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Delta Med - Renal > Renal 3 - Chronic renal Failure and Hypertension > Flashcards

Renal 3 - Chronic renal Failure and Hypertension Flashcards

1
Q

The number of patients requiring RRT in Australia is?

A

Plateauing

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2
Q

What is the leading cause of ESRF in Australia?

A

Diabetic Nephropathy

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3
Q

What are the top 5 causes of ESRF in Australia?

A
  1. DM nepropathy
  2. glomerulonephritis
  3. HTN
  4. PCKD
  5. Reflux nephropathy
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4
Q

What is the leading glomerulopathy causing ESRF and need for RRT in Australia?

A

IgA nephropathy

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5
Q

What is the effect of proteinura on progression of ESRF?

A

increases the rate of progression regardless of stage

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6
Q

What are features of the MDRD equation for calculating eGFR?

A

Doesn’t require height and weight.
More accurate than CG
Inaccurate above GFR >60

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7
Q

What risk factor is the best predictor of renal failure?

A

Reduced GFR (OR 3.01)

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8
Q

What is the best predictor of ESRF in pt with IgA nephropathy?

A
  1. Level of proteinuria
  2. Hypertension

Degree of proteinuria predicts need for RRT
Reducing proteinuria reduces risk for RRT

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9
Q

How does proteinuria cause CKD?

A

Hypefiltration
Tubular toxicity from resorbing certain proteins
Increased tubular work
Mesangial toxicity

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10
Q

What is the most appropriate screening test for diabetic nephropathy?

A

spot albumin:creatinine ratio

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11
Q

How does one convert PCR to g/day proteinuria?

A

if in g/mmol - x10 = g/day

mg/mmol /100 = g/day

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12
Q

In non-diabetics, what is the effect of treatment with ACEi in reducing proteinuria?

A

ACEi is better than lowering BP alone.

Lowering BP is better than doing nothing.

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13
Q

What were the findings of the IRMA study?

A

That in diabetic and hypertensive patients with microalbuminuria - irbesarten reduced the incidence of diabetic nephropathy

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14
Q

In diabetics what is the difference between ACEi and ARB wrt serum creat and urinary albumin excretion?

A

none!

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15
Q

What are issues with dual blockade in non-diabetics?

A

causes improvement in proteinuria, but leads to significant increases in serum potassium, with borderline significant reduction in GFR.

No long-term benefit in avoiding RRT has been proven in diabetics or non-diabetics

ONTARGET showed increase risk of renal impairment and increase in hyperkalemia

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16
Q

What is alternative agent for the reduction in proteinuria?

A

Can consider aldosterone antagonist - spironolactone
prelim data suggests reduced proteinuria and potential benefits for LVF

Hyperkalemia is restricting

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17
Q

What is the benefit of salt restriction in CKD?

A

salt restriction + ACEi is more effective than dual blockade in reducing BP and proteinuia.

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18
Q

What is an acceptable SBP target in patients with renal impairment and proteinuira?

A

125mmHg

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19
Q

What effect does lowering BP have in diabetic nephropathy?

A

Reduces rate of progression.

Aim for

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20
Q

What effect does intensive BSL control have in CKD?

A

IT prevents diabetic nephropathy and delays progression in diabetic nepropathy.

It also reduces rates of stroke, any Diabetic endpoint, DM death or microvascular complications.

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21
Q

What effects do statins have on CKD?

A

Statins reduce proteinuria significantly, but do not alter CKD progression

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22
Q

What is the effect of protein restriction on the progression of renal disease?

A

Equivocal benefit.
ACEi may improve impact of protein restriction
Difficult to sustain
Careful in renal failure
Vegetable protein may be better than animal.

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23
Q

What is the effect of bicarbonate in CKD?

A

in Pt w CKD4 and metabolic acidosis, it reduces the rate of progression to ESRF.

in Pt with CKD2 w/o acidosis and HTnephropathy, patients have a reduced rate of GFR decline.

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24
Q

What are indications for urgent dialysis?

A 
Hyperkalemia - gen w ECG changes
Fluid overload
Uraemic Sx:
 - pericarditis
 - pleuritis
 - encephalopathy
 - bleeding

Relative indication - urea >60 (creat irrelevant)

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25
Q

What are advantages and disadvantages of HD?

A

Adv:

  • efficient solute removal, reasonable fluid removal
  • intermittent - escape

Cons

  • intermittent - fluctuation in solute and fluid removal, BP
  • requires good cardiac function
  • Access can be difficult, esp in DM
  • Heparin exposure
  • Blood exposure to artificial circuit
  • Strict attention required to fluid and solute intake
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26
Q

What are advantages and disadvantages of peritoneal dialysis?

