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S2.6 Renal > AKI/CKD > Flashcards

AKI/CKD Flashcards

1
Q

What is the criteria for diagnosis of acute kidney injury?

A

Increase in serum creatinine with minimal or no urine output

Creatinine increase >26.5microM within 48 hours
- or 1.5x baseline presumed to have occurred in previous week
Urine <0.5mL/kg for 6 hours

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2
Q

What are the general comorbidity risk factors for acute kidney injury?

A 
Age >75
Previous AKI
Heart Failure
Liver disease
CKD
Diabetes
Vascular disease
Cognitive impairment
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3
Q

What are the different classifications of AKI causes?

A

Pre-renal - blood flow to kidney affected
Renal (intrinsic) - damage to renal parenchyma
Post-renal - urine obstruction

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4
Q

What are different pre-renal causes of AKI?

A

Volume depletion - haemorrhage/dehydration
Hypotension/shock
CHF/Liver failure

Sepsis and D&V can be precipitating factors
Arterial occlusion
Vasomotor - NSAIDs/ACEis

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5
Q

What are some intrinsic causes of AKI?

A 
Acute tubular necrosis - ischaemic
Toxin-related
Acute interstitial nephritis
Acute glomerulonephritis
Myeloma
Intra-renal vascular obstruction

Toxins

  • Drugs
  • Radiocontrast
  • Rhabodyolysis
  • Snake venom
  • Mushrooms

Obstruction

  • vasculitis
  • thrombotic microangiopathy
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6
Q

What are some post-renal causes of AKI?

A

Obstruction

  • intraluminal
  • intramural
  • extramural

Intraluminal

  • calculus
  • clot
  • sloughed papilla

Intramural

  • malignancy
  • ureteric stricture
  • radiation fibrosis
  • prostate disease

Extramural

  • RPF
  • malignancy
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7
Q

What is the most common cause of AKI?

A

Poor perfusion leading to established tubule damage

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8
Q

What are risk factors for someone developing radiocontrast-induced AKI?

A 
DM
Renovascular disease
Impaired renal function
Paraprotein
High volume of contrast
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9
Q

What is an important condition to consider that may present as AKI?

A

Multiple Myeloma

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10
Q

What are the symptoms/signs of AKI?

A

Oliguria/Anuria
- Abrupt anuria suggests acute obstruction, acute/severe glomerulonephritis, acute renal artery occlusion

Nausea, vomiting
Dehydration
Confusion

Hypertension
Abdomen distension (bladder enlargement)
Increased JVP, pulmonary/peripheral oedema
Pallor, rash, bruising - may suggest inflammatory or vascular disease

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11
Q

What are the clinical features of multiple myeloma?

A 
Anaemia
Back pain
Weight loss
Fractures
Infections
Cord compression
Markedly elevated ESR
Hypercalcaemia
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12
Q

What investigations might be performed in suspected AKI?

A 
Renal function etc
Urine - dipstick (blood, protein), albumin/creatinine ratio, culture, PCR
FBC
USS
Blood gases 
U+Es
LFTs
Bone
Clotting
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13
Q

What tests should be performed in suspected multiple myeloma?

A

Bone marrow aspirate - >10% clonal plasma cells
Serum paraprotein +/- immunoparesis
Urinary Bence-Jones protein (BJP)
Skeletal survey - lytic lesions

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14
Q

What are some immediately dangerous consequences of AKI?

A

Dependant on cause to an extent in the first few hours

Acidosis
Electrolyte imbalance
Intoxication (toxins)
Overload
Uraemic complications
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15
Q

What test result would suggest hyperkalaemia, and what are some possible complications of hyperkalaemia?

A

ECG changes

  • peaked T waves (tall, tented)
  • P waves widens and flattens
  • PR segment lengthens
  • P waves eventually disappear
  • Prolonged QRS
  • conduction block
  • sinus bradycardia, slow AF

Can cause cardiac arrest

  • asystole
  • VFib
  • PEA with bizarre, wide complex rhythm
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16
Q

What are the possible outcomes of AKI?

A

Short-term (hospital)
- death, dialysis, length of stay

Intermediate, long-term (post-discharge)
- death, CKD, dialysis, CKD related CV events

Mortality

  • dialysis-requiring AKI, 45-75%
  • non-dialysis-requiring still high
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17
Q

What is post-obstructive natriuresis and why does it occur?

A

If GFR recovers quicker than tubule resorptive capacity, excessive diuresis may result e.g. post-obstructive natriuresis

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18
Q

How is AKI prevented in those at risk?

A 
Avoid dehydration
Avoid nephrotoxic drugs
Review clinical status in those at risk and act on findings
? Hold medication
? Give fluids
Treat sepsis
STOP
S - sepsis
T - toxins
O - optimise BP and volume
P - prevent harm - daily U+Es, fluid balance and medication review
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19
Q

How is AKI managed?

