AKI - CKD Flashcards

1
Q

Define AKI

A

• An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.
o NOTE: this can occur in patients with previously normal kidneys or in patients with pre-existing renal disease (acute-on-chronic)

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2
Q

What is used to determine AKI (3)

A

KDIGO
o Increase in serum creatinine > 26 umol/L within 48 hrs
o Increase in serum creatinine to > 1.5 times baseline within the preceding 7 days
o Urine volume < 0.5 ml/kg/hr for >6 hours

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3
Q

Commonest causes of AKI (3)

A

sepsis, ischaemia, nephrotoxins (SIN)

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4
Q

Pre-renal causes of AKI (10)

A

• Pre-Renal (40-70%) – INADEQUATE PERFUSION
o Anything causing renal hypoperfusion
Hypotension (e.g. shock, sepsis, anaphylaxis)
Hypovolaemia (e.g. haemorrhage, severe vomiting)
Renal artery stenosis, ACEi, NSAIDs, ARBs
o Heart failure – cardiorenal syndrome
o Cirrhosis – hepatorenal syndrome

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5
Q

Intrinsic renal causes of AKI (13)

A

o Glomerular - glomerulonephritis, haemolytic uraemic syndrome, autoimmune such as SLE, drugs
o Tubular - acute tubular necrosis (ATN) is commonest intrinsic renal cause; often occurs as a result of pre-renal damage or nephrotoxins (e.g. aminoglycosides)
o Interstitial - acute interstitial nephritis (e.g. NSAIDs, autoimmune), drugs, infiltration with lymphoma/infection/tumour lysis syndrome following chemotherapy
o Vascular - vasculitides (e.g. Wegener’s granulomatosis), large vessel occlusion
o Eclampsia

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6
Q

Intrinsic AKI classifications (5)

A
Glomerular
Tubular
Interstiitial
Vascular
Eclampsia
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7
Q

Pre-renal AKI mechanisms (5)

A
Hypotension
Hypovolaemia
Renal artery stenosis
Heart failure
Cirrhosis
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8
Q

Post-renal AKI classification (3)

A

Luminal
Mural
Extrinsic compression

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9
Q

Post-renal causes of AKI (11)

A

o Luminal: stones, clots, sloughed papillae
o Mural: malignancy (ureteric, bladder, prostate), BPH, urethral strictures
o Extrinsic compression: malignancy (esp pelvic), retroperitoneal fibrosis, prostatic hypertrophy

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10
Q

RF of AKI (18)

A

Age over 75
CKD
Comorbidities (heart failure, peripheral vascular disease, chronic liver disease, DM)
Malignant hypertension
Connective tissue disease (SLE, scleroderma…)
Myeloproliferative disorders (multiple myeloma)
Sepsis
Hypovolaemia
Use of nephrotoxic medications (aminoglycosides, vancomycin, ACEi if overused, NSAIDs)
Poor fluid intake/increased losses
History of urinary symptoms

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11
Q

Nephrotoxic drugs? (4)

A

Vancomycin, NSAIDs, aminoglycosides, ACEi if overused

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12
Q

Epidemiology of AKI

A
  • 18% of adults admitted to hospital will develop an AKI

* Most common in the ELDERLY

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13
Q

S/s of AKI (17)

A
•	Depends on underlying CAUSE 
•	Oliguria/anuria
o	NOTE: abrupt anuria suggests post-renal obstruction
•	Nausea/vomiting 
•	Dehydration 
•	Confusion 
  • Hypertension or hypotension
  • Distended bladder – palpable
  • May have palpable kidneys (suggests polycystic disease)
  • May have renal bruit (sign of renovascular disease)
  • Dehydration - postural hypotension
  • Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
  • Pallor, rash, bruising (vascular disease)
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14
Q

Ix for AKI (metabolic 3, urinalysis 5, bloods 6, immunology 5, virology 2, imaging 3)

A

Basal metabolic profile (hyperkalaemia, high creatinine, metabolic acidosis)
• Urinalysis
o Blood - suggests nephritic cause
o Leucocyte esterase and nitrites - UTI
o Glucose
o Protein – suggests glomerular disease
o Urine osmolality
• Bloods
o FBC
o Blood film
o U&Es
o Clotting
o LFTs
o CRP
o Immunology
• Serum immunoglobulins and protein electrophoresis - for multiple myeloma
 Also check for Bence-Jones proteins in the urine
• ANA - associated with SLE
 Also check anti-dsDNA antibodies (high in active lupus)
• Complement levels - low in active lupus
• Anti-GBM antibodies - Goodpasture’s syndrome
• Antistreptolysin-O antibodies - high after Streptococcal infection
o Virology - check for hepatitis and HIV
• Renal Ultrasound
o Check for post-renal cause
o Can help distinguish obstruction and hydronephrosis
o Shows cysts, small kidneys, masses
• Other Imaging
o CXR - pulmonary oedema
o AXR - renal stones

Urine culture if suspicion of infection

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15
Q

What is urgent to check in AKI

A

K+ and ECG for hyperkalaemia

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16
Q

What do patients with glomerular disease show in a urine dip/exam

A

Patients with glomerular disease typically present with proteinuria and microscopic haematuria with hypertension and oedema.

