renal failure symposium Flashcards

1
Q

what is chronic kidney disease

A

GFR <60ml/min/1.73m2 for >3 months with or without kidney damage and/or
kidney damage >3 months with/without dec GFR via path abnormalities (markers like proteinuria) or UACR >30mg/g

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2
Q

what happens to the kidney in chronic disease

A
multiple injurious stimuli 
diabetes
hypertension
vascular disease
hyperfiltration
eg glomerulosclerosis, interstitial scarring or tubular atrophy
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3
Q

pathogenesis of manifestations of CKD

A

slow progressive loss of nephrons unnoticed
silent disease
maladaptive compensatory func
loss of renal func/adaptations lead to manifestations for failure

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4
Q

how is CKD classified

A
Stage 1 baseline 
2 Mild reduction (WRT normal for young adult)
3 mild-mod
4 sev reduction
5 Failure/ESRD
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5
Q

survival in ESRD

A

Dec with age

much less in diabetics

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6
Q

How does CVD affect CKD

A

can lead to uremic cardiomyopathy from atherosclerosis

heart failure and sudden cardiac death as a result

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7
Q

Benefits of good management of CKD

A

Prevent or slow progression to renal failure
Reduce morbidities
Improve quality of life
Reduce costs

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8
Q

how is kidney function measured

A

measured by serum creatinine clearance

relationship not linear - not completely accurate

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9
Q

what is eGFR

A
rough measure of the number of functioning nephrons
Actual GFR (by inulin clearance) not routinely measured in clinical settings
GFR is equal to the sum of the filtration rates in all of the functioning nephrons
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10
Q

what is MDRD

A

An equation used to estimate GFR in adults
uses Cr, Age, ethnicity & gender
Association of estimated GFR with measured iGFR in outpatients

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11
Q

how does cock-croft Gault estimate GFR

A

Age, Cr and Wt

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12
Q

Flaws with creatinine

A

indicator of excretory func
renal func more complicated eg acid-base, fluid, electrolyte, endocrine etc
eGFR only for stable CKD

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13
Q

Signs of kidney disease

A
accumulation of waste (uraemia)
fluid balace (oedema)
endocrine (anaemia or bone chemistry)
electrolyte (hyperkalaemia)
acid-base (metabolic acidosis with normal AG)
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14
Q

significance of proteinuria

A

Indicative of glomerular disease (leaky glomerular basement membrane)
Proteinuria is nephrotoxic (causes downstream renal tubular cell damage)
Marker for increased risk of progression of renal disease
Major benefit from lower BP target, and ACE inhibitors

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15
Q

how is proteinuria measured

A

Dipstick inaccurate, and can miss sig proteinuria
Different range for people without diabetes
No 24 hr urine collection
Spot urine sample for protein:creatinine or albumin:creatinine ratio usually sufficient
All patients with CKD stage 3 or worse should have proteinuria measured at least once

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16
Q

Estimating 24 hour urine protein excretion from the ACR & PCR

A

PCR/ACR (mg/mmol) x 10 ≈ 24 hour excretion (mg/24 hrs)

protein: creatinine ratio of 110 mg/mmol ≈ 1100mg proteinuria/ 24 hours (1.1g/24 hrs)
albumin: creatinine ratio of 15mg/mmol ≈ 150mg albuminuria/24 hrs (0.15g/24 hrs)

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17
Q

what is normal proteinuria in non diabetics

A

<30 ACR and <50 PCR

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18
Q

what is normal albuminuria in diabetics

A

<2.5
microalbuminuria 2.5-30
clinical proteinuria >30
3.5 women

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19
Q

lifestyle measures for CKD

A

dietetic history
salt restriction
no smoking

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20
Q

how does proteinuria related to BP targets

A

PCR <50 140/90
50-99 140/90 refer if haematuria present or GFR declines
>100 <130/80 and refer

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21
Q

how is Intraglomerular pressure effected at the afferent and efferent glomerular arterioles

A
afferent - NSAIDS relax
efferent - ACE inhibitors effect
RAS
Dehydration
Sepsis
Pump failure/hypoperfusion
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22
Q

