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Clincal - Renal > AKI And CKD > Flashcards

AKI And CKD Flashcards

1
Q

Define AKI

A

A syndrome of decreased renal function, measured by serum creatinine or urine output, occuring over hours-days

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2
Q

How can AKI be staged?

A

According to highest creatine rise of longest period /severity of oliguria

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3
Q

How can AKI be defined?

A

Rise in serum creatinine >26 micromol/L within 48 hours

Rise in creatinine 1.5 times baseline within 7 days

Urine output <0.5mL/kg/H for >6 consecutive hours

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4
Q

Name some risk factors for developing AKI

A

Pre-existing CKD

Age

Male

Comorbidities - DM, CVS disease, malignancy, chronic liver disease, complex surgery

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5
Q

Name 7 causes for AKI

A 
Sepsis 
Major surgery
Cardiogenic shock 
Other hypovolaemia
Drugs 
Hepatorenal syndrome 
Obstruction
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6
Q

How can AKIs be divided?

A

According to the

  • pre renal - decreased perfusion to the kidney
  • renal - intrinsic renal disease
  • post renal disease - obstruction to urine
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7
Q

Name 4 causes of pre-renal AKI pathology

A

Decreased vascular volume = haemorrhage, burns, D&V, pancreatitis

Decreased cardiac output = cardiogenic shock, MI

Systemic vasodilation = sepsis, drugs

Renal vasoconstriction = NSAIDs, ACEi, ARB, hepatorenal Syndrome

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8
Q

Name 3 causes of renal AKIs

A

Glomerular = glomerulonephritis, acute tubular necrosis (prolonged renal hypoperfusion causing intrinsic renal damage)

Interstitial = drug reaction, infection, infiltration

Vessels = vasculitis, DIC

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9
Q

Name two causes of post renal AKIs

A

Within renal tract - stone, renal tract malignancy, stricture, clot

Extrinsic compression - pelvic malignancy, prostatic hypertrophy, retro-peritoneal fibrosis

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10
Q

Name 3 life threatening complications from AKI

A

NEWS scoring - refer critical care

Pulmonary oedema - may require dialysis

Urgent K+

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11
Q

How would you treat hypovolaemia in AKI?

A

Bolus fluid 250-500ml, until volume replete

If 2L given without response - seek expert help

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12
Q

What needs to be monitored during AKI?

A

Fluid balance - consider catheter and hourly urine output

K+ - check response to treatment and at least daily creatinine until it falls

Observations - every 4 hours

Lactate - if signs of sepsis

Daily creatinine until decrease (lags 24 hours behind clinical response)

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13
Q

What investigations can be done for AKI?

A

Urine dipstick (pre-catheter) and quantification of proteinuria. Proteinuria and haematuria may suggest intrinsic renal disease

USS within 24 hours - unless obvious cause or AKI improving

Check liver function - (hepatorenal)

Check platelets - if low, requires blood film to check for haemolysis

Investigate intrinsic renal disease if indicated - immunoglobulins, paraprotein, complement, autoantibodies (ANCA, anti-GBM)

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14
Q

What do small kidneys <9cm on USS suggest?

What do asymmetric kidneys on USS suggest?

A

CKD

Asymmetry - renal Vascular disease

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15
Q

What is the management for AKI?

A

Treat sepsis

Stop nephrotoxic medication - NSAIDs, ACEi, ARBs, aminoglycosides

Stop drugs that increase complications e.g. diuretics (esp. K+ sparing) ,metformin, antihypertensives

Check drug dosages appropriate for renal impairment

Consider gastroprotection - H2/PPI and nutritional support

Avoid radiological contrast

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16
Q

What drugs may increase AKI complications?

A

Diuretics - especially K+ sparing

Metformin

Antihypertensives

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17
Q

What is the generic treatment for a pre-renal AKI?

A

Correct volume depletion and/or treat renal perfusion via circulatory/Cardiac Support, treat any underlying sepsis

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18
Q

What is the generic treatment for a renal AKI?

A

Refer for likely biopsy and specialist treatment of intrinsic renal disease

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19
Q

What is the generic treatment for a post-renal AKI?

A

Catheter, nephrostomy or urological investigation

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20
Q

What are the symptoms of hypovolaemia?

A

Decrease BP

Reduced urine output

Non-visible JVP

Poor tissue turgor

Increase pulse

Daily weight loss

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21
Q

What are the symptoms of fluid overload?

A

High BP

Increased JVP

Lung crepitations

Peripheral oedema

Gallop rhythm

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22
Q

What may be late signs of hypovolaemia?

A

Decreased BP

Skin turgor

Capillary refill time

DONT wait for these signs!

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23
Q

What is the 4 stage process to fluid resuscitation?

