Renal Flashcards

1
Q

Acute kidney injury
What is it

A

Acute deterioration in renal function and build up of waste products
Abrupt -1-7 dayy
Sustained >24 hours

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2
Q

RIFLE criteria

A

Risk: serum creat >1.5x increase
GFR >25-50% decrease
UO < 0.5ml/kg/hr for 6 hours

Injury: serum creat >2x increase GFR > 50-75% decrease
UO < 0.5ml/kg/hr for 12 h

Failure: creat 3x increase or >4mg/dL or decrease GFR> 75%
UO < 0.3ml/kg/hr or anuria for 12 h

Loss: persistent AKI complete loss function 4 weeks

ESRF: complete loss >3 m

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3
Q

AKIN criteria

A
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4
Q

AKIN criteria

A
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5
Q

KDIGO definition AKI

A
  1. UP <0.5ml/kg/hr for 6 hours
  2. Serum creat >1.5x normal in last 7 days
  3. Serum creat >0.3mg/dL in 48 hours
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6
Q

Severity AKI

A

Stage 1: 1.5-1.9 x baseline cr
>0.3mg/dL increase from baseline

Stage 2: 2-2.9 increase baseline scr

Stage 3: > 3.0 x baseline scr or RRT

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7
Q

Risk factors for AKI

A

Sepsis
Age>65
Race
Pre existing CKD
Surgical patients
cVs disease
Liver failure pts
Diabetes
Oligouria
Nephrotoxins
Contrast

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8
Q

Indications for dialysis

A

A: refractor acidaemia <7.2
E: electrolyte abnormalities K>7
I: ingestions toxins BLAST: barbiturates, lithium, alcohol, salicylates, theophyline
O: oedema apo
U: uraemia pericarditis, encephalopathy

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9
Q

Causes of AKI

A

Pre renal: hypo perfusion

Renal: structural/ functional changes at nephron ATN

Post renal: obstruction

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10
Q

Causes of pre renal aki

A
  • dehydration: blood loss, diarrhoea, diuretic, vomting, sepsis
  • shock: hypotension
  • low effective: heart failure: liver failure
    Anatomical: renal artery stenosis
    Drug induced: nsaids, acei
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11
Q

Causes of Renal AKI

A

ATN: most common
Nephrotoxins: nsaids, contrast, allopurinol, gentamicin, furosemide, herbicides, heavy metal ACEi
Glomerulonephropathies: nephrotic vs nephritic syndrome
HUS
Rhabdo: myoglobin
Severe HTN

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12
Q

Post renal aki

A

Obstruction
Ureters: stone or structure, retroperitoneal fibrosis
Bladder: cancer
Prostate: BPH: cancer
Urethra: stricture
External mass/ LN

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13
Q

Complications of AKI

A

Volume overload: CHF, HTN, APO
Metabolic acidosis: reduced albumin, impaired insulin’s action increase bsl
Electrolyte: low na and high K
Pulmonary oedema: low albumin and reduced oncotic pressure
ALI: neutrophils
Uraemia: encephalopathy, confusion, seizures, pericarditis
Haematological: reduce RBC reduce epo
GI: ulceration and haemorrhage
Pharmacology: reduce vd under or over dosing

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14
Q

Phases of AKI

A

Phase 1: onset: insult renal blood flow 25% of normal, UO<0.5ml/kg/hr
Phase 2: oligouric: OU <400mls/ day
Increase in urea and creat, electrolyte abnormalities
Phase 3: polyuric in UO>400mls/ day. Hypotension hypovolaemia
Increase GFR
Phase 4: recovery: normalisation of GFr 80% electrolyte and fluid UO normal

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15
Q

Management of AKI

A

IVF
Maintain UO, diuretics mannitol
Monitor K
Acidosis
Relief onstruction IDC/ nephrostomy
Withhold Nephrotoxins
GIH prophylaxis

A address drugs withhold nephrotoxic
B blood pressure fluid and tropes
C calculate fluid balance
D. Dip urine
E exclude obstruction catheter

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16
Q

Urea creatinine ratio
What is it? What does it mean?

