US of Renal Insufficiency in Neonates
Abstract
Congenital and acquired renal diseases that can produce renal insufficiency during the neonatal period may be classified according to their ultrasonographic (US) characteristics: increased parenchymal echogenicity (renal parenchymal diseases, angiotensin-converting enzyme inhibitor fetopathy, cortical necrosis), cystic disease (glomerulocystic kidney disease, autosomal recessive polycystic renal disease, multicystic dysplastic kidney, cystic renal dysplasia), obstructive uropathies (ureteropelvic junction obstruction, posterior urethral valves), infections (candidal infections and bezoars), and renal agenesis. High-resolution sector and linear-array transducers allow characterization of the underlying pathologic conditions in many cases. Findings of renal parenchymal disease will vary at Doppler US and, during the acute phase, diastolic flow can be decreased, absent, or reversed. In patients with glomerulocystic kidney disease, US shows bilaterally enlarged kidneys with diffusely increased echogenicity and retention of a reniform contour, loss of corticomedullary differentiation, and cortical cysts. Obstruction of the ureteropelvic junction, the most common cause of hydronephrosis in neonates, can be seen at US as a dilated renal pelvis with dilated and communicating calices, lack of dilatation in the distal portion of the ureter, changes of renal dysplasia with increased echogenicity of the renal parenchyma, and parenchymal cysts, depending on the severity and duration of the obstruction. High-resolution US provides improved characterization of the renal parenchyma and more precise description of renal architecture.
© RSNA, 2002
LEARNING OBJECTIVES FOR TEST 3
After reading this article and taking the test, the reader will be able to:
| •. | List the US features of a normal neonatal kidney. | ||||
| •. | Identify the US characteristics of lesions and conditions that result in renal insufficiency in neonates. | ||||
| •. | Describe the role of US in evaluating renal insufficiency in neonates. | ||||
Introduction
Renal insufficiency and failure can result from a variety of congenital, developmental, and acquired conditions in the newborn infant. Renal blood flow is proportionately lower in neonates than in older children and adults. The rate of renal plasma flow is 120–150 mL/min per 1.73 m3 in the premature infant and 140–200 mL/min per 1.73 m3 in the term infant, whereas in adults, it is 630 mL/min per 1.73 m3. This normal physiologic characteristic puts the neonate at risk for renal insufficiency and failure when blood flow is decreased by perinatal and postnatal events such as hypoxemia, anoxia, hypovolemia, cardiac failure, and patent ductus arteriosus. Drugs such as tolazoline hydrochloride, captopril, and indomethacin can also decrease flow (,1).
Renal failure in term neonates is suspected when the plasma creatinine concentration is greater than 15 mg/L for at least 24–48 hours while maternal renal function is normal. Renal insufficiency in neonates is suspected if the plasma creatinine level increases or fails to decrease during the 1st week of life in term neonates (,2). Renal failure in neonates admitted to the nursery intensive care unit has a reported prevalence of 8%–24%. The causes can be classified as prerenal, renal ,or postrenal. Depending on the population and clinical definition, renal insufficiency is usually a transient phenomenon, with a mortality of 1% (,3).
Because of its advantages of portability and noninvasiveness, ultrasonography (US) is the primary imaging modality used to elucidate the pathogenesis of renal insufficiency in neonates. High-resolution images obtained with high-frequency linear-array transducers allow excellent characterization of renal parenchymal architecture and pathologic conditions and, in some instances, enable more precise anatomic localization. High-frequency sector transducers also can be used and may be required in small premature infants because of the large size of the footplate of some linear-array transducers. This pictorial essay illustrates various US patterns of bilateral neonatal renal disease, including increased parenchymal echogenicity, cystic diseases, obstructive uropathies, infections, and miscellaneous causes.
Normal Findings at Neonatal Renal US
The US appearance of the kidneys in neonates and infants up to 6 months of age is distinctive and differs significantly from that in older children and adults. The renal cortex in neonates has echogenicity equal to or greater than that of the liver and spleen, whereas in older children and adults, the cortex is hypoechoic relative to those organs. The echogenicity of neonatal renal cortex is due to the relative concentration, as well as the increased cellular volume, of glomeruli. The medullary pyramids appear prominent and hypoechoic because of a relatively lower cortical volume (,Fig 1). By the time a child is 6 months old, the echogenicity of the renal parenchyma assumes an adult pattern. In addition, the intense echogenicity due to fat in the renal sinuses of older patients is relatively scant or absent in the newborn infant (,4).
