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1
Q

what are the pre renal causes of AKI

A

Shock - dehydration, hypovolaemia
 RAS
 Hepatorenal syn.

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2
Q

what are the renal causes of AKI

A

Glomerulonephritis
 Acute Tubular Necrosis
 Interstitial disease

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3
Q

what are the post renal causes of AKI

A
  1. Diseases of renal papillae, pelvis, ureters, bladder or urethra.

SNIPPIN

 Stone
 Neoplasm
 Inflammation: stricture
 Prostatic hypertrophy
 Posterior urethral valves
 Infection: TB, schisto
 Neuro: post-op, neuropathy
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4
Q

what are the presentations relating to AKI

A 
Uraemia / Azotaemia
 Acidosis
 Hyperkalaemia
 Fluid overload
 Oedema, inc. pulmonary  ↑BP(or↓)
 S3 gallop
 ↑ JVP
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5
Q

how would you assess for AKI clinically

A 
1. Acute or chronic?
 Can’t tell for sure: Rx as acute
 Chronic features
 Hx of comorbidity: DM, HTN
 Long duration of symptoms
 Previously abnormal bloods (GP records)
2. Volume depleted?
 Postural hypotension
 ↓ JVP
 ↑ pulse
 Poor skin turgor, dry mucus membranes
3. GU tract obstruction?
 Suprapubic discomfort
 Palpable bladder
 Enlarged prostate
 Catheter
 Complete anuria (rare in ARF)
4. Rare cause?
 Assoc.  ̄c proteinuria ± haematuria
 Vasculitis: rash, arthralgia, nosebleed
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6
Q

what are the investigations required in AKI

A

Bloods: FBC, U+E, LFT, glucose, clotting, Ca, ESR
 ABG: hypoxia (oedema), acidosis, ↑K+
 GN screen: if cause unclear. f blood and protein on urine dipstick – perform c-ANCA (PR3) + p-ANCA (MPO) too look for vasculitis, anti-GBM, ANA,
C3, C4 to look for lupus nephritis, serum immunoglobulins and electrophoresis to look for myeloma
 Urine: dip, MCS, chemistry (U+E, PCR, osmolality, BJP)
 ECG: hyperkalaemia
 CXR: pulmonary oedema
 Renal US: Renal size, hydronephrosis

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7
Q

describe how AKI is classified

A

RIFLE = 3 grades of AKI and 2 outcomes
Classification determined by worst criteria

table

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8
Q

in pre renal failure what is happens to osmolality and sodium

A

in pre-renal failure, urine is concentrated and Na is reabsorbed = increase osmolality, Na less than 20mM

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9
Q

what is the general management for AKI

A

 Identify and Rx pre-renal or post-renal causes
 Urgent US
 Rx exacerbating factors: e.g. sepsis
 Give PPIs
 Stop nephrotoxins: NSAIDs, ACEi, gent, vanc
 Stop metformin if Cr > 150mM

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10
Q

What are the features to be monitored in AKI

A

Catheterise and monitor UO
 Consider CVP
 Fluid balance  Wt.

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11
Q

what are the ECG changes seen in hyperkalamia

A 
ECG Features (in order)
 Peaked T waves
 Flattened P waves
 ↑ PR interval
 Widened QRS
 Sine-wave pattern → VF
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12
Q

how do you treat hyperkalaemia

A

10ml 10% calcium gluconate
 100ml 20% glucose + 10u insulin (Actrapid)  Salbutamol 5mg nebulizer
 Calcium resonium 15g PO or 30g PR
 Haemofiltration (usually needed if anuric)

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13
Q

how do you treat pulmonary oedema

A

Sit up and give high-flow O2
 Morphine 2.5mg IV (± metoclopramide 10mg IV)
 Frusemide 120-250mg IV over 1h
 GTN spray ± ISMN IVI (unless SBP <100)
 If no response consider:
 CPAP
 Haemofiltration / haemodialysis ± venesection

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14
Q

what are the indications for acute dialysis (in AKI)

A
  1. Persistent hyperkalaemia (>7mM)
  2. Refractory pulmonary oedema
  3. Symptomatic uraemia: encephalopathy, pericarditis 4. Severe metabolic acidosis (pH <7.2)
    reabsorbed → ↑osmolality, Na <20mM
  4. Poisoning (e.g. aspirin)
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15
Q

what are the life threatening complications in AKI

A

Hyperkalaemia

Pulmonary oedema

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16
Q

how do you manage acute renal failure

A

refer to notes

  1. A-E
  2. life threatening complications
  3. shock or dehydration
  4. monitor
  5. look for evidence of post renal causes
  6. hx and lx
  7. manage sepsis
  8. further management
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17
Q

what are the features of chronic renal disease?

