to functional impairment; since there is no sufficient blood reaching the
kidney to be cleared of these toxins.
In post-renal failure, the obstruction of the urinary tract results in
increasing the pressure above the level of the obstruction up to the
nephron including the urinary space of the renal glomeruli. When this
back pressure exceeds that of the filtration pressure in the renal glomeruli,
the process of urine formation will stop with progressive accumulation of
wastes and increase of serum creatinine and blood urea.
In renal failure (intrinsic renal failure), there is a damage involving
the glomeruli, renal tubules or tubulointerstitium with loss of their
functions. Consequently wastes accumulate with increase in serum
creatinine and blood urea.
I. Pre-renal Failure
Combination of hypotension, hypovolaemia resulting in diminished
renal perfusion is the most common cause of acute renal failure in
hospitalized patients.
When renal hypoperfusion (due to hypotension and/or
hypovolaemia) is not severe enough to cause renal tubular damage, it will
manifest as pre-renal failure in the form of oliguria and a rise in serum
creatinine and blood urea. Since there is no structural renal damage, early
diagnosis and correction of renal hypoperfusion results in immediate
diuresis and rapid drop in serum creatinine and blood urea levels. If
hypoperfusion is severe or neglected, renal compensatory mechanisms
will fail and acute tubular necrosis occurs. In this new situation, correction
of hypoperfusion will not be followed by diuresis or drop in serum