Increased Parenchymal Echogenicity
Increased renal parenchymal echogenicity is a subjective finding that has no direct correlation with specific renal pathologic conditions or parenchymal distribution of the disease (,5,,6). This finding is more difficult to determine with confidence in neonates because of the normally increased echogenicity of the cortex. Increased parenchymal echogenicity is usually a diffuse phenomenon and suggests diffuse renal parenchymal disease.
Renal Parenchymal Diseases
The causes of parenchymal disease in neonatal kidneys are predominantly prerenal in nature. Common pathogeneses include hypoperfusion caused by perinatal asphyxia; systemic diseases such as sepsis, surfactant deficiency, and severe congenital heart disease; and patent ductus arteriosus. A possible contributor to renal disease is medical therapy, especially the use of drugs such as prostaglandin inhibitors to prevent closure of a patent ductus arteriosus; tolazoline hydrochloride to treat pulmonary hypertension; neuromuscular blocking agents administered to improve pulmonary function during artificial ventilation and to reduce pulmonary barotrauma; amphotericin B; and intravenous contrast agents used in radiology. Renal perfusion may also be diminished by the presence of umbilical catheters and the use of positive pressure ventilation (,7).
US findings are dependent on the severity of renal involvement at the time of the study and can change over time. Cortical and medullary echogenicity varies from normal to increased, with or without preservation of corticomedullary differentiation (,,,Figs 2, ,3). Doppler US findings will vary, and during the acute phase, diastolic flow can be decreased, absent, or reversed (,,,Fig 2).
Angiotensin-converting Enzyme Inhibitor Fetopathy
Angiotensin-converting enzyme (ACE) inhibitors are a major advance in the treatment of hypertension over β-blockers and diuretics. Because they impede progression of diabetic nephropathy, these drugs are widely used by women of childbearing age. ACE inhibitors are transmitted to the fetus via the placenta and cause decreased ACE activity in the fetal kidneys. Reported adverse effects of exposure during the second and third trimesters of pregnancy include oligohydramnios and intrauterine growth retardation (,8,,9). The pathologic findings are thought to be secondary to hypotension and hypoperfusion with associated ischemia. Renal biopsies show renal tubular dysplasia. The adverse effects of exposure to ACE inhibitors are considered to be a fetopathy, a morbid condition that results from interference with normal fetal development, since no teratogenic effect is seen with periconceptional use or cessation of use during the first trimester.
The newborn infant with this fetopathy presents with hypotension and renal failure. At US, the kidneys can be of normal size and appearance or may show diffusely increased echogenicity and loss of corticomedullary differentiation (,Fig 4).
Cortical Necrosis
Renal cortical necrosis is most often caused by generalized cortical ischemia in the neonate. The ischemic injury may be secondary to chronic in utero hypoxia (eg, placental abnormalities), dehydration, sepsis, blood loss, or severe hypoxia. Renal arterial thrombosis is a less common cause of cortical necrosis in this age group.
At US, the kidneys are normal in size initially, with markedly increased cortical echogenicity and unusually prominent hypoechoic pyramids. Cortical thinning, with a resultant decrease in renal size, can develop later (,10) (,Fig 5).
Cystic Diseases
Glomerulocystic Kidney Disease
The term glomerulocystic kidney disease describes the morphologic appearance of the glomeruli in several conditions. Glomerulocystic kidney disease (GCKD) can be categorized into three groups: nonsyndromic (familial nonsyndromic GCKD), heritable (dominant GCKD), and sporadic forms. Glomerulocystic kidney disease can be a major component of heritable malformation syndromes (tuberous sclerosis, trisomy 13) and a minor component of abnormal or dysplastic kidney disease, some of them syndromic (diffuse cystic dysplasia, Meckel syndrome). Most patients present with palpable abdominal masses and renal failure (,10).
US shows bilaterally enlarged kidneys with diffusely increased echogenicity and retention of a reniform contour, loss of corticomedullary differentiation, and cortical cysts (,,,Fig 6). The cysts tend to be small and subcortical.
