Divided into three main types:

Pre-Renal Renal failure

(aka pre-renal impairment, pre-renal uraemia (PRU))
Caused by decreased perfusion of the kidneys due to extrarenal circulatory factors, e.g. hypotension, volume depletion secondary to haemorrhage or dehydration, heart failure or ACE inhibitors.

Common causes:
Extracellular Volume (ECV) Depletion: Haemorrhage, Burns, GI loss (vomiting, diarrhoea), Renal loss (osmotic diuretics, Addison's disease)

Normal or increased ECV with ineffective intravascular volume: Shock, Congestive cardiac failure, Third space fluid loss (pancreatitis, ascites, crush injury), ACE Inhibitors

Urine sodium concentration is very low (less than 20 mmol/l) and urine osmolality is high indicating that the tubules are functioning normally. Oliguria or anuria in this condition is usually of only a few hours' duration if treated aggressively - prerenal failure is readily reversible when the extrarenal circulatory disturbance is corrected, because there is no intrinsic abnormality in the kidneys. Failure to correct the prerenal causes will go on to result in intrarenal failure. (Decrease in BP to give ischaemia and death of tubules.)

Intra-renal renal failure

(aka acute renal failure, renal impairment, intra-renal impairment; intrinsic renal failure sometimes called ATN – acute tubular necrosis).
Variety of causes:

a) Ischaemic Any of the causes of pre-renal failure can lead to ischaemic ("hypotensive") acute renal failure if the defect in renal perfusion is too severe or prolonged. Renal failure persists after the extrarenal circulatory disturbance is corrected and may not resolve for several weeks. Urine sodium concentration is usually greater than 20 mmol/l and urine osmolality is low because of abnormalities in tubular function. This type of renal failure is often called "acute tubular necrosis" - a poor term to use as necrotic tubular epithelial cells are usually not apparent histologically although individual tubular epithelial cells may be missing. Recovery may take several weeks. Patients require dialysis.

b) Nephrotoxic Various pharmacologic agents and poisons (such as antibiotics (gentamicin), analgesics (paracetamol), carbon tetrachloride (CCl 4 ) can produce nephrotoxic acute renal failure which is clinically very similar to ischaemic acute renal failure but is associated with much more obvious damage to renal tubular epithelium histologically. Widespread frank necrosis of tubular epithelium is observed, particularly in the proximal convoluted tubules, so the term "acute tubular necrosis” (ATN) is more appropriate here.
Besides ischaemic and nephrotoxic acute renal failure there are a number of other less common renal parenchymal diseases which cause acute renal failure. These often have atypical clinical features, such as the presence of, haematuria, complete anuria, or signs of systemic disease. Examination of the urine sediment and, in selected cases, renal biopsy can be helpful in diagnosing these atypical forms of intrarenal acute renal failure.

c) Acute glomerulonephritis immune complex deposition may result in the destruction of the glomerular membrane e.g. Streptococcal infections and Goodpastures Syndrome.

d) Cortical Necrosis. This condition may be found in pregnant women who have abruptio placentae ("concealed accidental haemorrhage"). It is also found in the haemolytic uraemic syndrome (HUS), and in gram-negative septicaemia. It differs from ischaemic or nephrotoxic acute renal failure in that all elements of the cortex become necrotic, including the glomeruli. Recovery may take place.

e) Obstruction of Major Vessels. Acute renal failure may be produced by embolisation of a main renal artery, involvement of the larger intrarenal arteries by polyarteritis, or by sudden thrombosis of renal veins. Extensive tissue death occurs since the blood supply is cut off.

TREATMENT Maintain support of all the systems - fluid, acid base balance, infection (the patient will most likely require dialysis) until tubular regeneration occurs, usually after 3 weeks.

Post-Renal Acute Renal Failure

Caused by obstruction of the urinary tract. (eg. by tumour, stone, prostatic hypertrophy, blood clots.) Often results in complete anuria. The backpressure may cause a temporary defect in renal concentrating ability after relief of obstruction (post-obstructive nephropathy), but permanent renal damage only results from chronic obstruction.