A

Both freely filtered at the glomerulus
Creatinine is not reabsorbed
Urea is reabsorbed by the tubules
Can be used as an indicator of renal failure
If issue is intrinsic to kidney urea is not reabsorbed therefore the ratio is closer to one

If the issue is pre-renal the kidney is still working and urea is reabsorbed therefore the creatinine and ratio is further away from one

Urea: creatinine
Pre renal >100:1 or bun: Creat >20:1
Renal <40:1 or bun: creat <10:1

Ensure units are same

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17
Q

AKI
How to distinguish cause renal vs pre renal
Creat: urea ratio
Urine Na
Fraction excreted na
Urine osmolalitu

A

Urea: creat pre renal >100:1 Renal <40:1
Urine Na pre renal <20mEq/l renal: >20mEq
FENa pre renal <1% and renal >2%
Urine osmolality >500 renal >350 mOsmol/l

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18
Q

Bun: creat ratio.
Causes of high

A

Drivers can use GPS
D: dehydration, pre renal, haemorrhage vomting
C: corticosteroids
G: GIH
P: protein rich diet
S: severe catabolic state

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19
Q

Bun: creat ratio.
Causes of low

A

I am SIMPLE SR

S: severe liver failure
I: intrinsic renal damage
m: malnutrition/ starvation
P: pregnancy
L: low protein intake
E:
S: siadh
R: rhabdo

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20
Q

What is most common inheritance of polycystic kidney disease

A

Autosomal dominant
But also can be recessive

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21
Q

Most common cause of death in PCKD

A

Cardiac cause of death

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22
Q

Most common presenting symptoms of PCKD

A

Hypertension

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23
Q

Associated disease PCKD

A

Berry aneurysm: 8-10%
Thoracic aortic and cervicocephalic artery dissection
Coronary A aneurysm
MV prolapse
Defective sperm motility and infertility

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24
Q

PCKD where do cysts form

A

Kidney 100%
Liver 80%
Seminal vesicles 40%
Spleen 3%

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25
Q

PCKD diagnosis

A

On US in those at risk or with FH
Age
15-39: at least 3 in total
Age 40-59: at least 2 in each kidney
age 60: at least 4 in each kidney

If no family history >10 in total

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26
Q

Symptoms HUS

A

FAT RN
F: fever
A: microangiopathic anaemia
T: thrombocytopenia
R: renal failure
N: neurological impairment

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27
Q

What causes HUS
Main
Others

A

Diarrhoea associated: verocytotoxin producing bacteria EColi 0157:H7

Non diarrhoea HUS: strep pneumonia, pregnancy, drugs, HIv

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28
Q

Investigations HUS

A

Microangiopathic haemolytic anaemia, ARF and thrombocytopenia

Low plts
Low HB schistocytes and spherocytes
Increase reticulocytes
Reduced haptoglobins
Increase LDH
Unconjugated hyperbilirubinaemia
Urinary urobilinogen
Variable neutrophilia
Increase urea and crest

Renal biopsy: thrombotic microangiopathic with swollen glomerular endothelial cells and red cells and plts in capillaries

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29
Q

Managed of HUS

A

Supportive
ABX may worsen
Plts contraindicated
Plasmopheresis if unsure
Plasma exchange and transfusion
No evidence for steroids, heparin, aspirin
Tx arf fluid restriction, antihypertensive, avoid Nephrotoxins

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30
Q

Renal cell carcinoma % all malignancy
What syndrome associated with

A

3%

80% pts with von hippel Lindau disease

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31
Q

What is HSP
Who most common in: age and gender

A

IGA vasculitis

Immune mediated small vessel vasculitis

IGA and complement C3 deposition in walls- inflammation
Post URTI

Children age 4-6 year
Male> female

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32
Q

What difference petechia and purpura

A

Petechia: smaller <3mm non blanching
Purpura: larger > 3mm

33
Q

Symptoms of HSP

A

Purpura and petechia: LL and buttocks palatable
Abdominal pain:50% GIh and intussception
Joint pain: arthralgia and swelling, hips, legs, knees
Frothy urine: proteinuria
Haematuria: 50%
Fever

34
Q

Diagnosis HSP

A

Palpable purpura and 1 of
Diffuse abdo pain
Arthralgia
Renal involvement
Typical histopatholofy

35
Q

Management HUS and prognosis

A

Supportive
Panadol
Pred

6montly BP urinalysis
When normal x2 can be discharged

Relapse 30-40%
Renal failure 1%

36
Q

What is most common cause of AKI in hospital

A

ATN

37
Q

Causes of ATN

A

Ischaemic: prolonged hypotension, haemorrhage- this is most common cause
Nephrotoxins; aminoglycosides, nsaids, acei, amphoceterin, cistoplatin, heavy metals, tacrilimus
Pigments: myoglobin, hb

38
Q

Most common cause of nephrotic disease in children

A

Minimal change diseases

39
Q

Physiology of minimal change disease

A

Loss of glomerular foot processes

40
Q

Symptoms of minimal change disease

A

Nephrotic syndrome
1. Proteinuria >3.5g/ day
2. Hypoalbuminaemia
3. Oedema
4. Hypercoagulability: reduced antithrombin 3 and protein S, losss in urine. Increase plt activation
5. Htn

41
Q

Treatment minimal change disease

A

Prednisolone and dietary restrictions

42
Q

Nephrotic syndrome six

A
  1. Proteinuria >3.5g/ day
  2. Hypoalbuminaemia <30
  3. Oedema
  4. Hyperlidipiademia
  5. Hyper-coagulable
43
Q