A

Pros:

  • smooth removal of solute and fluid
  • eliminates peaks and troughs
  • cardiac friendly
  • no heparin, no artificial circuit
  • independence

Cons

  • peritonitis and exit site infection
  • inefficient - requires residual renal function
  • respiratory embarrassment
  • requires dexterity and vision
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27
Q

What is the microbiology of PD peritonitis?

A

Gram positive - 50% - skin (Coag -ve staph, S. aureus, enterococcus, streptococcus)
Gram negs - 15% - GUT
Culture negative - 20%
Polymicrobial infection 4% - remove tenckhoff
- mult gram negs, gram +ve and gram -vs

Exit site infection 13%
Peritoneal fluid leak 3%
Hospitalisation 31% - most Rx in Community

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28
Q

What is the initial therapy of PD peritonitis?

A

Intraperitoneal antibiotics

  • need gram +ve and -ve activity
  • typically 1st and 4th gen cephalosporins +/- gentamicin
  • ETG - cefazolin + gentamicin - if systemic feat, change cefazolin to vanc, or if MRSA colonised.

If multiple organisms:
- require lapartotomy if enteric

Recurrent peritonitis can = sclerosing peritonitis

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29
Q

What improves survival in HD patients?

A

dialysis duration?

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30
Q

How is dialysis adequacy measured and what is the goal?

A

URR = pre urea - post urea / pre-urea

Goal is >70%

Mortality is increased in patients with

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31
Q

What is the general goal of dialysis time?

A

15hrs/week, 5hrs x 3 days generally

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32
Q

What is the general overall mortality rate in HD patients?

A

10%/year, average 40-50% survival at 5 years.

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33
Q

What is the most likely cause of death in a patient commencing dialysis?

A

Cardiovascular event

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34
Q

What are significant comlpications of renal failure?

A 
Cardiovascular disease
Anaemia
Renal bone disease
Hypertension
Hyperlipidaemia
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35
Q

What is the OR of CV disease in patients with ESRF

A

20-1000 - the MOST POTENT Risk factor

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36
Q

What are traditional risk factors for CVD in patients?

A 
Age
Gender
Smoking
HTN**
DM**
Lipids**
LVH**
Physical inactivity**
FHx
Obesity

** All have increased incidence in renal failure

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37
Q

What is the significance of lipid status in ESRD patients?

A

Lowering lipids does not afford a reduction in CV risk, addit of statins does not improve mortality in ESRD patients.

SHARP study

continue if already on statins, likely calcific disease vs lipid rich plaques

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38
Q

What is the prevalence of LVH in Dialysis patients?

A

70%

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39
Q

What impact does LVH have upon survival?

A

Survival is reduced in patients with severe LVH, in ESRD patients

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40
Q

What is the effect of BP control in haemodialysis patients?

A

BP 170-79 increases mortality, however meta-analysis favours treatment. ? LVH management.

Aim for

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41
Q

What is the effect of obesity in ESRF patients?

A

Increasing BMI reduces mortality.

42
Q

What are non-traditional risk factors in ESRD?

A 
Anaemia
Uraemic retention solutes
Oxidative stress products
Advanced glycation end products
Inflammation (IL-6 and CRP)
Pro-coagulant factors
Hyperphophataemia (Ca x PO4 product)
PTH
Homocysteine
Neuropeptide Y
Malnutrition
43
Q

What is the Hb range target in renal failure patients?

A

110-130g/dl

44
Q

What is the relationship between Hb and outcomes in renal failure patients

A

Higher Hb levels are associated with lower rates of mortality and hospitalisation (>120),

45
Q

What is the effect of Hb >130 in HD patients?

A

Increased mortality
Pt feel better with Hb >120
Mortality likely 2ndary to higher EPO dose

46
Q

What are targets for Ferritin and transferrin saturation in ESRF patients?

A

Aim for ferritin >200, and transferrin saturation >20%
IV is better than oral in HD patients.
HD patients lose 2g of iron /year

47
Q

What is the strongest clinical parameter in increasing motrality via CV risk in HD patients?

A

Serum phosphate

48
Q

What effect does vit D have on renal excretion of Ca and P

A

Decreases BOTH

49
Q

What effect does PTH have on Ca and P renal excretion?

A

Decreases Ca, Increases P

50
Q

What effect does calcitonin have on renal excretion of Ca and P?

A

Increases BOTH

51
Q

What effect does FGF23 have on Ca and P excretion in the kidney?

