Renal Flashcards
Acute kidney injury
What is it
Acute deterioration in renal function and build up of waste products
Abrupt -1-7 dayy
Sustained >24 hours
RIFLE criteria
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
AKIN criteria
AKIN criteria
KDIGO definition AKI
- UP <0.5ml/kg/hr for 6 hours
- Serum creat >1.5x normal in last 7 days
- Serum creat >0.3mg/dL in 48 hours
Severity AKI
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
Risk factors for AKI
Sepsis
Age>65
Race
Pre existing CKD
Surgical patients
cVs disease
Liver failure pts
Diabetes
Oligouria
Nephrotoxins
Contrast
Indications for dialysis
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
Causes of AKI
Pre renal: hypo perfusion
Renal: structural/ functional changes at nephron ATN
Post renal: obstruction
Causes of pre renal aki
- dehydration: blood loss, diarrhoea, diuretic, vomting, sepsis
- shock: hypotension
- low effective: heart failure: liver failure
Anatomical: renal artery stenosis
Drug induced: nsaids, acei
Causes of Renal AKI
ATN: most common
Nephrotoxins: nsaids, contrast, allopurinol, gentamicin, furosemide, herbicides, heavy metal ACEi
Glomerulonephropathies: nephrotic vs nephritic syndrome
HUS
Rhabdo: myoglobin
Severe HTN
Post renal aki
Obstruction
Ureters: stone or structure, retroperitoneal fibrosis
Bladder: cancer
Prostate: BPH: cancer
Urethra: stricture
External mass/ LN
Complications of AKI
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
Phases of AKI
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
Management of AKI
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
Urea creatinine ratio
What is it? What does it mean?
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
AKI
How to distinguish cause renal vs pre renal
Creat: urea ratio
Urine Na
Fraction excreted na
Urine osmolalitu
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
Bun: creat ratio.
Causes of high
Drivers can use GPS
D: dehydration, pre renal, haemorrhage vomting
C: corticosteroids
G: GIH
P: protein rich diet
S: severe catabolic state
Bun: creat ratio.
Causes of low
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
What is most common inheritance of polycystic kidney disease
Autosomal dominant
But also can be recessive
Most common cause of death in PCKD
Cardiac cause of death
Most common presenting symptoms of PCKD
Hypertension
Associated disease PCKD
Berry aneurysm: 8-10%
Thoracic aortic and cervicocephalic artery dissection
Coronary A aneurysm
MV prolapse
Defective sperm motility and infertility
PCKD where do cysts form
Kidney 100%
Liver 80%
Seminal vesicles 40%
Spleen 3%
PCKD diagnosis
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
Symptoms HUS
FAT RN
F: fever
A: microangiopathic anaemia
T: thrombocytopenia
R: renal failure
N: neurological impairment
What causes HUS
Main
Others
Diarrhoea associated: verocytotoxin producing bacteria EColi 0157:H7
Non diarrhoea HUS: strep pneumonia, pregnancy, drugs, HIv
Investigations HUS
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
Managed of HUS
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
Renal cell carcinoma % all malignancy
What syndrome associated with
3%
80% pts with von hippel Lindau disease
What is HSP
Who most common in: age and gender
IGA vasculitis
Immune mediated small vessel vasculitis
IGA and complement C3 deposition in walls- inflammation
Post URTI
Children age 4-6 year
Male> female