Nephritic syndrome is

A

Haematuria
Htn
Proteinuria <3.5g/day
Oligouria
Red cells casts

44
Q

What is in urinalysis of nephritis syndrome

A

Red cell casts

45
Q

Post strep glomerulonephritis
Caused by
Symptoms

A

Group A beta haemolytic streptococcus
Nephritic
Htn haematuria and periorbital oedema

46
Q

Diagnosis of post strep glomerulonephritis

A

Asymptomatic, microscopic haematuria nephritic syndrome
+ evidence of recent strep infection
GAS skin/ throat swab
Low c3/ Ch50

47
Q

Prognosis post strep glomerulonephritis
Children and adults

A

Children: excellent complete recovery
Adults: poorer prognosis more likely ckd, htn

48
Q

5 causes of nephrotic disease

A

Minimal change nephropathy
Focal segments glomerulosclerosis
Membranous glomerulonephropathy
Amyloidosis
SLE

49
Q

Most common cause of nephrotic syndrome in adults

A

Membranous glomerulonephropathy

50
Q

Causes of nephritic syndrome

A

Immune complex disease
Post strep glomerulonephritis
IgA GN: Bergers disease
Membranoproliferative GN
Others: sle, bacterial endocarditis
Pauci immune complex
Granulomatosis and polyangitis: cANCA
Eosinophilia granulomatosis and polyangitis: pANCA

Anti GBM goodpastures
Ab against type 4 collagen
Lung and kidney hameoptysis and renal failure

51
Q

Treatment of goodpastures

A

Plamsopheresis
Get rid of antibodies
Pred and immunosuppressant

52
Q

General management of nephrotic syndrome

A

General supportive
Salt and water restriction
Duiresis: loop diuretics
ACEi and ARB reduce proteinuria
vte prophylaxis
Pneumococcal vaccine and statin

Specific
Steroids —- immunosuppressant

53
Q

What is ass allport syndrome

A

Hereditary disease
Glomerulonephritis and sensorineural hearing loss
Bilateral — progresses 85% boys hearing loss by 15 year

54
Q

What acute renal injuries associated with rheumatic heart disease

A

Group a strep is cause
Post strep glomerulonephritis

55
Q

Treatment of scleroderma renal crisis

A

ACEi

56
Q

Is acute renal artery occlusion painful or painless

A

Painful if acute painless is gradual

57
Q

How does papillary necrosis present

A

Fever
Flank pain
Haematuria

58
Q

Is acute renal failure often symptomatic

A

Acute renal failures is often asymptomatic until uraemia occurs

59
Q

Pre renal cause of Aki is what percentage

A

70%

60
Q

What % hospital acquired aki are pre renal

A

20%

61
Q

% aki caused by intrinsic renal cause in community vs hospital acquired

A

20% vs 70%

62
Q

Post renal % aki in community and hospital

A

10%

63
Q

% community acquired aki are reversible

A

90%

64
Q

What is most common cause of intrinsic renal failure

A

Tubular
Acute tubular necrosis

65
Q

4 types of intrinsic renal failure

A

Glomerular, tubular, interstitial, small vessel disease

66
Q

What is most common cause of death associated acute renal failure

A

Sepsis / infection

67
Q

Mortality rates in children with arf

A

25%

68
Q

Second most common cause of death in ARF

A

Cardio/ resp

69
Q

What drugs cause reduced GFR

A

ACEi, NSAIDS, ARBs

70
Q

What electrolyte abnormality do ACEI cause

A

Hyperkalaemia
Suppression or ag II
Reduced aldosterone
Reduced excretion K+

71
Q

Do nsaids
Selective and non selective effect kidney

A

Both COXi interfere with prostaglandin synthesis and can cause glomerular arteriolar vasoconstriction with diminished renal flow and GFR

72
Q

Risk factors for getting contrast induced nephropathy

A

GFR<60
Pt factors: age >75
Diabetes
Shock
Hypotension
CHF
Sepsis
Nephrotic agents

73
Q

When should we repeat EUCs in patients high risk COntrast induced nephropathy

A

48-72 hrs peaks at 3 days post

74
Q

What reduced incidence of contrast induced nephropathy

A

IV fluids

75
Q

What % patients reciving dialysis get pericarditis

A

20%

76
Q

What is uraemic pericarditis friction rub and ecg like compared to normal

A

Pericardial friction rub louder and often palpable
Do not penetrate myocardium - nil ecg changes

77
Q

AV fistula
Natural vs Graft
What has higher complications

A

Graft

78
Q

What is most common av fistula complication

A

Low flow: thrombosis/ stenosis
infection

79
Q

What is most common av fistula infectious organism

A

Staph aureus