Autosomal Recessive Polycystic Renal Disease
Autosomal recessive polycystic renal disease is a hereditary condition characterized by renal cystic disease and hepatic fibrosis in varying degrees of severity. Neonatal patients have prominent renal enlargement with renal failure and minimal liver dysfunction. Approximately 30%–50% of affected infants die during the perinatal period owing to pulmonary hypoplasia and pulmonary insufficiency. Those that survive have progression of the renal and liver disease, with increasing amounts of fibrosis. The hepatic fibrosis might be progressive but is not of clinical importance in this group of patients (,11).
At US, the kidneys are massively enlarged and diffusely echogenic bilaterally (,,,,Figs 7, ,,,8). Corticomedullary differentiation is absent. High-resolution US (linear-array transducer, 7.5 mHz or greater) allows visualization of numerous cylindrical cysts in the medulla and cortex, which represent ectatic collecting ducts. These cysts are oriented in a radial pattern in the distribution of the collecting ducts (,11). A subcapsular area devoid of cystic involvement has been described in some cases and represents an area that lacks collecting or connecting ducts (,12) (,,,,Fig 7).
Multicystic Dysplastic Kidney
Multicystic dysplastic kidney is the second most common cause of an abdominal mass in the neonate, after hydronephrosis. The condition is thought to be caused by severe ureteral obstruction early during gestation. Multicystic dysplastic kidney most often occurs unilaterally and does not affect renal function unless the contralateral kidney has other associated anomalies. Common associated abnormalities include obstruction of the ureteropelvic junction (10%–20% of cases) or reflux nephropathy (30%–40%) (,13,,14).
The US appearance of multicystic dysplastic kidney is a mass of noncommunicating cysts of variable size. Unlike severe hydronephrosis, in which the largest cystic structure (the renal pelvis) lies in a central location and is surrounded by dilated calices, in multicystic dysplastic kidney the cyst distribution shows no recognizable pattern. Scant dysplastic, echogenic parenchyma may be visible between the cysts, but no normal renal parenchyma is seen (,,,Fig 9).
Cystic Renal Dysplasia
Cystic renal dysplasia that is bilateral usually differs etiologically from multicystic dysplastic kidney. Bilateral involvement can result from a primary dysplasia of the renal parenchyma or from obstruction of the bladder outlet or urethra early during gestation. Such dysplastic kidneys usually retain a reniform shape and have more abundant parenchyma than classic multicystic dysplastic kidney. The kidneys are normal to small in size with highly echogenic cortex, loss of corticomedullary differentiation, and scattered cysts that are smaller than those commonly seen with multicystic dysplastic kidney (,,,Fig 10).
Obstructive Uropathies
Obstruction of the Ureteropelvic Junction
Obstruction of the ureteropelvic junction is the most common cause of hydronephrosis in neonates. The flow of urine is restricted at the ureteropelvic junction. When ureteropelvic junction obstruction is identified prenatally, it is due to an area of stenosis caused by replacement of smooth muscle by collagen or the presence of bands, kinks, or rarely, an aberrant vessel (,15–,17). The diagnosis is frequently made at prenatal US. After birth, the abnormality is apparent as a palpable abdominal mass, hematuria, infection, or an incidental finding. Bilateral ureteropelvic junction obstruction is not uncommon. In such cases, renal insufficiency can occur, depending on the degree of obstruction and renal dysplasia present.
At US, a dilated renal pelvis, with dilated and communicating calices, is seen. The ureter is not dilated distally. Changes of renal dysplasia, with increased echogenicity of the renal parenchyma, and parenchymal cysts can be seen, depending on the severity and duration of the obstruction (,,,,Fig 11).
Posterior Urethral Valves
Posterior urethral valves are the most common cause of urethral obstruction in boys. The urethral valves are obstructive folds of urethral tissue that cause increased resistance to urine flow. Renal dysplasia associated with posterior urethral valves is probably the result of a complex interaction that involves (a) high-pressure vesicoureteral reflux, present in about 50% of patients with posterior urethral valves; (b) outflow obstruction; and (c) renal dysplasia, which occurs early during embryogenesis owing to the pressure insult. At the time of diagnosis, 40%–50% of patients will have some degree of renal dysfunction, commonly with renal failure (,18). US reveals bilateral hydronephrosis and hydroureter, with a thickened and sometimes trabeculated bladder wall. The dilated prostatic urethra may be visible at US (,19–,21). Those patients with renal dysplasia have increased parenchymal echogenicity and loss of corticomedullary differentiation (,,,,Fig 12). Cortical cysts are a common US feature (,4).