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17
Q

What happens in prerenal azotemia

A

decreased renal flow stimulates salt and water retention to restore volume and pressure.

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18
Q

Mx of AKI (including for 3 types of KI)

A

• Begin with ABCDE approach along side checking for hyperkalaemia and treating if needed (10 ml 10% calcium gluconate, then 10 units actrapid in 50ml 20% glucose)
• Assess volume status – BP, JVP, skin turgor, capillary refill, urine output
• Aim for euvolaemia
• Stop nephrotoxic drugs such as ACEi, NSAIDs, ARBs, gentamicin, amphotericin, metformin
• Monitor – fluid status, daily U&Es
• Nutrition is vital in critically unwell patient – aim for normal calorie intake and protein.
• Treat the underlying cause
o Pre-renal: correct volume depletion with appropriate fluids/sepsis with antibiotics
o Post-renal: catheterise and consider CT of renal tract and urology referral if obstruction likely cause – requires urgent relief
o Intrinsic renal: refer to nephrology, check for signs of systemic disease
• Renal replacement therapy - dialysis

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19
Q

When is renal replacement therapy considered (4)

A

o Hyperkalaemia refractory to medical management
o Pulmonary oedema refractory to medical management
o Severe metabolic acidaemia
o Uraemic complications

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20
Q

Complications of AKI (5)

A
  • Pulmonary oedema
  • Acidaemia
  • Uraemia
  • Hyperkalaemia
  • Bleeding
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21
Q

Indicators of poor prognosis for patients with AKI (5)

A
o	Age 
o	Multiple organ failure 
o	Oliguria
o	Hypotension 
o	CKD
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22
Q

Define CKD

A
  • Progressive loss of kidney function over a period of months or years
  • Defined as impaired renal function for >3 months with or without evidence of kidney damage i.e. GFR <60ml/min
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23
Q

Classifications of CKD

A
•	Classification of CKD
o	Stage 1: Normal
•	eGFR > 90 ml/min per 1.73 m2 with other evidence of CKD (microalbuminuria, proteinuria, haematuria, structural abnormalities, biopsy showing glomerulonephritis)
o	Stage 2: Mild Impairment
•	eGFR 60-89 ml/min per 1.73 m2 with other evidence of CKD 
o	Stage 3a: Moderate Impairment
•	eGFR 45-59 ml/min per 1.73 m2
o	Stage 3b: Moderate Impairment
•	eGFR 30-44 ml/min per 1.73 m2
o	Stage 4: Severe Impairment
•	eGFR 15-29 ml/min per 1.73 m2
o	Stage 5: Established Renal Failure
•	eGFR < 15 ml/min per 1.73 m2 or on dialysis
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24
Q

RF of CKD in developed countries (7)

A

GOD CHAP
o Glomerulonephritis – commonly IgA nephropathy
o Obesity
o Diabetes mellitus (20%) – T2>T1DM

o Cardiovascular disease
o Hypertension or renovascular disease
o Age
o Pyelonephritis and reflux nephropathy

25
Q

Other RF of CKD bar GOD CHAP (8)

A
o	Arteriopathic renal disease 
o	Nephropathies
o	Family history 
o	Neoplasia 
o	Myeloma 
o	Systemic disease (e.g. SLE) 
o	Smoking 
o	Chronic use of NSAIDs
26
Q

Epidemiology of CKD

A
  • COMMON
  • Risk increases with age
  • Associated with other diseases (e.g. CVD)
27
Q

S/s of CKD (16)

A
•	Often ASYMPTOMATIC
•	May be an incidental finding of a routine blood or urine test 
•	Symptoms of Severe CKD:
o	Anorexia
o	Nausea and vomiting 
o	Fatigue 
o	Pruritus 
o	Peripheral oedema 
o	Muscle cramps 
o	Pulmonary oedema 
•	Sexual dysfunction is common 
•	Physical examination rarely reveals many clues 
•	May show signs of underlying disease (e.g. SLE) 
•	May show complications of CKD (e.g. anaemia) 
•	Signs of CKD:
o	Skin pigmentation 
o	Excoriation marks 
o	Pallor 
o	Uraemic tinge to skin – yellowish
o	Purpura 
o	Hypertension 
o	Peripheral vascular disease 
o	Signs of fluid overload
28
Q