how do ace inhibitors effect diabetic neuropathy

A

slow

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23
Q

what should be given to diabetics with CKD

A

statins to lower lipids

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24
Q

what is AKI

A
a rapid (hours to days) decline in excretory kidney function
Sig mortality (often CVD or infection)
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25
classification of AKI
``` Serum Cr AKIN 1 1.5-2fold inc from baseline 2 >2-3 3 >3 ```
26
are classifications of AKI useful
Diagnosis of AKI could be made Within 6h of onset of oliguria Within 48h of 50% rise in Cr OR Cr rise by at least 26.5 µmol/l
27
what are most cases of AKI from
community missed diagnosed/lack of intervention on the inc
28
how can AKI predict mortality
inc risk of mortality and morbidity | predicts progression to advanced CKD, ESRD
29
How does AKI link to CKD
recovery from AKI predicts outcome and likely progression to CKD
30
Why is AKI associated with terrible morbidity and mortality
distant organ effects - inflammatory disease | bone, heart, brain, lungs, liver
31
who is at risk of AKI
``` Pre-existing CKD Age >60 Comorbidity Diabetes Cardiac failure Liver disease Iatrogenic/Pathological derangements Sepsis Hypovolaemia Hypotension Contrast Post-op Drugs ```
32
Potentially Reversible/Actively Treatable Causes of AKI
Obstruction Rapidly progressive glomerulonephritis Multiple myeloma
33
Type and cause of AKI
Pre renal eg sepsis, hypotension, HF post renal eg stones, tumours intrinsic AKI eg injury, myeloma, nephrotoxins
34
how is AKI assessed
``` Sepsis - screen and test Toxins - drugs/iv contrast Optimise BP/vol status Prevent harm eg identify cause and treat complications AKI ```
35
how is hypotension treated
Clinical fluid assessment Maintain BP and therefore renal blood flow filling – crystalloid (unless haemorrhagic shock) Inotropes in patients with vasomotor shock
36
how is fluid overload treated
``` When full give diuretics maintain urine flow reduces metabolism of tubular cells protects from ischaemia no diuretics to prevent or treat, only to manage ```
37
how is acidosis treated
Treat with NaHCO3 (isotonic)
38
how is hyperkalaemia treated
Correct acidosis Insulin/Dextrose is only a temporary measure Other electrolytes Ca, Mg
39
when should AKI be taken to a specialist
AKIN 2 & 3 AKIN 1 unresolving despite simple measures Worried about Inflammatory disease/RPGN/Myeloma
40
Indications for urgent renal replacement therapy
Uncontrollable fluid overload Uncontrollable, severe metabolic acidosis Uncontrollable hyperkalaemia Uraemic pericarditis / encephalopathy Poisoning – ethylene glycol, lithium, NSAIDs
41
role of nurse specialist in CKD
prolong renal function Empower patients to make appropriate treatment choices Prepare patients physically and psychologically for their treatment choice
42
Treatment choices for CKD
transplant peritoneal/haemodialysis physidia - new tech max conservative care - support, symptom control
43
how is anaemia treated with CKD
``` Target Hb 100-120 g/L transferrin sat >20% serum ferritin 100-140 mcg/L oral iron - GI upset IV iron ```
44
what is ESA
Erythropoietin stimulating agent injections or pen when req + monitoring 3 monthly iron stores
45
dietary interventions for renal patients
``` energy protein potassium phosphate fluid/salt fibre vits and mins other ```
46
individual patient assessment for dietary needs
``` bloods type (AKI, CKD, Stage) Type of treatment fluid balance MUST other health conditions medications ```
47
role of nutrition in preserving kidney function
``` avoiding xs protein/inc diet quality as inefficient filtering inc net endogenous acid and accelerates nephron damage optimising blood glucose BP weight management keep active ```
48
modifiable risk factors for CKD
``` glucose in diabetes hypertension anti-hypertensiive agents DASH/med diet less sodium no smoking reg exercise weight loss lower lipids ```
49
CKD related malnutrition
``` dietary and fluid restrictions poor appetite (uraemia and taste change) long treatment restricts time multiple morbidities XS protein catabolism micronutrient def due to dialysis/meds ```
50
protein recommendations for renal patients
0.8g per kg in low clearance/transplant pts 1-1.2g dialysis conservative management - protein restriction
51
fluid for renal patients
No kidney function 500-750mls per day Impaired kidney function- generally encourage to drink Transplant- Generally drink lots post transplant Haemodialysis- 500mls plus 24 hour urine Peritoneal dialysis- 750mls plus 24 hour urine Hypervolemia = Oedema, pleural effusions, hypertension, congestive Heart failure (CHF) Sodium- A no added salt diet advised
52
important differentials for fluid
Poor diabetes control Urine output has decreased Patient is unaware of fluid restriction
53
potassium in renal patients
4- 6mmol/l dialysis 3.2- 5.5mmol/l Low clearance K balance for muscle/cardiac function
54
high potassium food
Bananas, dried fruit, exotic fruits Mushrooms, parsnips, sprouts, spinach, tomatoes Chips, jacket potato Coffee, hot chocolate, milk, fruit juice, cider, strong beer and stout Chocolate, nuts Lo salt, Marmite, Bovril
55
important differentials for potassium
``` Acidosis Inadequate dialysis dose Medications (especially ACE inhibitors), Poor diabetic control Constipation Blood transfusions Haemolysed samples Catabolism/sepsis ```
56
phosphate in renal patients
1.1 – 1.7 mmol/L dialysis. 0.9 – 1.5 mmol/L low clearance Low phosphate diet plus phosphate binders/ alfacalcidol (PTH) Low PO4 = Assess malnutrition risk. Ca and PO4 homeostasis required for bone health. Pruritis (Itchiness).
57
high phosphate foods
``` Dairy products Reduce or switch to lower phosphate alternatives Oily fish with bones Shellfish Offal Nuts/chocolate Processed foods- additives dark fizzy drinks eg. Coke, Pepsi, Dr Pepper ```
58
what are phosphate binders
Often required in addition to a low phosphate diet. Prescribed to take with meals. Difficult to remember for some patients. Lots of different types/ preparations.
59
important differentials for phosphate
Binders taken at the wrong time Unable to swallow binders Forgetting to take binders Binder dose needs titrating up
60
micronutrients in renal patients
Avoid fat soluble vitamins in end stage kidney disease (A, D, E and K) Routine supplementation of water soluble vitamins for all dialysis patients.
61
Managing nutrition for multiple health conditions
``` Diabetes Malnutrition Obesity Gastro complications Depression Special diet burnout ```