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THE RENAL TRACT 185
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hydronephrosis in isolation is not a reason for
nephrostomy.
Vascular anatomy The main transplant artery
and vein are anastomosed to the recipient’s
external iliac artery and vein respectively and
can normally be visualized throughout their
length. Overall global perfusion can be assessed
with colour Doppler and the smaller vessels at
the periphery of the kidney (Fig. 7.24) should
be discernible. The normal spectral Doppler
waveform is a low-resistance waveform with
continuous forward end diastolic flow.
Perirenal fluid A small amount of free fluid is
not unusual postoperatively. This usually resolves
spontaneously. Fluid collections around the
kidney are a common complication. They may
resolve on further scanning; drainage is only
peformed for good clinical reasons (see below).
Postoperative complications
Ultrasound has an essential role in assessing the
transplant and makes a significant contribution
towards graft survival through the early recognition
of postoperative complications. Complications
are varied and include acute rejection, ureteric
obstruction, vascular occlusions, perirenal fluid
collections, renal dysfunction (of various aetiologies)
and infection. Drug toxicity from the
immunosuppressive therapy can also compromise
graft function. Finally, in the long term, the original
disease, for which transplantation was performed,
may recur.
Complications can be divided into three main
categories: immediate postoperative complications,
primary and secondary renal dysfunction.
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Immediate
—non-perfusion, normally the result of an
occluded or twisted renal artery; correction
is surgical
—haematoma
Primary dysfunction
—non-perfusion (arterial occlusion), total or
lobar
—acute tubular necrosis
—renal vein thrombosis
—obstruction
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—acute or accelerated acute rejection
Secondary dysfunction
—acute rejection
—ciclosporin nephrotoxicity
—acute tubular necrosis
—obstruction
—RAS
—postbiopsy fistula
—infection
—chronic rejection.
Renal transplant dilatation
A mild degree of PCS dilatation is normal postoperatively,
due to oedema at the site of the vesicoureteric
anastomosis. This phenomenon is
usually transient, and serial scans in conjunction
with biochemistry (urea, creatinine) is normally all
that is required. More severe dilatation may be
indicative of obstruction, especially if the individual
calyces are also dilated. A trend of increasing
dilatation is a poor prognostic indicator. A ratio
between the area of the PCS and the renal outline
in two planes, the dilatation index, has been found
to predict obstruction and differentiate obstructive
from non-obstructive dilatation 30 (Fig. 7.25).
The degree of dilatation of the PCS correlates
well with the severity of obstruction.
Obstruction of the transplant kidney may be due
to an ischaemic related stricture at the vesicoureteric
anastomosis, or may be the result of a blood clot or
infected debris in the ureter. Haematoma or debris
within the PCS may appear echogenic but requires
to be differentiated from fungal balls.
Percutaneous nephrostomy is the method of
choice to relieve obstruction.
Rejection
This can be acute or chronic. Acute rejection may
be responsible for delayed graft function whereas
chronic rejection is a gradual deterioration in renal
function that may begin any time after 3 months of
transplantation. Ongoing episodes of acute rejection
should raise the possibility of non-compliance
with therapy. Acute rejection cannot be differentiated
on ultrasound from other causes of delayed
function, particularly acute tubular necrosis, and
therefore biopsy is invariably necessary.