A

Remove/treat cause if possible
Pre-renal - fluid/BP support
Renal (intrinsic) - remove precipitant
Post-renal - catheter?

Fluid balance

  • volume resuscitation if volume deplete
  • fluid restriction if volume overload

Optimise BP

  • give fluid/vasopressors
  • stop ACEi/anti-hypertensives

Stop nephrotoxic drugs

  • NSAIDs
  • aminoglycosides
20
Q

How is hyperkalaemia treated?

A

Stabilise myocardium - calcium gluconate
Shift K+ intracellularly - salubtamol, insulin-dextrose
Remove - diuresis, dialysis, anion exchange resins

21
Q

How is the role of the kidney replaced in more severe AKI?

A

Haemodialysis

Haemofiltration

22
Q

What are the pros/cons of haemodialysis and haemofiltration

A 
Dialysis
\+ rapid correction
\+ efficient in hypercatabolic patients
- can cause haemodynamic instability
- intermittent - fluid removal only during treatment

Filtration
+ slower removal associated with better haemodynamic instability
+ absence of fluctuation in volume/solute
- needs continuous anticoag
- may delay mobilisation
- may not have adequate clearance in hypercatabolic patients

23
Q

Why is the kidney susceptible to hypoperfusion?

A

Intrarenal heterogeneity of

  • blood supply
  • oxygenation
  • metabolic demand

The cortex is richly perfused, whereas the medulla receives around 10-15% of renal blood flow
Medulla hypoxic, yet metabolically active

24
Q

What is chronic kidney disease

A

Irreversible and significant loss of renal function

Therefore problems with

  • filtration - excretion
  • filtration - reabsorption/prevention of excretion
  • anatomy
25
Q

How is the diagnosis of chronic kidney disease made?

A

Presence of either:

  • kidney damage - abnormal blood, urine, or x-ray findings
  • OR GFR <60mL/min/1.73m2

That is present for >3 months

26
Q

What are the risk factors for CKD?

A

Renovascular disease - artery stenosis, decreased perfusion
IgA nephropathy
Systemic illnesses - DM, SLE, malignancy, hypertension
Drug exposure - NSAIDs, penicillins, ACEi/ARB, chemotherapy
Pre/post renal factors - CHF, diuretics, dehydration, cirrhosis, prostatic disease
Myeloma

27
Q

What are the symptoms/signs of CKD?

A

Uraemic symptoms

  • nausea, anorexia, vomiting
  • pruritus
  • weight loss
  • weakness, fatigue drowsiness

SOB - fluid overload, anaemia, IHD
Pallor secondary to anaemia of CKD

Urine output change - oliguria, nocturia, proteinuria
Haematuria - bleeding from immune injury to glomerular capillary wall, differentiated from lower tract bleeding via microscopy

Peripheral oedema - renal sodium retention, exacerbated by reduced oncotic gradient in nephrotic syndrome, because of hypoalbuminaemia

Hypertension - primary or secondary effect
Cognitive changes - increases risk of cognitive impairment by 65%

28
Q

What investigations are done in CKD?

A

Assess excretory function

  • GFR (used for staging) - creatinine/inulin clearance/isotope GFR, estimating equations
  • 24 hour urine collection + blood test

Assess filtering function - should be no blood or protein

  • urinalysis
  • albumin/creatinine ratio

Assess anatomy

  • histology - biopsy
  • radiography - USS, XR, CT, nuclear, MRI

Chemistry - U+Es, Bicarb, total protein/albumin, calcium, phosphate, CK, Ig, serum protein electrophoresis

Haematology
- FBC (Hb, MCV, MCH, WBC, Platelets, %hypochromic RBCs)

Coagulation screen

  • PT
  • APPT
  • +/- fibrinogen
29
Q

What investigations are done to exclude active disease?

A

Blood count and film - haemolytic uraemic syndrome
Serum and urine electrophoresis - myeloma
Urine protein:creatinine ratio - intrinsic renal disease
CK - rhabdomyolysis
Anti-GBM - anti-GBM disease
ANCA - ANCA associated vasculitides
C3, C4 autoantibody screen - connective tissue diseases, SLE, etc.

30
Q

How is CKD staged?

A 
Stage 1 - normal or high GFR (GFR > 90 mL/min)
Stage 2 Mild CKD - 60-89
Stage 3A Moderate CKD - 45-59
Stage 3B Moderate CKD - 30-44
Stage 4 Severe CKD - 15-29
Stage 5 End Stage CKD - <15

Can be asymptomatic up to stage 4 or 5

31
Q

How is CKD managed?