Ix for CKD (3 assessments of renal function, bloods 4, biochemistry 6, serology 5, urinalysis checking for 3, imaging 3, and 1 more)

A

• Assessment of Renal Function
o Urea - not ideal because it varies massively depending on hydration status and diet
o Creatinine - useful but has limitations. Renal function can drop considerably with minimal change in serum creatinine
o Isotopic GFR - GOLD STANDARD but expensive
• Bloods – Hb, ESR, U&Es, glucose
• Biochemistry
o Glucose - check for undiagnosed diabetes and diabetic control
o Potassium - raised
o Also check sodium, bicarbonate, calcium, phosphate
• Serology
o Antibodies
• ANA - SLE
• c-ANCA - granulomatosis with polyangiitis (Wegener’s)
• Anti-GBM - Goodpasture’s syndrome
o Hepatitis serology
o HIV serology
• Urinalysis
o Check for proteinuria/haematuria
o 24 hr urine collection
o Serum or urine protein electrophoresis - check for multiple myeloma
• Imaging
o Ultrasound - check for structural abnormalities
o CT/MRI
o X-Ray KUB - check for stones
• Renal Biopsy – if rapidly progressive disease or unclear cause and normal sized kidneys

29
Q

Define amyloidosis

A

• Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils

30
Q

What are amyloid fibrils

A
  • Amyloid fibrils are polymers of low-molecular-weight subunit proteins
  • These are derived from proteins that undergo conformational changes to adopt an anti-parallel beta-pleated sheet configuration
31
Q

Examples of localised amyloidosis (5)

A

in pancreatic islets of Langerhans (T2DM), cerebral cortex (Alzheimer’s), cerebral blood vessels (amyloid angiopathy), and in bones and joints.

32
Q

3 types of amyloidosis and what do they affect

A

o Type AA - serum amyloid A protein
Also known as secondary amyloidosis
Affects kidneys, liver and spleen
o Type AL - monoclonal immunoglobulin light chains
Also known as primary amyloidosis
Affects kidneys, heart, nerves, gut, vascular
o Type ATTR (familial amyloid polyneuropathy) - genetic-variant transthyretin
Also known as familial amyloidosis
Usually causes a sensory or autonomic neuropathy +/- renal or cardiac involvement

33
Q

Epidemiology of each type of amyloidosis

A
  • AA - incidence of 1-5% amongst patients with chronic inflammatory diseases
  • AL - 300-600 cases in the UK per year
  • Hereditary Amyloidosis - accounts for 5% of patients with amyloidosis
34
Q

Renal s/s of amyloidosis (3)

A

• Renal - proteinuria, nephrotic syndrome, renal failure

35
Q

Cardiac s/s of amyloidosis (4)

A

• Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina

36
Q

GI s/s of amyloidosis (5)

A

• GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding

37
Q

Neurological s/s of amyloidosis (4)

A

• Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome

38
Q

Skin s/s of amyloidosis (5)

A

• Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules

39
Q

Joints s/s of amyloidosis (2)

A

• Joints - painful asymmetrical large joints, enlargement of anterior shoulder

40
Q

Haematological s/s of amyloidosis (1)

A

• Haematological - bleeding tendency

41
Q

Which parts of the body does amyloidosis affect (7)

A

Renal, cardiac, GI, neuro, skin, joints, haematological

42
Q

S/s of amyloidosis (3 renal, 4 cardiac, 5 GI, 4 euro, 5 skin, 2 joints, 1 haem 5 other)

A
  • Renal - proteinuria, nephrotic syndrome, renal failure
  • Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina
  • GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding
  • Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome
  • Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules
  • Joints - painful asymmetrical large joints, enlargement of anterior shoulder
  • Haematological - bleeding tendency
Raised JVP
Lower extremity oedema
Tiredness
Weight loss
Dyspnoea on exertion
43
Q

Ix for amyloidosis

A

• Urine - check for proteinuria, free immunoglobulin light chains (in AL)
• Bloods
o CRP/ESR
o Rheumatoid factor
o Immunoglobulin levels
o Serum protein electrophoresis
o LFTs
o U&Es
• SAP Scan - radiolabelled SAP will localise the deposits of amyloid
• Tissue Biopsy – to diagnose amyloidosis and identify amyloid fibril protein

44
Q

RF of amyloidosis (6)

A

Monoclonal gammopathy of undetermined significance
Inflammatory polyarthropy (rheumatoid arthritis, ankylosing spondylitis…)
Chronic infections (bronchiectasis, chronic UTI’s…)
IBD particularly Crohn’s

45
Q

Ix for amyloidosis (7)

