Diagnostic ultrasound ( PDFDrive )

1798 PART V Pediatric Sonography
developing world, acquired causes of CKD predominate, particularly
infection-related glomerulopathies. he worldwide
incidence and prevalence of CKD are greater for boys than for
girls because of the higher incidence of congenital causes of
CKD in boys. 80
As with AKI, ultrasound is the primary imaging modality
used to investigate CKD. Congenital anomalies such as UPJO,
PUV, duplex collecting systems and ureters, and ectopic ureteral
insertion are well depicted by sonography. Determination of
kidney size is critical for long-term follow-up. Enlarged kidneys
can occur in the setting of obstruction, cystic disease, and
glomerulonephritis. Hypoplastic and scarred kidneys usually are
small. A gradual reduction in kidney size usually occurs in patients
with CKD. With progressive CKD, a concomitant loss of corticomedullary
diferentiation usually occurs, and most kidneys
will have echogenic parenchyma. However, increased renal
parenchymal echogenicity is a nonspeciic inding and is not
correlated with the severity of disease. Dysplastic kidneys have
disordered development that usually results in a combination
of echogenic parenchyma and cysts (Fig. 52.35). Dysplasia may
be focal or difuse and is usually depicted sonographically as
echogenic tissue without identiiable corticomedullary diferentiation.
80 Renal vascularity relects functional status and will decrease
in persons with CKD. he renal arterial resistive index (RI)
correlates with creatinine levels and appears to be an independent
risk factor for the progression of CKD. 83
URINARY TRACT CALCIFICATION
Renal Cortical Calciication
Renal cortical calciication most commonly occurs as a result
of acute cortical necrosis or chronic glomerulonephritis. 84
Additional causes are listed in the accompanying box. In the
setting of acute cortical necrosis, the renal cortex will appear
echogenic by ultrasound within a few weeks of injury, with
calciication increasing over time (Fig. 52.36). Progressive renal
atrophy also occurs. 85
Causes of Cortical Nephrocalcinosis
Renal cortical necrosis
Chronic glomerulonephritis
Renal transplant rejection
Alport syndrome
Ethylene glycol poisoning
Hyperoxaluria
Acquired immunodeiciency syndrome–associated
infections
With permission from Bedard M, Wildman S, Dillman J. Embryology,
anatomy, and variants of the genitourinary tract. In: Coley BD, editor.
Caffey’s pediatric diagnostic imaging. 12th ed. Philadelphia: Elsevier
Saunders; 2013. 86
Medullary Nephrocalcinosis
In more than 90% of children with nephrocalcinosis, calciication
is mainly located in the medullary pyramids. he most common
causes in children are metabolic disorders resulting in hypercalcemia
and hypercalciuria, renal tubular acidosis, and diuretic
therapy. Additional causes are listed in Table 52.8.
Prolonged administration of diuretics such as furosemide is
a signiicant cause of medullary nephrocalcinosis in neonates.
In these conditions an increased calcium load is presented to
the kidney. he mineral content within the kidney increases
progressively from the glomerulus to the collecting ducts, and
thus the greatest concentration of calcium is found in the pyramids,
especially at their tips. he “Anderson-Carr-Randall
progression” of calculus formation postulates that microscopic
calciications within a renal pyramid may fuse to form a plaque
that migrates toward the calyceal epithelium, eventually
FIG. 52.35 Renal Dysplasia. Longitudinal image of right kidney
demonstrates echogenic parenchyma with absent corticomedullary
differentiation and peripheral cysts (arrows). *, Dilated renal pelvis; L,
liver.
FIG. 52.36 Acute Cortical Necrosis in Infant With History of Aortic
and Vena Caval Thromboses and Severe Renal Functional Impairment.
Longitudinal image reveals thin, echogenic parenchyma with loss
of corticomedullary differentiation and cortical calciications (arrows).