A

Detect underlying cause - treatment specific
Slowing rate of decline of renal function - generic therapies
Assessment of complications related to reduced GFR - prevention/treatment
Preparation for renal replacement therapy (dialysis)

Potential interventions to slow the rate of renal decline

  • BP control
  • control proteinuria (particularly ACEis/ARBs)
  • reverse other contributing factors - treat causes

Others

  • allopurinol
  • dietary protein restriction
  • fish oils
  • lipid lowering
  • control acidosis

High BP associated with faster decline so treatment slows progression, particularly with proteinuria

32
Q

When is renal replacement therapy indicated in CKD?

A 
Advanced uraemia (GFR 5-10mL/min)
Severe acidosis (bicarb <10mM)
Treatment resistant hyperkalaemia (>6.5mM)
33
Q

What are the different options in renal replacement therapy?

A

Renal transplant
Haemodialysis
Peritoneal dialysis
Conservative kidney management

34
Q

What are possible complications of CKD? How are they managed?

A

Acidosis - not usually seen until GFR <20 - bicarb
Anaemia - usually when GFR <20 - erythropoietin, iron
Bone disease - will see low Ca, high phosphate - diet, phosphate binders
Cardiovascular - BP/atheroma control, aspirin, exercise/weight
Death and Dialysis
Electrolytes - diet, drugs
Fluid overload - salt/fluid restriction, diuretics
Gout - optimise medications
Hypertension - weight/diet, fluid balance, drugs
Iatrogenic issues

More likely with worsening eGFR
Mortality increases with worsening renal function

35
Q

What are the different forms of access for haemodialysis?

A

Permanent - arteriovenous fistula, AV prosthetic graft

Temporary - tunnelled venous catheter, temporary venous catheter

36
Q

What are possible complications of haemodialysis?

A

CV problems

  • intra-dialytic hypotension and cramps
  • arrhythmias

Coagulation

  • clotting of vascular access
  • heparin related problems

Other

  • allergic reactions to dialysers and tubing
  • catastrophic dialysis accidents (Rare)
37
Q

What are the different forms of peritoneal dialysis?

A

Continuous ambulatory peritoneal dialysis
Automated peritoneal dialysis
Hybrid

38
Q

What are possible complications of peritoneal dialysis?

A

Infection

  • exit site infection
  • tunnel infection
  • peritonitis (Gram + = skin contaminant, -ve = bowel, can be mixed e.g. perforation)

Mechanical

  • tube malfunction
  • abdominal wall herniae

Ultrafiltration problems

39
Q

What restrictions do dialysis patients face?

A

Fluid restriction - dictated by residual urine output, interdialytic weight gain

  • Haemodialysis- usually restricted to 500-800mL/24hr (~ urine + insensible loss)
  • PD - usually more liberal intake as continuous ultrafiltration is often achieved

Dietary restriction
- potassium, sodium, phosphate

40
Q

What other treatments are dialysis patients commonly on?

A

Anaemia

  • erythropoietin injections
  • IV iron supplements

Renal bone disease

  • activated vit D e.g. calcitriol
  • phosphate binders with meals (CaCO3)

Heparin
Water soluble vitamins
?Antihypertensives

41
Q

What are some common immunosuppressant agents used in renal transplant? What are some side effects?

A

Corticosteroids
Calcineurin inhibitors - tacrolimus, cyclosporin
Anti-proliferatives - mycophenolate mofetil, azathioprine
mTOR inhibitors - sirolimus
Costimulatory signal blockers - belatacept
Depleting agents - basiliximab, anti-thymocyte globulin, rituximab

Hypertension, infection, hyperglycaemia
- common side effects

42
Q

What is the protocol/order of immunosuppressant use in transplant?

A

Induction - basiliximab
Maintenance - tacrolimus + mycophenolate + steroids
Steroid free is possible
Others - CNI free using belatacept

43
Q

What are some complications of renal transplant?

A

Rejection

  • cell mediated
  • humoral (Ab mediated)

Cardiovascular

  • underlying renal disease
  • CRF
  • hypertension
  • hyperlipidaemia
  • PT Diabetes

Infective

  • bacterial
  • viral
  • fungal

Malignancy

  • skin
  • lymphoma
  • solid cancers
44
Q

What are the different forms of organ rejection?

A 
Hyperacute rejection (pre-existing alloreactivity to donor)
Acute rejection - T cell mediated or antibody mediated
45
Q

What is the most important transplant-related infection? What are some other important infections to consider

A

Cytomegalovirus
Affects 8% of patients
High mortality and morbidity

Also consider BK and JC viruses (polyomaviridae)

46
Q

What are common malignancies that can present after renal transplantation?

A 
Non-melanoma skin, kaposi sarcoma, non-hodgkins lymphoma
Renal
Melanoma, leukaemia, cervical
Testicular, bladder
Colon, lung, breast

S2.6 Renal (8 decks)

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