A
  1. Give 500ml crystalloid over 15mins
  2. Reassess fluid state. Get expert help if unsure or if patient remains shocked
  3. Further boluses of 250-500ml crystalloid with clinical review after each
  4. Stop when euvolaemic or seek expert help when 2L given

Crystalloid solution = normally 0.9% saline

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24
Q

What may 0.9% saline solution cause?

A

Hyperchoraemic acidosis

Contains increased chloride and is non-buffered

25
Q

Name a balanced/buffered crystalloid

When does caution need to be given if using this solution?

A

Hartman’s
Because they are balanced they are often used preferentially

However, they contain 4-5mmol/L of K+ so caution if hyperkalaemia and oligio/anuria

26
Q

When is a colloid bolus used?

A

Blood component should be used in resuscitation due to haemorrhage

27
Q

How do you manage hypervolaemia (fluid overload)?

A

Oxygen supplementation if required

Fluid restriction - consider oral and IV volumes. Give antibiotics in minimal fluid and consider concentrated nutritional preparations

Diuretics - only in symptomatic fluid overload. They are ineffective and potentially harmful if used to treat oliguria without fluid overload

Renal replacement therapy

28
Q

When are diuretics used to treat hypervolaemia?

A

Only if patient is symptomatic with fluid overload

They are ineffective and potentially harmful if used to treat oliguria without fluid overload

29
Q

How do you treat acidosis?

A

Treat the underlying cause which will stop acid production

30
Q

What are the ECG changes seen in hyperkalaemia?

A

Tall tented T waves

Increased PR interval

Small or absent P waves

Widened QRS complex

31
Q

What is the 4 stage process for treating hyperkalaemia?

K+ >6.5mmol/L or with any ECG changes

A
  1. 10ml of 10% Calcium chloride - cardioprotective but does not treat K+ level
  2. IV insulin and dextrose - stimulates intracellular uptake of K+. Monitor hourly for hypoglycaemia
  3. Salbutamol - causes intracellular K+ shift but high doses are required and tachycardia can limit use
  4. Definitive treatment requires K+ removal. If underlying pathology cannot be corrected renal replacement may be indicated
32
Q

What are the 4 possible indications for renal replacement therapy in AKI?

What does it aim to do?

A

Fluid overload unresponsive to medical treatment

Severe/prolonged acidosis

Recurrent/persistent hyperkalaemia despite medical treatment

Uraemia e.g. pericarditis, encephalopathy

Aim = provide organ support and prevent complications, rather than waiting for them to occur

33
Q

What are the possible complications for renal replacement therapy in AKI?

A

Risk of dialysis catheter insertion and maintenance

Procedural hypotension

Bleeding due to the requirement for Anticoagulation

Altered nutrition

Altered drug clearance

34
Q

Define CKD

A

Abnormal kidney structure or function present for >3months, with implications for health

35
Q

What 3 ways can CKD be classified?

A

GFR category table

Presence of albuminuria as a marker of kidney damage

Cause of kidney disease

36
Q

What is the GFR for category 1,2,3a,3b,4,5?

A 
1 = GFR >90 
2 = 60-89  (only CKD if evidence of kidney damage)
3a = 45-59   mild - moderate
3b = 30-44   moderate - severe 
4 = 15-29 - severe 
5 = <15 = kidney failure
37
Q

What are the three most common causes of CKD?

A

Diabetes

Glomerulonephritis

Increased BP/renovascular disease

38
Q

What does decreased GFR and albuminruria increase the risk of?

A

Mortality

CVS mortality

Progressive kidney disease and kidney failure

AKI

39
Q

What are the three things to clarify in a patient with suspected CKD?

A

Does the patient really have CKD? - does eGFR reflect true GFR? Is it corrected for ethnicity and drugs? Requires evidence of chronicity >3months

Possible causes - previous UTI? PMH of DM, increased BP, IHD? Drug history and when meds were started? Family history? Rule out malignancy?

Current state - patients may have symptoms of CKD if GFR <30. Symptoms of fluid overload e.g. SOB, peripheral oedema, nausea, vomiting, restless legs, weakness, pruitis, bone pain

40
Q

What symptoms will a person with GFR <30 show?

A

Fluid overload - SOB, peripheral oedema

Anorexia

Nausea/vomiting

Restless legs

Fatigue

Weakness

Pruitis

Bone pain

Amenorrhoea

Impotence

41
Q

What signs may you seen on examination of the face in a person with CKD?

A

Anaemia

Xanthelasma

Yellow tinge (uraemia)

Jaundice (hepatorenal)

Gum hypertrophy (ciclosporin)

Cushingoid (steroids)

Periorbital oedema (nephrotic syndrome)

42
Q

What signs may you seen on examination of the periphery in a person with CKD?

