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Life Maintenance > Renal medicine > Flashcards

Renal medicine Flashcards

1
Q

What are the main functions of the kidney?

A 
Acid-base balance
Water balance
Electrolytes
Toxin removal
Blood pressure regulation
EPO synthesis
D (vitamin) D 1a hydroxylation
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2
Q

How do renal syndromes correlate with disease?

A

One clinical disease can manifest in several different renal syndromes

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3
Q

How is kidney function measured?

A

Blood tests: creatinine
Urine output
Elimination of radioisotopes

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4
Q

How is eGFR calculated?

A

(current guidance) CKD-EPI algorithm based on serum creatinine
adjustments included for gender, race and age

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5
Q

In which contexts is CKD-EPI not a useful eGFR indication?

A

extremes of muscle mass, other ethnicities (aside from black or caucasian), fluctuating GFR)

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6
Q

What are the 3 broad tempos of renal failure?

A

Acute - occurs within days of an insult or injury
Chronic - progressively deteriorating renal function over years
(also a MODERATE type where renal failure occurs over weeks-months)
Acute on chronic - idea that those with chronic renal impairment are more susceptible to acute insults

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7
Q

How common is AKI?

A

It affects 20% of all emergency admissions

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8
Q

What is the mortality rate of AKIs?

A

25-40%
even a minor increase in serum [creatinine] has impact on mortality risk
20-30% of AKIs are preventable

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9
Q

What are the long term complications of AKIs?

A

CKD
End stage renal failure (ESRF)
death

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10
Q

What are the different stages of AKI severity?

A

Stage 1: SCr increase >26 umol/L in <48hr or >1.5-1.9x baseline; urine output < 0.5ml/kg/hr for 6hr (consecutive)
Stage 2: SCr > 2-2.9x baseline; urine output <0.5ml/kg/hr for 12hr
Stage 3: SCr >3x baseline or SCr >354 umol/L or initiated on RRT; urine output <0.3ml/kg/hr or anuria for 12hr

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11
Q

What are pre-renal causes of AKI?

A

Hypovolemia
Hypoperfusion
Drugs (ACEi, NSAIDs)

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12
Q

How do ACEi/ARBs affect GFR?

A

ACEi prevent vasoconstriction of the efferent arteriole, thus resulting in vasodilation and reduced GFR -> reduced systemic BP

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13
Q

How do NSAIDs affect GFR?

A

NSAIDs inhibit production of prostaglandins which normally cause vasodilation of afferent arteriole. As a result, there is vasoconstriction of the afferent arteriole which reduces the systemic blood volume entering the kidney and can cause hypoperfusion as well as reduces the GFR

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14
Q

What are the intrinsic renal causes of AKI?

A

Glomerular (glomerularnephritis, systemic disease)
Tubular (acute tubular necrosis)
interstitial (interstitial nephritis)

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15
Q

What the main types of glomerular disease?

A

nephrotic disease: proteinuria and oedema

nephritic disease: inflammation and haematuria (some proteinuria may also be present0

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16
Q

What are the main principles to consider with glomerular disease?

A

Primary vs. Secondary
Primary should be considered under clinical syndrome, histopath. and pathogenesis
There are often no good clinicopathological correlations
Redundant terminology (multiple names for one pathology)
Pathogenesis is unknown in many cases

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17
Q

What are the main types of PRIMARY glomerular disease?

A 
nephrotic syndrome
nephritic syndrome
asymptomatic urinary abnormalities
rapidly progressive GN
CKD
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18
Q

What are post-renal causes of AKI?

A

Bladder stones
Tumours post-renal
enlarged prostate
hydronephrosis/hydroureter (enlargement)

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19
Q

What is the immediate management of hyperkalaemia?

A

Calcium gluconate: cardioprotective as decreases responsiveness of cardiac muscle to potassium in blood
Glucose/insulin: shift of K+ ions into cells via increased activity of Na+ K+-ATPase pump
(Acidosis may be managed with HCO3- infusion)

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20
Q

What is the consideration when giving bicarbonate to correct metabolic acidosis in AKI?