A

NO effect on Ca, increases P

52
Q

What effect does vitamin D and PTH have on Ca and P in bone?

A

Increases lability of both into serum, Calcitonin reduces mobilisation from bone

53
Q

What is the relative effect of phosphate and Ca on mortality?

A

PO4-»> Ca++ wrt mortality

Can look at Ca PO product instead

54
Q

What is the effect of arterial calcification in ESRD patients?

A

increased arterial calcification predicts higher risk of CV mortality

55
Q

What is the goal of treatment of hyperphosphataemia in ESRD patients?

A

Reduce PO4-

  • phosphate binders or dialysis
  • avoid calcium based PO4- binders if calcium is high

Prevent hyperparathyroidism

  • replace vitamin D to maintain normal serum Ca
  • use vit D as suppressive therapy
  • If non responder consider calcimimetics or PTHectomy (if PTH >100)
56
Q

What effect do phosphate binders have in ESRD patients?

A

they reduce rates of all cause and cardiovascular mortality.

very mild preference with regard to overall mortality for non-calcium binders (0.87)

57
Q

What is the effect of calcimimetics on mortality?

A

NONE - removed from PBS for this reason.

58
Q

What are the mechanisms of renal bone disease?

A

Hyperparathyroidism - osteitis fibrosa/osteomalacia (subperiosteal resorption on X-ray)

Low active form of Vit D - reduced bone mineralisation

Adynamic bone disease/aluminium deposition
- severe aluminium toxicity can result in: anaemia, encephalopathy and hypercalcaemia

59
Q

What is most likely to increase serum phosphate in chronic renal failure?

A

Calcitriol

60
Q

What is calciphylaxis?

A

subepidermal calcific obstruction of small vessels.
may be precipitated by hypotension
central type associated with mortality of >50%
treatment is difficult - hyperbaric oxygen, sodium thiosulphate

61
Q

What must be reduced to reduce vascular calcification?

A

Must reduce serum:

  • phosphate
  • PTH
  • Calcium
  • and CaxPO4 product

(phosphate is the MOST IMPORTANT)

62
Q

What is the relationship between serum albumin and mortality in ESRF?

A

lower albumin increased risk of death, esp

63
Q

What are properties of IL-6 in HD patients?

A

IL-6 more predictive of CV mortality than CRP
IL-6 has atherogenic properties on plts, endothelium and coag factors
Strong and independent predictor of progression of carotid atherosclerosis and mortality in pre-dialysis patients.

64
Q

What is the classification of BP in adults?

A

Normal =160 or >=100

65
Q

What is essential hypertension?

A 
Unknown cause, 80-95% of HTN
RFs
 - salt
 - obesity
 - alcohol
 - angiotensin excess
 - sympathetic excess
 - FHx
66
Q

What is the impact of hypertension?

A

Most important cause of stroke (ischaemic or ICH) and premature cardiovascular disease.

Major cause of renal failure, heart failure and LVH

67
Q

What are prognostic factors in HTN?

A 
History
smoking, male, age
Fundi - grade III or IV changes
Heart - LVH or cardiac failure
Kidneys - renal failure, albuminuria (and urinary casts), microalbuminuria
Assoc disease
 - IHD, DM, hyperlipidaemia
68
Q

What is the effect of HTN treatment?

A

Reduces stroke by 35-40%
MI by 20-25%
Heart failure by 50%

69
Q

What are expected red in SBP with lifestyle interventions?

A

Wt reduction 5-20mmHg/10kg lost
DASH eating plan 8-14mmHg
Dietary sodium restriction (

70
Q

What are 1st line drugs in HTN management?

A

ACEi/ARB OR CCB or Low dose thiazide in >65 yo

71
Q

What are 2nd line options in HTN management if targets not reached?

A

ACEi/ARB + CCB or ACEi/ARB + thiazide

72
Q

What are 3rd line options in HTN management if targets are not reached?

A

ACEi/ARB + CCB + thiazide

73
Q

Which agents reduce the risk of stroke the most?

A

Calcium channel blockers?

74
Q

What agents are shown to reduce the risk of coronary heart disease?

A

Thiazides, ACEi, CCB (not B-blockers)

All agents are better than placebo with respect to Stroke and CHD

75
Q

Which agents reduce risk of coronary heart disease after acute MI?

A

Beta blockers

76
Q

At what level is treatment of HTN indicated?

A

At most levels of hypertension there is a benefit

77
Q

What is better - single drug or multidrug regimen?

A

Three drugs at 1/2 the standard dose provide a greater benetfit than one drug at a standard dose.

