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
What difference petechia and purpura
Petechia: smaller <3mm non blanching
Purpura: larger > 3mm
Symptoms of HSP
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
Diagnosis HSP
Palpable purpura and 1 of
Diffuse abdo pain
Arthralgia
Renal involvement
Typical histopatholofy
Management HUS and prognosis
Supportive
Panadol
Pred
6montly BP urinalysis
When normal x2 can be discharged
Relapse 30-40%
Renal failure 1%
What is most common cause of AKI in hospital
ATN
Causes of ATN
Ischaemic: prolonged hypotension, haemorrhage- this is most common cause
Nephrotoxins; aminoglycosides, nsaids, acei, amphoceterin, cistoplatin, heavy metals, tacrilimus
Pigments: myoglobin, hb
Most common cause of nephrotic disease in children
Minimal change diseases
Physiology of minimal change disease
Loss of glomerular foot processes
Symptoms of minimal change disease
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
Treatment minimal change disease
Prednisolone and dietary restrictions
Nephrotic syndrome six
- Proteinuria >3.5g/ day
- Hypoalbuminaemia <30
- Oedema
- Hyperlidipiademia
- Hyper-coagulable
Nephritic syndrome is
Haematuria
Htn
Proteinuria <3.5g/day
Oligouria
Red cells casts
What is in urinalysis of nephritis syndrome
Red cell casts
Post strep glomerulonephritis
Caused by
Symptoms
Group A beta haemolytic streptococcus
Nephritic
Htn haematuria and periorbital oedema
Diagnosis of post strep glomerulonephritis
Asymptomatic, microscopic haematuria nephritic syndrome
+ evidence of recent strep infection
GAS skin/ throat swab
Low c3/ Ch50
Prognosis post strep glomerulonephritis
Children and adults
Children: excellent complete recovery
Adults: poorer prognosis more likely ckd, htn
5 causes of nephrotic disease
Minimal change nephropathy
Focal segments glomerulosclerosis
Membranous glomerulonephropathy
Amyloidosis
SLE
Most common cause of nephrotic syndrome in adults
Membranous glomerulonephropathy
Causes of nephritic syndrome
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
Treatment of goodpastures
Plamsopheresis
Get rid of antibodies
Pred and immunosuppressant
General management of nephrotic syndrome
General supportive
Salt and water restriction
Duiresis: loop diuretics
ACEi and ARB reduce proteinuria
vte prophylaxis
Pneumococcal vaccine and statin
Specific
Steroids —- immunosuppressant
What is ass allport syndrome
Hereditary disease
Glomerulonephritis and sensorineural hearing loss
Bilateral — progresses 85% boys hearing loss by 15 year
What acute renal injuries associated with rheumatic heart disease
Group a strep is cause
Post strep glomerulonephritis
Treatment of scleroderma renal crisis
ACEi
Is acute renal artery occlusion painful or painless
Painful if acute painless is gradual
How does papillary necrosis present
Fever
Flank pain
Haematuria
Is acute renal failure often symptomatic
Acute renal failures is often asymptomatic until uraemia occurs
Pre renal cause of Aki is what percentage
70%
What % hospital acquired aki are pre renal
20%
% aki caused by intrinsic renal cause in community vs hospital acquired
20% vs 70%
Post renal % aki in community and hospital
10%
% community acquired aki are reversible
90%
What is most common cause of intrinsic renal failure
Tubular
Acute tubular necrosis
4 types of intrinsic renal failure
Glomerular, tubular, interstitial, small vessel disease
What is most common cause of death associated acute renal failure
Sepsis / infection
Mortality rates in children with arf
25%
Second most common cause of death in ARF
Cardio/ resp
What drugs cause reduced GFR
ACEi, NSAIDS, ARBs
What electrolyte abnormality do ACEI cause
Hyperkalaemia
Suppression or ag II
Reduced aldosterone
Reduced excretion K+
Do nsaids
Selective and non selective effect kidney
Both COXi interfere with prostaglandin synthesis and can cause glomerular arteriolar vasoconstriction with diminished renal flow and GFR
Risk factors for getting contrast induced nephropathy
GFR<60
Pt factors: age >75
Diabetes
Shock
Hypotension
CHF
Sepsis
Nephrotic agents
When should we repeat EUCs in patients high risk COntrast induced nephropathy
48-72 hrs peaks at 3 days post
What reduced incidence of contrast induced nephropathy
IV fluids
What % patients reciving dialysis get pericarditis
20%
What is uraemic pericarditis friction rub and ecg like compared to normal
Pericardial friction rub louder and often palpable
Do not penetrate myocardium - nil ecg changes
AV fistula
Natural vs Graft
What has higher complications
Graft
What is most common av fistula complication
Low flow: thrombosis/ stenosis
infection
What is most common av fistula infectious organism
Staph aureus