A

Additional HCO3- will push equilibrium of Henderson-Hasselback equation to left and therefore generate more CO2
This may exacerbate respiratory compensation or status
Not ideal where resp. function is compromised (e.g. COPD)

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21
Q

Why does administration of glucose/insulin correct hyperkalaemia?

A

Leads to movement of K+ ions into the cell as insulin promotes uptake of glucose.
This occurs secondary to increased Na+/K+ ATPase activity

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22
Q

Why may treatment of hyperkalaemia result in an initial worsening acidosis?

A

Influx of K+ into cells means that there is a simultaneous efflux of H+ out of cells
This may result in more acidosis or be converted into CO2 (respiratory excretion)

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23
Q

When should renal replacement therapy (RRT) be commenced?

A

AKI is established and unavoidable

BUT complications have not yet developed

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24
Q

What are the main risks of RRT?

A

VTE
Bacteremia (sepsis)
Haemorrhage from anticoagulants

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25
Q

What are the main indications for starting RRT?

A

Urgent: hyperkalaemia, volume overload

Non-urgent: Uraemia, acidosis

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26
Q

What are the biochemical indicators for initiating dialysis in AKI?

A

Refractory hyperkalaemia > 6.5 mmol/l

serum urea > 30 mmol/l
Refractory metabolic acidosis pH ≤ 7.1

Hyponatraemia / hypernatraemia / hypercalcaemia

Tumour lysis syndrome with hyperuricaemia and hyperphosphataemia

Urea cycle defects, and organic acidurias resulting in hyperammonaemia, methymalonic acidaemia

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27
Q

What are the clinical indicators for starting dialysis in AKI?

A

Urine output < 0.3 ml/kg for 24 h or complete anuria >12 hrs

AKI with multiple organ failure

Refractory volume overload

End organ damage

Create intravascular space for plasma and other blood product infusions and nutrition

Severe poisoning or drug overdose

Severe hypothermia or hyperthermia

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28
Q

When may RRT be deferred even if some clinical and/or biochemical indicators are present?

A

When the underlying clinical conditions is improving

Or there are some early clinical signs of renal recovery

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29
Q

What are the main functions of dialysis?

A

removes nitrogenous waste
corrects electrolytes
removes water
corrects acid-base disturbances

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30
Q

Which renal functions can dialysis NOT do?

A

Red blood cell production
Blood pressure control
Vitamin D activation

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31
Q

How is chronic kidney disease (CKD) staged?

A 
Stage 1 (Kidney damage) 
GFR >90 mL/min
Stage 2 (mild GFR) 
GFR = 60-89 mL/min

Stage 3 (moderate GFR)
3a, GFR 45-59
3b, GFR 44-30

Stage 4 (severe GFR)
GFR 15-29
Stage 5 (kidney failure)
GFR <15 or dialysis
32
Q

What proportion of the UK population is affected by CKD stages 3-5?

A

8.5%

consumes ~2% of budget

33
Q

What are the traditional risk factors for cardiovascular disease in CKD?

A 
Age 
gender
hypertension
diabetes
hyperlipidemia
smoking 
obesity
34
Q

What are the uraemia related risk factors for cardiovascular disease in CKD?

A 
Inflammation
oxidative stress
anaemia
calcification
homocysteine
malnutrition
Vit D def
35
Q

What are the general measures used to manage chronic renal failure?

A
  • aim to slow down the progression of disease

- treat symptoms and/or complications

36
Q

What specific therapies available for chronic renal failure?

A

Immunosuppression: for autoimmune conditions such as SLE, vasculitis

Tolvaptan for polycystic kidney disease
Used to treat hyponatraemia. Improved urine output w/o losing too much Na+

37
Q

What benefits can be brought by slowing down the rate of disease progression?

A

Maintains kidney function for longer
Minimises systemic side effects for other organs
Staves off need for dialysis

38
Q

What are the main methods by which disease progression is slowed?

