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CHAPTER 18 Organ Transplantation 651

sign of potential dysfunction. Other gray-scale indings include

increased cortical thickness, increased or decreased cortical

echogenicity, reduction of the corticomedullary diferentiation,

loss of the renal sinus echoes, and prominence of the pyramids

(Fig. 18.34).

Color Doppler assessment may be normal or may occasionally

show difuse decreased blood low. he RI of the intraparenchymal

arteries is also nonspeciic in these conditions and may be normal

or elevated. In severe cases, there may be a complete lack of low

in diastole or a reversal of diastolic low 44 (Fig. 18.35). Despite

the lack of speciicity of gray-scale and Doppler ultrasound in

these acute conditions, serial spectral Doppler measurements,

in combination with clinical assessments and biochemical indings,

provide a useful guide to the clinician in terms of monitoring

the allograt function and in determining the need for percutaneous

biopsy.

FIG. 18.32 Normal Renal Transplant Doppler. Color Doppler shows

low throughout kidney (top). Intrarenal spectral traces of upper, middle,

and lower poles show a resistive index of less than 0.8 and continuous

low throughout diastole. The main renal artery shows continuous low

with peak velocities less than 200 cm/sec (bottom).

hypotension. It is most common in the early postoperative period

and is the major cause of delayed grat function (deined as the

need for dialysis within the irst week of transplantation). 45,55 In

patients requiring dialysis, recovery is usually in the irst 2 weeks

of transplantation but may be delayed by up to 3 months. ATN

occurs in most cadaveric grats and is observed infrequently in

living related renal transplants because of the relatively short

cold ischemic time of the donor kidney. 44

Transplants afected by hyperacute rejection are rarely imaged

because grat failure occurs immediately at the vascular anastomosis

during surgery. 45 Acute rejection occurs in up to 40% of

patients in the early transplant period, peaking at 1 to 3 weeks

ater surgery, and is an adverse long-term prognostic indicator.

Most patients with acute rejection are asymptomatic, but a small

proportion may have lulike symptoms, malaise, fever, and grat

tenderness. Provided that the diagnosis can be rapidly established,

acute rejection usually can be promptly reversed with high-dose

steroids or antibiotic therapy. 44,56

he imaging features of ATN and acute rejection are almost

identical on gray-scale and Doppler ultrasound. Both conditions

can produce increases in renal volume of the allograt.

However, precise volumetric comparisons between interval

studies can prove diicult; subtle changes in two-dimensional

(2-D) measurements have not been adopted as a strong clinical

Chronic Rejection

Chronic rejection is deined as a reduction in allograt function

starting at least 3 months ater transplantation in association

with ibrous intimal thickening, interstitial ibrosis, and tubular

atrophy on histology. It is the most common cause of late grat

loss. he most frequent predisposing risk factor for development

of chronic rejection is recurrent previous episodes

of acute rejection. 44,45 On ultrasound, there is progressive

thinning of the renal cortex, prominence of the central renal

sinus fat, and a reduction in the overall size of the transplant.

Dystrophic calciications may be seen scattered throughout

the residual parenchyma. In the end-stage renal transplant, the

entire renal cortex can become calciied, appearing as a sharp

echogenic interface associated with clean distal shadowing

(Fig. 18.36).

Infection

Over 80% of patients with renal allograts will experience an

episode of infection within the irst year ater transplant surgery. 57

Transplant pyelonephritis can result from an ascending infection,

hematologic seeding, or contiguous spread from an adjacent

infected luid collection. Ultrasound indings include a focal or

difusely granular, echogenic renal cortex associated with loss

of the corticomedullary junction; increased echogenicity and

thickening of the perirenal fat secondary to extension of inlammation

or infection into the surrounding tissue; and uroepithelial

thickening (Fig. 18.37).

Pyonephrosis may occur occasionally in a chronically

obstructed transplanted kidney. In the early stages, the lumen

of the dilated collecting system appears anechoic. Once the lumen

becomes illed with purulent material, low-level echoes develop

within the calyceal system and ureter, sometimes associated with

luid-debris levels. Echogenic material within the collecting system

may also result from intraluminal blood or other illing defects,

or it may be artifactual as a result of scatter or s1ide-lobe artifact

(see Fig. 18.37).

Abscesses can arise from infection of a previously sterile

collection. On ultrasound, abscesses appear as a complex cystic

structure and may be associated with luid-luid levels or intraluminal

air (Fig. 18.38).

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