A

Kidney damage ≥3mo indicated by ↓ function
 Symptoms usually only occur by stage 4 (GFR<30)
 ESRF is stage 5 or need for RRT

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18
Q

how is CKD classified

A

based on eGFR
stage 1 = Greater than 90 ml/min, with some sign of kidney damage on other tests (if all the kidney tests* are normal, there is no CKD)

stage 2 = 60-90ml/min if kidney tests are normal, no CKD
stage 3a = 45-59ml/min
stage 3b = 30-44ml/min
stage 4 = 15- 29ml/min
stage 5 = less than 15 ml/ min = dialysis or kidney transplant needed

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19
Q

what are the common causes of CKD

A

Common
 DM
 HTN = Chronic raised BP causing nephrosclerosis.

Other
 RAS
 GN
 Polycystic disease
 Drugs: e.g. analgesic nephropathy 
 Pyelonephritis: usually 2O to VUR 
 SLE
 Myeloma and amyloidosis
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20
Q

describe the inheritance pattern for adult polycystic disease and chr affected by type 1 and 2

A

2 Types (both are autosomal dominant)
 Type 1 (85%; PKD1 mutation on Chromosome 16)
 Type 2 (15%; PKD2 mutation on Chromosome 4)

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21
Q

what are sx seen in APKD

A

size of the kidney, infection of the cysts (flank pain, haematuria, and fever) or can be asymptomatic

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22
Q

what are the factors affecting anaemia in chronic kidney disease

A

Decreased production of erythropoietin from the kidney
Absolute iron deficiency (poor absorption and malnutrition)
Functional iron deficiency (inflammation, infection) Blood loss
Shortened Red Blood Cell survival
Bone marrow suppression from uraemia Medication induced
Deficiency of Vit B12 and folate

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23
Q

in CKD, mineral bone disease leads

A

CKD leads to
Increased Fibroblast Growth Factor-23 Increased Alkaline Phosphatase and PTH Increase Phosphate
Decreased Serum Calcium
decreased 1,25 - vitamin D

24
Q

describe tertiary hypothyroidism in CKD

A

Occurs when PTH release continues despite raised serum Calcium levels (independently)
• As a result of parathyroid gland nodular hyperplasia
• Consequence of advanced CKD

25
Q

how is anaemia of CKD managed

A

Measure haematinics – Vitamin B12, Folate, Ferritin, Iron, Transferrin Saturation, CHr
If deficient in any of above – replace this first
• IV Iron may be better tolerated than PO Discuss with renal team regarding starting ESA
aim for Hb 100-120

26
Q

describe management of ADPKD

A

Control BP
 As per CKD management
 Tolvaptan (Vasopression receptor-2 antagonist) is
available for some patients to slow progression of
CKD.
 Genetic counselling and testing

27
Q

how id ADKPD DX

A

Family history is KEY

USS

28
Q

describe the pathophysiology and investigations for HTN nephropathy and treatment

A

Chronic raised BP causing nephrosclerosis.

Investigations to identify if primary or secondary HTN (based on clinical findings and index of suspicion):
 24 hour Urinary metanephrines (Phaeochromocytoma)
 Aldosterone: Renin ratio (Primary aldosteronism)
 Cortisol & Dexamethasone suppression test
(Cushing’s syndrome)
 TSH (hyperthyroidism)
 MRA (Renal artery stenosis)

Treatment
Anti-hypertensives (see ABCD guidelines)

29
Q

in CKD what are questions to ask

A 
past UTI
HTN, DM
FH
DH
sx
30
Q

what are the investigations in CKD

A

BLOOD = ↓Hb, U+E, ESR, glucose, ↓Ca/↑PO4, ↑ALP, ↑PTH
 Immune: ANA, dsDNA, ANCA, GBM, C3, C4, Ig, Hep
 Film: burr cells