A
Serum immunofixation
Urine immunofixation
Immunoglobulin free light chain assay
Bone marrow biopsy
Tissue biopsy showing positive green birefringence with Congo red dye
SAP scan to localise deposits of amyloid
46
Q

Define BPH

A
  • Slowly progressive nodular or diffuse hyperplasia of the periurethral (transitional) zone of the prostate gland
  • The inner transitional zone enlarges rather than peripheral layer expansion seen in prostate carcinoma
47
Q

RF of BPH (2)

A

FHx

Age over 50

48
Q

Mnemonic for LUTS (9)

A
FUND (irritative)
Frequency
Urgency
Nocturia
Dysuria
HIIPS (obstructive)
Hesitancy
Incomplete voiding
Intermittency
Poor stream
Smell
49
Q

S/s of BPH (chronic and acute) (8 symptoms) obvious signs

A

Weak stream, hesitancy, intermittency, straining, incomplete emptying, and post-void dribbling.
Frequency, urgency, and nocturia.

•	Acute Retention Symptoms
o	Sudden inability to pass urine 
o	Associated with SEVERE PAIN
•	Chronic Retention Symptoms
o	Painless
o	Frequency - with passage of small volumes of urine 
o	Nocturia is a major feature 

• DRE - the prostate is usually smoothly enlarged with a palpable midline groove
• NOTE: there is poor correlation between the size and the severity of the symptoms
• Signs of Acute Retention
o Suprapubic pain
o Distended, palpable bladder
• Signs of Chronic Retention
o A large distended painless bladder (volume > 1 L)
o Signs of renal failure

50
Q

Ix for BPH (9)

A

• Urinalysis
o Check for UTI signs and blood
• Bloods
o U&Es - check for impaired renal function
o PSA – rule out cancer
• Midstream Urine
o MC&S
• Imaging
o US of urinary tract (check for hydronephrosis)
o Bladder scanning to measure pre- and postvoiding volumes
o Transrectal Ultrasound Scan (TRUS) - allows assessment of bladder size and volume - +/- biopsy
o Flexible Cystoscopy

51
Q

Mx of BPH (emergency, conservative, medical 2, surgical)

A

• In Emergency (acute urinary retention)
o Catheterisation
• Conservative (if mild)
o Watchful waiting
o Lifestyle: avoid caffeine, alcohol to reduce urgency. Relax when voiding and control urgency by practising distracting exercises.
• Medical – useful when waiting for surgery
o Selective a-blockers (e.g. tamsulosin) are 1st line - relax the smooth muscle of the internal urinary sphincter and prostate capsule
o 5a-reductase inhibitors (e.g. finasteride) will inhibit the conversion of testosterone to dihydrotestosterone, which can reduce prostate size by around 20%. Excreted in semen so should use condom.
• Surgery
o TURP: transurethral resection of prostate
o TUIP: transurethral incision of prostate – less destruction so less risk to sexual function but gives smaller benefit
o Open prostatectomy

52
Q

Complications of UTI (8)

A
  • Recurrent UTI
  • Acute or chronic urinary retention
  • Urinary stasis
  • Bladder diverticula
  • Stone development
  • Obstructive renal failure
  • Post-obstructive diuresis
  • Complications of TURP
53
Q

Prognosis of BPH

A
  • Mild symptoms are usually well controlled medically

* Most patients get significant relief from surgery

54
Q

What cell types are involved in bladder cancer (2)

A

o Most bladder cancers are transitional cell carcinomas (90%)
o RARELY, bladder cancers may be squamous cell carcinomas associated with chronic inflammation (e.g. schistosomiasis)

55
Q

RF for bladder cancer (9)

A
Smoking
Aromatic amines (rubber industry, dye stuffs (naphthylamine, arsenic and benzidine)
Schistosomiasis
Males
FHx
Chemotherapy
Age >55 years
56
Q

What carcinogens are particularly at play in bladder cancer (3)

A

arsenic, naphthylamine and benzidine

57
Q

Epidemiology of bladder cancer

A
  • 2% of cancers
  • 2nd most common cancer of the genitourinary tract
  • 2-3 x more common in MALES
  • Peak incidence: 50-70 yrs
58
Q

S/s of bladder cancer (7)

A
•	Painless macroscopic haematuria 
•	Irritative/storage symptoms
o	Frequency
o	Urgency
o	Nocturia
o	Voiding irritability 
•	Recurrent UTIs 
•	Rarely: ureteral obstruction
  • Often NO SIGNS
  • Bimanual examination may be performed as part of disease staging
59
Q

Ix for bladder cancer (5)

A
  • Cystoscopy - allows visualisation, biopsy or removal - cystoscopy + biopsy is diagnostic
  • Urine microscopy/cytology – malignancy can cause sterile pyuria
  • Ultrasound
  • Intravenous urography
  • CT/MRI for staging