A

Early, good treatment/control of DM
BP control <130/80
ACEi or ARBs
Healthy lifestyle

^^ this should be done early on in renal failure progression

39
Q

What complications can occur in chronic renal failure?

A

Salt and water retention:(glomerular disease)

Salt and water loss:
(tubulointerstitial disease)

Retention of urea and creatine:
(Uraemia)

hyperkalaemia due to K+ retention

Problems with Ca2+, phosphate, Vit. D and PTH:
(renal bone disease)

Lack of EPO:
(Anaemia)

40
Q

Why does renal bone disease occur in chronic renal failure?

A

Kidneys: 1-alpha hydroxylation of vitamin D3 -> activation
- reduced GFR
- reduced filtered phosphate load
- phosphate retention
- reduced 1, 25 hydroxylation -> reduced Ca2+
- increased PTH secretion
= secondary hyperparathyroidism and bone disease (LONG TERM)

41
Q

What is renal anaemia?

A

reduced EPO synthesis by kidney

Functional iron deficiency caused by increased hepcidin

42
Q

What is hepcidin?

A

hepatic bactericidal protein

LOSS of hepcidin causes increased/excessive iron absorption in duodenum
This causes iron overload = haemachromotosis

EXCESS hepcidin (e.g. during inflammation or infection)
- iron dysregulation and anaemia
43
Q

What biochemical parameters need to be regulated in chronic renal failure?

A 
Na+, water
BP
Diet (K+, phosphate, [protein])
Vitamin D (1-alpha OH)
EPO
44
Q

What options are available to patient as kidney function reaches end stage?

A

conservative management

transplantation

haemodialysis

peritoneal dialysis

palliative care

45
Q

What are the demographics of renal disease?

A

CKD is major public health issue
number of patients needing RRT (dialysis or transplantation) is increasing
~ 6-8% per annum

46
Q

In which demographic group, has the growth in patients needing dialysis been the biggest?

A

Elderly

47
Q

What are the options regarding transplantation for CKD?

A

deceased donor: brain death
deceased donor: cardiac death
living donor: pre-emptive, related, kidney sharing scheme, altruistic, ABO/HLA incompatible

48
Q

How are patients connected to a haemodialysis machine?

A

long term haemodialysis: via AV fistula

acute/short term haemodialysis: via subclavian (central venous catheter)

49
Q

What is peritoneal dialysis?

A

Dialysis solution is inserted into the abdomen via a permanent catheter and then removed

Abdomen is used as the dialysis membrane via which waste is excreted and other useful molecules are retained

This solution is usually enriched in glucose (osmotic agent)
It is also high in NaCl, hydrogen carbonate

PD is less efficient than HD for waste removal

50
Q

How does peritoneal dialysis remove fluid/toxins?

A

By osmosis
water molecules and (dissolved) uraemic toxins diffuse across semi-permeable membrane into dialysis fluid in peritoneum
Glucose moves from the peritoneum into the intra- and extra-cellular space (interstitial)

51
Q

What are the main functions of dialysis?

A
  • removes nitrogenous waste
  • corrects electrolytes
  • removes water/fluid
  • corrects acid-base imbalance
52
Q

What are the mortality figures for survival from day 0 RRT?

A

80% survival at 2yr
70% survival at 3yr
60% survival at 5yr
50% survival at 10yr

53
Q

How is CKD monitored over time?

A 
measure eGFR
proteinuria or haematuria?
intrinsic renal disease?
tempo of disease (acute vs chronic)
kidney size?
biopsy?
general and specific treatments
manage consequences of poor eGFR: vitamin D deficiency, EPO deficiency, dialysis, transplantation
54
Q

What are the main causes of hyperkalaemia?

A 
M: medications e.g. ACEi, NSAIDs
A: acidosis (metabolic or respiratory) 
C: cellular destruction e.g. burns, trauma
H: hypoaldosteronism, haemolysis
I: intake (excess)
N: nephron damage, renal failure
E: excretion (impaired)
55
Q

What is reseeding syndrome?

