cells

A

tubular/interstitial damage

48
Q

what is the likely diagnosis of a urinalysis of uric acid crystals

A

uric acid nephropathy

49
Q

what are the mechanisms of pre renal failure

A
  1. volume depletion- eg. diuretics or cytotoxic therapy

2. prostaglandin inhibition- eg. NSAIDS or ACEI

50
Q

which patients are at risk of NSAID induced renal impairment

A
  • age>60 years
  • sex F> M
  • underlying renal disease
  • concurrent medication
  • decrease in effective circulating blood volume
51
Q

describe how direct toxicity can occur

A
  1. ATN- acute tubular necrosis: common
    - direct chemical insult to proximal tubule (eg. aminoglycosides, aciclovir, ciclosporin)
  2. interstitial damage- papillae necrosis rare
    - chronic exposure to analgesics or analgesic/antipyretic mixtures (aspirin and paracetamol)
    - ingestion> 1-3kg
52
Q

describe how immunological damage can occur

A
  1. allergic vasculitis- rare, part of generalised allergic reaction caused by thiazides
  2. acute interstitial nephritis- hypersensitivity reaction and extra renal involvement (eg rash, fever)
    - recovery usually associated with drug removal
    - causes= gold, penicillins, allopurinol, loop and thiazides
  3. glomerular damage- immune mediated (Ag/Ab complex)
    - causes= thiazides, gold, penicillamine, captopril, NSAID
53
Q

describe how obstructive uropathy can occur

A
  1. retroperitoneal haemorrhage
  2. retroperitoneal fibrosis (overgrowth of fibrous tissue)
  3. ureteric obstruction
  4. tubular blockage (Hb- drug induced haemolysis)
54
Q

what cautions should be noted when prescribing in renal impairment

A
  1. recognise at risk patients and avoid nephrotoxic agents
  2. suggest alternatives where possible or appropriate monitoring if use unavoidable
  3. recommend appropriate dosage adjustments for renal excreted agents
  4. where renal failure occurs, recommend action relating to drug therapy
  5. educate patients of potential problems and how they could be managed
55
Q

list the sequence of steps to take in treating renal failure

A
  1. treat underlying cause- slowing progression
  2. manage the complications
  3. supportive therapy- dialysis
  4. cure- organ transplantation
56
Q

give examples of complications that may need to be managed in renal failure

A

hypertension, fluid retention, electrolyte control (potassium, calcium and phosphate), anaemia

57
Q

what are some of the complications of hypertension

A

cerebrovascular accident, myocardial infarction, aortic dissection, renal failure

58
Q

describe the core concepts of treatment of hypertension

A

renal disease is both a cause and consequence of hypertension
- reduction of blood pressure reduces the risk of developing both renal and cardiovascular disease

59
Q

what are the consequences of renal damage in hypertension

A
  • decrease in GFR
  • proteinuria
  • glomerular basement membrane changes
  • expanded mesangial matrix
  • glomerulosclerosis
  • tubule-interstitial fibrosis
60
Q

what does better blood pressure control reduce

A

reduces:

  • strokes by one third
  • serious deterioration of vision by one third
  • death related to diabetes by one third
61
Q

what does better glucose control reduce

A

reduces:

  • early kidney damage by one third
  • major diabetic eye disease by one fourth
62
Q

how can hypertension be treated using non pharmacological measures

A
  1. weight reduction (to ibw)
  2. reduced salt intake
  3. limited alcohol consumption
  4. dynamic exercise
  5. increased fruit and veg intake
  6. reduce overall CVS risk (stop smoking, reduce saturated fat intake)
63
Q

how can fluid retention be managed in renal disease

A
  1. fluid restriction- 800-1000ml/day
  2. low salt diets
  3. loop diuretics (effective when GFR as low as 5ml/min)/thiazides (ineffective if GFR<25ml/min)
  4. metolazone- synergism with loop diuretics (short term therapy)
  5. avoid potassium sparing diuretics- hyperkalaemia
64
Q

how can renal disease cause electrolyte disturbances

A
  1. hyperkalaemia- mainly excreted by active tubular secretion
    - small contribution from aldosterone
    - when GFR<5ml/min potassium rises rapidly
    - life threatening condition when >7mmol/L (cardiac arrhythmia)
  2. calcium and phosphate balance
    - deficiency in vitamin D synthesis (hypocalcaemia)
    - decreased phosphate clearance (hyperphosphataemia)
65
Q

describe how hyperkalaemia can be treated

A
  1. care with diet- bananas, coffee, spinach, nuts, chocolate
  2. care with all nephrotoxic drugs and k+ sparing drugs
  3. if potassium between 5-6.5mmol/L use calcium resonium
  4. if K+>6.5mmol/L: 10mls of 10% calcium gluconate over 10 mins, plus 10 units of soluble insulin
    - give in 50mls of 50% dextrose
    - ECG monitoring should be carried out
66
Q

how can calcium and phosphate imbalance be treated

A
  1. active vitamin D, alfacalcidol or calcitriol
  2. oral phosphate binders- complex phosphate in GIT, calcium carbonate or aluminium hydroxide
  3. dietary control
67
Q

how can reduced kidney function cause anaemia

A
  1. kidney is unable to send as much of the hormone to the bone marrow
  2. bone marrow produces fewer red blood cells, causing anaemia
  3. fewer red blood cells carry less oxygen through bloodstream
  4. less oxygen is made available to the organs, which can lead to severe complications
68
Q

how is iron deficiency managed in chronic renal failure patients receiving erythropoietin

A
  1. iron losses are high, especially in haemodialysis patients
  2. oral iron cannot maintain adequate iron stores in haemodialysis patients receiving EPO
  3. EPO stimulates erythropoiesis to >normal levels, leading to functional iron deficiency
  4. prevented by regular use of intravenous iron
  5. transferrin saturation is best indicator of iron availability
  6. serum ferritin is best indicator of tissue iron stores
69
Q

what would usually be found on a typically chronic renal failure prescription

A
  1. oral hypoglycaemic or insulin
  2. antihypertensive
  3. loop diuretic- controls fluid balance
  4. phosphate binder
  5. active vitamin D
  6. iron supplementation- according to degree of anaemia
  7. EPO- according to degree of anaemia
  8. ion exchange resins- to bind potassium
    - avoid potassium sparing drugs
    - consider influence of resin on bioavailability of other drugs

Renal (12 decks)

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