A

Peripheral oedema

Vasculitic rash

Signs of peripheral vascular disease or neuropathy

AV fistula

Signs of immunosuppression - bruising from steroids, skin malignancy

Uraemia flap/encephalopathy

43
Q

What investigation can you do for suspected CKD?

A

Blood test - U&Es, Hb,

Urine dipstick - microscopy, culture, stain

Imaging

Histology - consider renal biopsy in progressive disease, nephrotic syndrome, systemic disease, AKI without recovery

44
Q

What renal monitoring should be completed in a CKD patient?

A

GFR and albumin at least annually according to risk

High risk = monitor every 6 months

Small fluctuations are common but a drop in eGFR stage >25%

45
Q

What are the risk factors for CKD decline?

A

DM

Increased BP

Metabolic disturbance

Volume depletion

Infections

NSAIDs

Smoking

All CKD has increased superimposed risk of AKI and needs monitoring and prompt treatment during intercurrent illness

46
Q

What 5 things does management of CKD require?

A
  1. Appropriate referral to nephrology
  2. Treatment to slow renal disease progression
  3. Treatment of renal complications of CKD
  4. Treatment of other complications of CKD
  5. Preparation for renal replacement therapy e.g. dialysis/transplant
47
Q

What treatment can be offered to slow renal disease progression?

A

BP - target 140/90mmHg.
If DM or albumin:Creatinine ratio >70 then BP aim 130/80mmHg

RAAS antagonist - do not combine RAAS antagonist due to risk of hyperkalaemia and hypotension. Check K+ and renal function, prior to and within 1-2weeks of starting treatment/changing dose

Glycaemic contra - target HbA1c of 7% unless risk of hypoglycaemia, comorbidity or limited life expectancy

Lifestyle - exercise, healthy weight, smoking cessation, reduce salt intake

48
Q

Why should RAAS antagonists not be combined when using them to slow renal disease progression?

What should be checked prior to starting RAAS antagonist?

Name two RAAS antagonists.

A

Due to risk of hyperkalaemia and hypotension.

Check K+ and renal function, prior to and within 1-2weeks of starting treatment/changing dose

ACEi or ARB

49
Q

Name some renal complications of CKD

A

Anaemia

Acidosis

Oedema

Bone-mineral Disorders

Restless legs/cramps

50
Q

When should sodium bicarbonate supplements be considered in CKD?

When should caution be given?

A

Patients with eGFR <30 and low serum bicarbonate

Used to treat acidosis

Patients with hypertension and fluid overload due to sodium component

51
Q

How do you treat oedema caused by CKD?

A

Restrict fluid and sodium intake

High loop diuretics may be needed

Can combine loop and thiazide diuretics to have powerful effect

52
Q

How is anaemia as a result of CKD treated?

A

Investigate and treat deficiencies - iron, folate, B12

Iron therapy may need to be given IV

Consider treatment with erythropoietin stimulating agent like ‘Epo’ if Hb <110g/L and likely to benefit in terms of function and quality of life

53
Q

What bone mineral disorders occur as a complication of CKD?

How are they treated?

A

Increased serum phosphate and reduced hydroxylation of vitamin D by the kidney

Treat phosphate >1.5mmol/L with dietary restriction and phosphate binders

Give vitamin D supplements if deficient
If increased PTH persists/increases treat with activated vit D analogue

54
Q

What needs to be excluded with symptoms of restless legs/cramps as a result of CKD?

A

Exclude iron deficiency as possible exacerbating factor

Give sleep hygiene advice

Treatment for severe cases - gabapentin/ pregabalin/ dopamine agonists is off licence

55
Q

What treatment may be given for CVS complications of CKD?

A

Antiplatelets (low dose aspirin)- for those CKD patients at risk of atherosclerosis unless bleeding risk outweighs benefit

Atorvastatin 20mg for primary and secondary prevention of CVS disease

GFR< 60 nay affect troponin and BNP values - interpret results carefully

56
Q

When should planning for renal replacement therapy for CKD begin?

A

Progressive CKD where the risk of renal failure is 10-20% within a year.

Referral to nephrology less than 1 year before RRT is required is considered a late referral

57
Q

What should you check prior to prescribing in renal failure?

A

How administration of the drug should be altered due to decreased GFR - determined largely to the extent to which the drug is renally excreted

Significant for aminoglycosides, penicillins, cephalosporins, heparin, lithium, opiates, and digoxin

Loading doses should not be changed

58
Q

Name some drugs with renal excretion

A 
Aminoglycosides
Penicillins
Cephalosporins
Heparin
Lithium
Opiates 
Digoxin

Clincal - Renal (5 decks)

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