A

causes a large release of insulin
this causes rapid influx of K+, PO4 and Mg2+ into the cell
= hypokalaemia, hypophosphataemia, and hypomagnesemia

56
Q

What is the risk of prescribing trimethoprim alongside an ACE inhibitor?

A

trimethoprim (antibiotic)
Ramapril (ACEi)

Can cause life-threatening hyperkalaemia (which can be fatal)

57
Q

What is the mechanism of action of amiloride?

A

= K+ sparing diuretic

inhibits Na+ channels in the cortical collecting ducts

58
Q

What is the mechanism of action of thiazide diuretics?

A

inhibit the Na+ Cl- cotransporter in the distal convoluted tubule.

59
Q

What is the mechanism of action of loop diuretics?

A

inhibit Na+ K+ 2Cl- cotransporters in the thick ascending loop of Henle.

60
Q

What is the mechanism of action of Spironolactone?

A

= K+ sparing diuretic

inhibits the Na+/K+ exchanger in the cortical collecting ducts by blocking the action of aldosterone on aldosterone receptors.

61
Q

What kind of dietary intervention is contra-indicated in microalbuminaria a T2DM patient?

A

high protein diet

persistent microalbuminaria is indicative of early diabetic nephropathy

high protein diet has been shown to accelerate glomerulosclerosis in established renal disease
this can exacerbate renal function (reduced GFR)
High protein can also stimulate secretion of GH and IGF-1 which promotes renal decline

62
Q

Where does the bladder receive sympathetic innervation from?

A

superior and inferior HYPOGASTRIC plexuses

This maintains detrusor capacity (by preventing PNS contraction of the bladder)

63
Q

What are the 2 types of potassium-sparing diuretics?

A
  1. epithelial sodium channel blockers (amiloride and triamterene)
  2. aldosterone antagonists (spironolactone and eplerenone)
64
Q

What is amiloride?

A
  • weak diuretic
  • blocks epithelial sodium channel in the DCT
  • usually given with thiazides or loop diuretics as alternative to K+ supplementation
65
Q

What is spironolactone?

A
  • aldosterone antagonist

- acts at the DCT

66
Q

What are the clinical indications for K+ sparing diuretics?

A
  • ascites (cirrhosis patients can develop secondary hyperaldosteronism)
  • Heart failure
  • nephrotic syndrome
  • Conn’s syndrome (primary hyperaldosteronism)
67
Q

What are the main clinical features of nephrotic syndrome?

A
  • oedema
  • proteinuria
  • hypercholesterolaemia
  • hypoalbuminaemia

-> fluid retention leading to hypervolaemic hyponatraemia

68
Q

What type of epithelium lines the bladder?

A

transitional epithelium

69
Q

How does transitional epithelium aid bladder function?

A

when these cells are stretched (e.g. full bladder), they become flatter

Plasticity between stretched and empty bladder allow the bladder to cope with varying fluid levels
also a barrier between urine and bloodstream

70
Q

Which part of the renal tubule is impermeable to water?

A

thin ascending limb of loop of Henlé

71
Q

What are foods that are high in potassium?

A
  • salt substitutes

- bananas, kiwifruit, oranges, avocado, spinach

72
Q

What is the risk of beta blockers in renal failure?

A

Hyperkalaemia

Can interfere with potassium transport (salbutamol, a SABA may be used as emergency Rx)

73
Q

What is the risk of heparin in potassium levels?

A

hyperkalaemia

both unfractionated and low MW heparin can do this

thought to be caused by inhibition of aldosterone secretion

74
Q

What regulates plasma potassium levels?

A
  • aldosterone levels
  • acid-base balance
  • insulin levels
75
Q

What ECG changes are seen in hyperkalaemia?

A
  • tall tented T waves
  • small P waves
  • widened QRS complex (sinusoidal pattern and systole)
76
Q

Which medications can cause hyperkalaemia?

A
  • potassium sparing diuretics
  • ACEi
  • ARBs
  • spironolactone
  • ciclosporin
    [- heparin
  • beta blockers]

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