Give 2 clinical methods for defining AKI
• Increase in serum creatinine by >26.5 umol/L within 48 hours OR
• Increase in serum creatinine by >1.5 times baseline within 7 days OR
• Urine volume <0.5 ml/kg/h for 6 hrs - oligouria
What are the 3 main types of AKI?
1) Pre-renal 2) Renal 3) Post-renal
What is pre renal AKI? What causes pre renal AKI?
• Reduction in renal perfusion
• Is a physiological response to renal hypoperfusion
Pre-renal failure can also be caused by a reduction in the effective ECF volume such as in hypovolemia due to blood loss, systemic vasodilation as in anaphylaxis and sepsis, or in cardiac failure.
How can the autoregulatory mechanisms of the renal system be overcome to cause pre renal AKI?
o NSAIDS – prevent vasodilation of afferent arteriole
o ACE inhibitors – prevents vasoconstriction of efferent arteriole
o Disease of afferent arteriole – diabetes mellitus, hypertension etc.
What happens in acute tubular necrosis? What is it caused by?
ATN – Renal cells damaged, cannot be immediately reversed. Damaged cells cannot reabsorb salt and water efficiently or expel excess water
How would you differentiate between pre renal and ATN? Why does this method work?
• Na+ reabsorbed in pre-renal AKI to restore volume but reduced in renal AKI due to tubular cell damage
• Can therefore use sodium reabsorption to tell what stage the AKI is in.
• Fractional Sodium Excretion = (urine Na+/Plasma Na+) / (urine Creatinine / plasma creatinine) x 100
• In pre-renal the FENa is <1%. In ATN the FENa is >1%.
What is a nephrotoxin?
Damage the epithelial cells lining the tubules and cause cell death and shedding into the lumen. Can be endogenous or exogenous e.g. drugs
Give 2 examples of an endogenous nephrotoxin
myoglobin, urate, bilirubin
Give 2 examples of an exogenous nephrotoxin
drugs (e.g. ace inhibitors, NSAIDs, gentamicin), x-ray contrast, other poisons.
What is rhabdomyolysis and how does it cause AKI? In whom does it occur?
• Muscle necrosis results in large release of myoglobin.
• Can occur from drug users, elderly, wars, natural disasters
• Results in AKI
What is acute glomerulonephritis? What forms can it take?
o Immune disease affecting the glomeruli
o Can be primary (only affecting kidneys) or secondary (systemic)
o Secondary e.g. systemic lupus erythematosis
How does endothelium damage lead to RBC destruction?
o Endothelium damage results in platelet thrombus, which results in partial obstruction of small arteries and the destruction of RBCs
Give the pathology of a post-renal AKI
1) Obstruction with continuous urine production results in rise in intraluminal pressure
2) Results in dilatation of renal pelvis
3) Which produces a decrease in renal function
Give the 3 types of post renal AKI
1) Obstruction within the lumen
2) Obstruction within the wall
3) Obstruction by pressure from the outside
Give 2 things that can cause an obstruction in the lumen of the ureters
• Blood clots
• Papillary necrosis – sloughed papillae following infection and ischaemia
• Tumour of renal pelvis, ureter, bladder
Give 2 causes of post renal AKI within the wall of the ureters
• Pelviureteric neuromuscular dysfunction
• Megaureter – Dilated ureter
• Neurogenic bladder – lack of bladder control
• Ureteric stricture e.g. post-TB
Give 3 causes of post renal AKI due to pressure from the outside
• Prostatic hypertrophy
• Aortic aneurysm
• Accidental ligation of ureter
What indications in serum biochemistry would occur in AKI?
Increased urea and creatinine in all causes of AKI
What is a RBC cast?
Cylindrical structure in urine made up of RBC
How would you treat pre renal AKI?
• Immediate infusion of IV fluids to increase renal perfusion
• Avoid nephrotoxins
• Can force alkaline diuresis to remove myoglobin – use a drug to make the urine alkaline to draw out myoglobin
How would you treat ATN?
• Prevent volume overload by restricting dietary NA and water intake (<1L per day)
• Prevent hyperkalaemia – restrict dietary K, Ca gluconate, dextrose and insulin (uptake of K into cells),
• Prevent acidosis – Protein restriction, sodium bicarbonate infusion
When would you use dialysis for ATN?
• Metabolic acidosis where sodium bicarbonate infusion is not appropriate
• Fluid overload refractory to diuretics
• Presence of dialyzable nephrotoxin
• High K+ refractory to treatment (not treatable with treatment due to refractory period)
What are the 3 main types of proteinuria? Define them
1) Glomerular proteinuria – An increase in the permeability of the glomerulus to protein due to damage of the bowman’s capsule
2) Tubular proteinuria – Tubulointersitial disease impairs reabsorption of low molecular weight proteins at the PCT
3) Overflow proteinuria – Overproduction of smaller proteins leads to a rate of filtration that exceeds the transport maximum for reabsorption at the PCT.
Define nephrotic syndrome
Defined as proteinuria sufficient to cause hypoalbuminaemia and hence peripheral oedema. Proteinuria needs to exceed 5g/24hr.
Describe how lowered oncotic pressure can lead to oedema in 2 ways
1) Lowered oncotic pressure --> oedema
2) Hypovolemia results which stimulates RAS --> increase in aldosterone production
3) Aldosterone stimulates salt and water retention --> increased oedema.
What is nephrological and urological haematuria?
Nephrological haematuria – results from glomerular inflammation and bleeding
Urological haematuria – Due to renal stones, renal cell carcinoma, tubular cell carcinoma
What features would suggest nephrological as opposed to urological haematuria? Give 3 things
o Abnormal renal function
o Salt and water retention
o Young age (uroepithelial malignancy unlikely)
What 2 urinary features would you find in glomerulonephritis?
• Dysmorphic red cells
• Red cell cast