Urine: dip, MCS, PCR, BJP

Imaging
 CXR: cardiomegaly, pleural/pericardial effusion, oedema
 AXR: calcification from stones
 Renal US
 Usually small (<9cm)
 May be large: polycystic, amyloid
 Bone X-rays: renal osteodystrophy (pseudofractures)
 CT KUB: e.g. cortical scarring from pyelonephritis

renal biopsy if cause unclear and size normal

31
Q

what are the complications of CKD

A

CRF HEALS

Cardiovascular disease
 Renal osteodystrophy
 Fluid (oedema)
 HTN, Hypothyroidism secondary and tertiary
 Electrolyte disturbances: K, H
 Anaemia
 Leg restlessness
 Sensory neuropathy
32
Q

describe the features our renal osteodystrophy

A

osteoporosis: ↓ bone density

 Osteomalacia: ↓ mineralisation of osteoid (matrix)

33
Q

describe the mechanism of renal osteodystrophy

A

↓ 1α-hydroxylase → ↓ vit D activation → ↓ Ca → ↑ PTH
 Phosphate retention → ↓ Ca and ↑ PTH (directly)
 ↑ PTH → activation of osteoclasts ± osteoblasts
 Also acidosis → bone resorption

34
Q

describe the management of CKD

A

MDT focused

general = rx reversible causes
stop nephrotoxic drugs

lifestyle = exercise, healthy weight, stop smoking, Na, fluid and PO4 restriction

CV risk = statins, low dose aspirin, manage DM

HTN = target 140/90 and 130/80 if DM. in DM kidney disease give ACEi/ARB

ACEi/ ARB = reduce proteinuria

Oedema = furesomide

Bone disease = phosphate binders = sevelamar. vit D analogues - alfacalcidiol. Ca supplements

Anaemia = exclude IDA and ACD. EPO to raise Hb to 11g/dl (higher thrombosis risk)

Restless legs = clonazepam

Refer for fistula
o Venous mapping
 Refer for PD tube insertion
 Work-up for transplant
o Further tests
o Refer to Transplant work-up clinic
35
Q

describe RRT options

A

H.D
P.D
kidney transplant

36
Q

diabetic nephropathy is the biggest cause of…

A

ESKD

37
Q

describe the pathology of diabetic nephropathy

A

Hyperglycaemia → renal hyperperfusion → hypertrophy and ↑ renal size
 Hypertrophy and metabolic defects inc. ROS production → glomerulosclerosis and nephron loss
 Nephron loss → RAS activation → HTN

38
Q

clinically, what are the progression of diabetic nephropathy

A

Microalbuminuria (30-300mg/d or albumin:creatinine >3)
 Strong independent RF for CV disease
 Progresses to proteinuria (albuminuria >300mg/d)
 Diabetic retinopathy usually co-exists and HTN is
common

39
Q

describe screening for diabetic nephropathy

A

T2DMs should be screened for micrroalbuminuria 6 monthly

40
Q

how is diabetic nephropahty managed

A

Good glycaemic control delays onset and progression BP target 130/80
Start ACEi/ARB even if normotensive
Stop smoking
Combined kidney pancreas Tx possible in selected pts

41
Q

renal transplant is the treatment of choice in …

A

ESRF

42
Q

what factors needs to be checked/ or assessed before renal transplant

A

Virology status: CMV, HCV, HBV, HIV, VZV, EBV
 CVD
 TB
 ABO and HLA haplotype

43
Q

what are the contraindications to renal transplant

A

Active infection
 Cancer
 Severe HD or other co-morbidity

44
Q

what are the types of renal graft?

A

cadaveric: brainstem death ̄c CV support

 Non-heart beating donor: no active circulation

 Live-related = Optimal surgical timing + HLA-matched + Improved graft survival

 Live unrelated

45
Q

what immunosuppression is required in renal transplant

pre and post op

A 
pre = campath/alemtuzumab 
post = pred short term and tacrolimus/ciclosporin long term
46
Q

what is the prognosis for cadaveric renal allografts

A

15 years

47
Q

what are the complications of renal transplant

A 
Post-op
 Bleeding
 Graft thrombosis
 Infection
 Urinary leaks
Hyperacute rejection (minutes)
 ABO incompatibility
 Thrombosis and SIRS