78
Q

When is HTN treatment indicated in those >60 years?

A

when SBP >=150, DBP >=90, treat to goal

79
Q

When is HTN treatment indicated in the general population

A

Init w DBP >=90, and treat to DBP =140, and treat to

80
Q

In >18y and CKD, when is HTN treatment indicated?

A

> =140mmHg or DBP >=90mmHg.

81
Q

In 18y and DM, when is HTN treatment indicated?

A

SBP >=140 or DBP >=90mmHg.

82
Q

In the non black population incl DM, what is initial management?

A

Thiazide, CCB, ACEi, or ARB

83
Q

In the black population, including DM, what is initial management?

A

Thiazide or CCB

84
Q

In CKD, what is initial management?

A

ACEi or ARB, regardless of race or diabetes

85
Q

What are recommended drugs in HTN with CHF?

A

Diuretic, BB, ACEi, ARB or Aldo ANT

86
Q

What are recommended drugs in HTN post-MI?

A

BB, ACEi or Aldo ANT

87
Q

What are recommended drugs in HTN with High CAD risk?

A

Diuretic, BB, ACEi, CCB

88
Q

What are recommended drugs in HTN with DM?

A

Diuretic, BB, ACEi, ARB, CCB

89
Q

What are recommended drugs in HTN with CKD?

A

ACEi or ARB

90
Q

What are recommended drugs in HTN with recurrent stroke prevention?

A

Diuretic, ACEi

91
Q 
What Antihypertenstives are C/I in the following conditions?
Angioedema
Bronchospastic disease
Depression
Liver disease
Pregnancy
2nd/3rd degree HB
A 
Angioedema - ACEi
Bronchospastic disease - Beta Blockers
Depression - Reserprine
Liver disease - methyldopa
Pregnancy - ACEi or ARB
2nd/3rd degree HB - Beta blocker, nondihydropyridine CCB
92
Q

When is ambulatory blood pressure monitoring useful?

A 
suspected white coat HTN
Apparent drug resistance
hypotensive symptoms with antihypertensive meds
episodic hypotension
autonomic hypotension
93
Q

What are common causes of 2ndary hypertension?

A 
Intrinsic renal disease
renovascular disease
mineralocorticoid excess/aldosteronism
OSA
Meds - OCP, NSAIDS
94
Q

What are uncommon causes of 2ndary hypertension?

A

Phaeochromocytoma
Glucocorticoid excess/cushing’s disease
Coarctation of the aorta
Hyper/hypothyroidism

95
Q

When should testing for primary aldosteronism be considered?

A 
Hypertension and hypokalaemia
Resistant hypertension
Adrenal incidentaloma and hypertension
Onset of HTN =160/>=100
Whenever considering 2ndary hypertension
96
Q

What is the first line test in testing for primary aldosteronism?

A

Morning blood pressure in seated patient:
Plasma aldosterone concentration (PAC)
Plasma renin activity (PRA or PRC)

If PAC elevated, or reduced PRA or PRC AND PAC/PRA ratio >= 555 or >=20 investigate for primary aldosteronism

97
Q

What are confirmatory tests for hyperaldosteronism

A
  1. Oral salt loading
  2. IV salt loading
  3. Fludrocortisone suppression

Goal is to determine if aldosterone can be suppressed - if not after salt or fludro with salt then primary aldosteronism can be Dx

98
Q

What drugs should be avoided prior to testing for hyperaldosteronism?

A

aldosterone blockers
eplerenone
high dose amiloride

Probably ok on ACEi or ARB

99
Q

What is the next test when primary aldosteronism is confirmed?

A

Adrenal CT scan

If normal or micronodularity or bilateral masses and low prob of AHA - likely idiopathic hyperaldo - treat pharmacologically.

If high prob APA and above, for AVS - if lateralisable - APA or PAH - laparoscopic adrenalectomy

If unilateral hypodense nodule >1cm or 40, for lateralisation. if

100
Q

When should renovascular hypertension be considered?

A 
young pts with HTn
severe or refractory HTN
increased Creat with ARB/ACEi
Flash APO (more common in bilateral)
Known vascular disease and HTN

Screening not useful unless treatment is planned

101
Q

What are tests for RAS?

A

Angiography - gold std
CT angiogram - most Sn test
MRI/A - beware if CrCl 0.8, predicts poor outcome with angiography

102
Q

What was the outcome of the CORAL study?

A

NO benefit in treatment of renal artery stenosis with stents over and above medical therapy wrt hard endpoints, however still can attempt stenting if there is failure of medical therapy to control HTN etc.

Delta Med - Renal (3 decks)

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