Renal failure Flashcards
What is the anatomy of the kidneys, ureter and bladder?
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
What is associated with AKI?
Falling urine output, rising serum urea and creatinine
What does AKI result from?
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
What are common causes of prerenal AKI?
Hypovolaemia (dehydration and haemorrhage)
Hypotension (cirrhosis or septic shock)
Low cardiac output
What are common infrarenal causes of AKI?
NSAIDs
ACE inhibitors
Amphotericin B and calcineurin inhibitors
What are common causes of post renal AKI?
Bladder outflow obstruction (prostate disease)
Bilateral ureteric obstruction (stones or tumours)
What is renal parenchymal AKI?
Most commonly (80-90%) due to acute tubular necrosis Ischaemia or direct tubular toxins
How do you tell the difference between prerenal and intrinsic causes of renal failure?
Urine osmolality: high in prerenal, low in intrinsic
Urien sodium: low in prerenal, high in intrinsic
What are the causes fo acute tubular necrosis?
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
What are the biochemical abnormalities seen in AKI?
Hyperkalaemia Metabolic acidosis (unless vomiting) Hyponatraemia Hypocalcaemia Hyperphosphataemia
What are the symptoms of uraemia?
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
What are the investigations for a uraemic emergency?
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
What are the complications of an AKI?
Sepsis- impaired immune defence and instrumentation
Renal function recovers in 1-3 weeks
What are the indications for dialysis and/or haemofiltration in AKI?
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
What criteria indicates a AKI?
Urine output <0.5ml/kg/h for 6 hours
>50% rise in creatinine over 7 days
>26micromol rise in creatinine over 48h
What is stage 1 AKI?
Serum creatinine: 150-200% increase or 25micromol/l increase in 48h
Urine output: <0.5ml/kg/h for 6h
What is stage 2 AKI?
Serum creatinine: 200-300% increase
Urine output: <0.5ml/kg/h for 12h
What is stage 3 AKI?
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
What is pre-renal AKI aetiology?
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
What is post-renal AKI aetiology?
Urinary tract outflow obstruction –> hydronephrosis
Ureter stones, stricture, clots, malignancy
Bladder outlet obstruction (prostatic enlargement, urethral stricture, phimosis/paraphimosis)
What causes acute tubular necrosis?
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
What are the first line investigations for an AKI?
Hypotension/hypertension (CKD) Palpable bladder? Bloods: FBC (renal anaemia in CKD), U&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)
What are common electrolyte abnormalities in AKI?
Rapidly progressing uraemia (anorexia, vomiting, pruritis, encephalopathy, haemorrhagic episodes)
Hyperkalaemia
Hypernatraemia (unless pre-renal)
Metabolic acidosis
Hypocalcaemia/hypophosphataemia (more in CKD)
What is CKD stage 1?
GFR 90+ but other long-term evidence of kidney disease e.g.
proteinurea/haematuria
Genetic diagnosis
Structural abnormality