Acute Rejection (<6mo)
 ↑ing Cr (± fever and graft pain)
 Cell-mediated response
 Responsive to immunosuppression

Chronic Rejection (>6mo)
 Interstitial fibrosis + tubular atrophy
 Gradual ↑ in Cr and proteinuria
 Not responsive to immunosuppression

Ciclosporin / tacrolimus nephrotoxicity

 Acute: reversible afferent arteriole constriction → ↓GFR
 Chronic: tubular atrophy and fibrosis

↓ Immune Function
 ↑ risk of infection: opportunists, fungi, warts
 ↑ risk of malignancy: BCC, SCC, lymphoma (EBV)

Cardiovascular Disease
 Hypertension and atherosclerosis

48
Q

what are differentials for raising Cr in Tx pt

A

Rejection
 Obstruction
 ATN
 Drug toxicity

49
Q

what are the causes of hyperkalaemia

A

CKD, K rich diet with CKD (dried fruit, potatoes, oranges, tomatoes, avocados, nuts)
 Drugs (ACEi/ARBs/Spironolactone/Amiloride/NSAIDs/ Heparin/ LMWH/Cyclosporin or calcineurin inhibitors/High dose Trimethoprim/ Digoxin toxicity/B- blockers)
 Hypoaldosteronism (T4RTA), Addison’s disease, Acidosis, DKA (insulin deficiency), Rhabdomyolysis, tumour lysis, Massive haemolysis, Succinylcholine use
 Rarer – Hyperkalaemic periodic paralysis, Gordon’s syndrome
 Artifact Hyperkalaemia – haemolysis, leucocytosis, thrombocytosis

50
Q

what does each drug used in hyperkalaemia do?

A

Treatment of hyperkalaemia involves:
1. Stabilizing the myocardium to prevent arrhythmias
 10mls of 10% Calcium Gluconate over 5-10 minutes

  1. shifting potassium into intracellular space
    IV fast acting insulin (actrapid)
     10 units and IV glucose/dextrose 50% 50mls
    Sodium Bicarbonate
     500mls of 1.4% Sodium Bicarbonate
     Only effective at driving Potassium intracellullarly
    if the patient is acidotic
    Salbutamol
     5-10mg via nebulizer
  2. Eliminating Potassium From the Body: Calcium Resonium
     15-45g orally or rectally, mixed with sorbitol or lactulose
    Frusemide
     20-80mg depending on hydration status
    Dialysis
     If resistant to medical treatment
51
Q

what are sx of hypokalaemia

A

Fatigue, constipation, proximal muscle weakness, paralysis, cardiac arrhythmias, worsened glucose control in diabetics, hypertension

52
Q

what are the causes of hypokalaemia

A

Pseudohypokalaemia – acute leukaemia
 Extra-renal losses - Inadequate PO intake, Gut
losses (vomiting, NG losses, secretory Diarrhoea, laxatives, VIPoma, Zollinger-Ellison, Ileostomy, enteric fistula)
 Redistribution – Delirium tremens, beta agonists, insulin, caffeine, theophylline, alpha-blockers (Doxazosin), hypokalaemic periodic paralysis (inherited or acquired from thyrotoxicosis – Asian males)
 Refeeding syndrome, alkalosis, vigorous exercise, glue-sniffing (Toluene can cause Fanconi/RTA II with renal potassium wasting)
 Primary hyperaldosteronism (conn’s syndrome) Cushing’s syndrome, Secondary hyperaldosteronism (liver failure, heart failure, nephritic syndrome),
 Renal losses (diuretics, RTA, Tubulopathies - Bartters/Liddles/Gittelmans), liquorice, glucocorticoids, hypomagnesaemia.

53
Q

what are the ECG changes seen in hypokalaemia

A

ECG Changes
 Small T waves
 U wave (after T)
 Increased PR interval

54
Q

what are the rx of AKI

A 
Diabetes
 CKD
 IHD/CCF/CVD
 Any major medical co-morbidity
 Elderly >75
 Sepsis
 Medications – ACEi, ARBs, NSAIDs, Antibiotics
55
Q

how is hypokalaemia treated

A

Replace magnesium
 Oral K replacement
 IV K replacement (Usually in 0.9% NaCl - avoid in
dextrose as induces further hypokalaemia)

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