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CP1 Textbook > Renal failure > Flashcards

Renal failure Flashcards

1
Q

What is the anatomy of the kidneys, ureter and bladder?

A

Kidneys- T12-L3
Ureters- 25cm long, arise from renal pelvis to ureteropelvic junction, descend through abdomen along the poses major (retroperitoneal) at the sacroiliac joint the ureters cross the pelvic brim then cross the bifurcation of the common iliac arteries

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2
Q

What is associated with AKI?

A

Falling urine output, rising serum urea and creatinine

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3
Q

What does AKI result from?

A

Prerenal, reduced kidney perfusion leads to falling GFR
Renal parenchymal disorders (injury to glomerulus, tubule or vessels)
Urinary tract obstruction (post renal, functioning kidneys cannot excrete urine with back pressure affecting function

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4
Q

What are common causes of prerenal AKI?

A

Hypovolaemia (dehydration and haemorrhage)
Hypotension (cirrhosis or septic shock)
Low cardiac output

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5
Q

What are common infrarenal causes of AKI?

A

NSAIDs
ACE inhibitors
Amphotericin B and calcineurin inhibitors

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6
Q

What are common causes of post renal AKI?

A

Bladder outflow obstruction (prostate disease)

Bilateral ureteric obstruction (stones or tumours)

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7
Q

What is renal parenchymal AKI?

A 
Most commonly (80-90%) due to acute tubular necrosis 
Ischaemia or direct tubular toxins
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8
Q

How do you tell the difference between prerenal and intrinsic causes of renal failure?

A

Urine osmolality: high in prerenal, low in intrinsic

Urien sodium: low in prerenal, high in intrinsic

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9
Q

What are the causes fo acute tubular necrosis?

A 
Haemorrhage
Burns
Diarrhoea and vomiting, fluid loss from fistulae
Acute pancreatitis
Diuretics
Myocardial infarction
Congestive cardiac failure
Endotoxic shock
Snake bite
Myoglobinaemia
Haemoglobinaemia (due to haemolysis, e.g. in falciparum malaria, ‘blackwater fever’)
Hepatorenal syndrome
Radiological contract agents
Drugs, e.g. aminoglycosides, NSAIDs, ACE inhibitors, platinum derivatives
Abruptio placentae
Pre-eclampsia and eclampsia
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10
Q

What are the biochemical abnormalities seen in AKI?

A 
Hyperkalaemia
Metabolic acidosis (unless vomiting)
Hyponatraemia
Hypocalcaemia
Hyperphosphataemia
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11
Q

What are the symptoms of uraemia?

A

Weakness, fatigue, anorexia, nausea and vomiting
Mental confusion, seizures and coma
Pruritus and bruising (impaired platelets)
Breathlessness (anaemia dn pulmonary oedema secondary to fluid overload)
Pericardiits in severe untreated
Infection

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12
Q

What are the investigations for a uraemic emergency?

A

Blood count- anaemia and high ESR (myeloma or vasculitis)
Urine dip- haematuria and proteinuria (glomerulonephritis)
Urinary electrolytes
Serum calcium, phosphate and uric acid
Renal USS(exclude obstruction)
Histological investigations- renal biopsy in unexplained and normal sized kidneys

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13
Q

What are the complications of an AKI?

A

Sepsis- impaired immune defence and instrumentation

Renal function recovers in 1-3 weeks

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14
Q

What are the indications for dialysis and/or haemofiltration in AKI?

A

Progressive uraemia with encephalopathy or pericarditis
Severe biochemical derangement, especially if there is a rising trend in an oliguric patient and in hypercatabolic patients
Hyperkalaemia not controlled by conservative measures
Pulmonary oedema
Severe metabolic acidosis: pH<7.1
For removal of drugs causing the AKI, e.g. gentamicin, lithium, severe aspirin overdose

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15
Q

What criteria indicates a AKI?

A

Urine output <0.5ml/kg/h for 6 hours
>50% rise in creatinine over 7 days
>26micromol rise in creatinine over 48h

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16
Q

What is stage 1 AKI?

A

Serum creatinine: 150-200% increase or 25micromol/l increase in 48h
Urine output: <0.5ml/kg/h for 6h

17
Q

What is stage 2 AKI?

A

Serum creatinine: 200-300% increase

Urine output: <0.5ml/kg/h for 12h

18
Q

What is stage 3 AKI?

A

Serum creatinine: >300% increase or >350micromol/l with acute rise of >45micromol/l in 48h
Urine output: <0.3ml/kg/h for 24h or anuria for 12h

19
Q

What is pre-renal AKI aetiology?

A

Inadequate renal perfusion (75%)
Shock: hypovolaemic, cardiogenic, distributive
Renovascular obstruction: embolus, aortic dissection, renal artery stenosis (RAS), thrombosis, ACEIs given in bilateral RAS
Prolonged = acute tubular necrosis –> pourous tubular membranes
Initially, urine osmolarity is high (>500mosmol/kg) + low sodium
If ATN occurs, urine is isotonic with plasma + high sodium

20
Q

What is post-renal AKI aetiology?

A

Urinary tract outflow obstruction –> hydronephrosis
Ureter stones, stricture, clots, malignancy
Bladder outlet obstruction (prostatic enlargement, urethral stricture, phimosis/paraphimosis)

21
Q

What causes acute tubular necrosis?

A

85% of renal AKI
Drugs/toxins damaging tubular cells
Drugs: aminoglycosides (antibiotic ‘-mycin’), cephalosporins (antibiotic ‘cef-‘), radiological contrast mediums, NSAIDs
Toxins: heavy metal poisoning, myoglobinuria, haemolytic uraemic syndrome

22
Q

What are the first line investigations for an AKI?

A 
Hypotension/hypertension (CKD)
Palpable bladder? 
Bloods: FBC (renal anaemia in CKD), U&amp;Es, bicarbonate, phosphate, CRP, clotting (hepatorenal disease may need invasive procedures), creatine kinase (raised in myoglobinurea) 
Nephritic screen if cause unclear 
ABG 
Urine dip and MCS 
ECG (risk of hyperkalaemia) 
Renal USS (post-renal causes) 
Non-contrast CT (if suspect obstucting calculus) 
Echo (if suspect uraemic pericarditis)
23
Q

What are common electrolyte abnormalities in AKI?

A

Rapidly progressing uraemia (anorexia, vomiting, pruritis, encephalopathy, haemorrhagic episodes)
Hyperkalaemia
Hypernatraemia (unless pre-renal)
Metabolic acidosis
Hypocalcaemia/hypophosphataemia (more in CKD)

24
Q

What is CKD stage 1?

A

GFR 90+ but other long-term evidence of kidney disease e.g.
proteinurea/haematuria
Genetic diagnosis
Structural abnormality

25
Q

What is CKD stage 2?

A

GFR 60-89 + other long-term evidence of kidney disease e.g.
proteinurea/haematuria
Genetic diagnosis
Structural abnormality

26
Q

What are the stages of CKD 3+?

A

3: GFR 30-59
4: 15-29
5: <15

27
Q

What re the investigations for CKD?

A

Bloods: FBC, U&Es, LFTs, calcium, phosphate, PTH levels, glucose
Urinalysis & MCS - quantify proteinurea, exclude infection, look for casts
24h urinary protein/creatinine clearance - assess severity/nephrotic syndrome
CXR if pulmonary oedema suspected
Renal USS is obstructive causes suspected
DTPA scan - investigate vascular supply
Renal biopsy if cause unknown
Bone imaging - renal bone disease

CP1 Textbook (36 decks)

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