Candidal Infections and Bezoars
Candida albicans is the most common cause of fungal urinary tract infection. Although candidiasis is uncommon in the term infant, premature infants are susceptible owing to decreased immunity, frequent use of indwelling catheters, hyperalimentation, and long-term antibiotic therapy.
The kidneys may appear normal in patients with candidemia, even when Candida organisms are found in the urine. Candidal overgrowth in the kidneys can lead to fungemia bezoars (fungus balls) within the collecting structures, often with ensuing obstruction. Local environmental predisposing factors include a low urine pH, urine stasis due to poor urine output, and congenital renal anomalies (,22). The US findings of candidiasis include increased parenchymal echogenicity, abscesses, caliceal and pelvic debris, and bezoars (,23). If the fungal bezoars are large and bilateral, obstruction can occur, resulting in decreased urine output (,24) (,,,,Fig 13).
Renal Agenesis
Bilateral absence of kidneys and ureters is caused by early vascular insult to the developing ureteral bud. Renal agenesis is incompatible with life, and infants usually die shortly after birth owing to pulmonary hypoplasia. Renal agenesis occurs in one in 3,000 births and accounts for one-third to one-fifth of newborns with the Potter phenotype: Widely separated eyes with epicanthic folds, low-set ears, a flat and broad nose, a receding chin, and associated limb anomalies and contractures are present. Associated anorectal, cardiovascular, genital, and skeletal abnormalities are seen (,18,,25).
At US, the kidneys are absent, as are the renal arteries. Flattened and oval or elongated adrenal glands, due to lack of molding by the kidney, are identified in the renal fossa (,Fig 14). The bladder is hypoplastic and may be absent (,4).
Conclusions
US is an integral part of the evaluation of renal insufficiency and failure in neonates. High-resolution US allows improved characterization of the renal parenchyma and more precise description of renal architecture. Recognition of the US appearance and characteristics of different pathogeneses aids in the establishment of a differential diagnosis. Prompt diagnosis permits earlier intervention and may prevent progression of renal insufficiency to renal failure in some patients.
Figure 1. Normal kidney in a 2-week-old girl. US scan shows the prominent medullary pyramids (p), which should not be mistaken for dilated calices.
Figure 2a. Severe perinatal asphyxia in a 6-day-old boy. (a) US scan shows increased echogenicity of the renal parenchyma, with loss of corticomedullary differentiation. (b) US examination shows abnormal resistive index (RI) of 0.81 (normal ≤ 0.75).
Figure 2b. Severe perinatal asphyxia in a 6-day-old boy. (a) US scan shows increased echogenicity of the renal parenchyma, with loss of corticomedullary differentiation. (b) US examination shows abnormal resistive index (RI) of 0.81 (normal ≤ 0.75).
Figure 3. Meningitis and sepsis in a 2-week-old girl. US scan shows diffusely increased echogenicity of the parenchyma, with incomplete loss of corticomedullary differentiation.
Figure 4. ACE inhibitor nephropathy in a female newborn of 31 weeks gestational age. Longitudinal US scan of the kidney shows increased echogenicity of the parenchyma, with loss of corticomedullary differentiation. The kidneys are in the upper limits of normal to slightly enlarged in size for this newborn.
Figure 5. Cortical necrosis due to placental insufficiency in a 3-day-old boy. US scan of the right kidney shows thinning and markedly increased echogenicity of the renal cortex. Corticomedullary differentiation is preserved.
Figure 6a. Glomerulocystic kidney disease in a newborn girl. US scans of right (a) and left (b) kidneys show diffusely echogenic, enlarged (>95% for gestational age) kidneys with no corticomedullary differentiation. Multiple, predominantly cortical cysts are identified bilaterally.
Figure 6b. Glomerulocystic kidney disease in a newborn girl. US scans of right (a) and left (b) kidneys show diffusely echogenic, enlarged (>95% for gestational age) kidneys with no corticomedullary differentiation. Multiple, predominantly cortical cysts are identified bilaterally.
Figure 7a. Bilateral autosomal recessive polycystic renal disease in an 11-hour-old term male newborn. (a) US scan shows bilaterally enlarged and echogenic kidneys. (b) High-resolution US scan, obtained with a linear-array transducer, shows tubular cortical and medullary cysts, with a radial array of cysts in the medullary area (arrows). (c) US scan shows a subcapsular area spared of cysts (arrows).
Figure 7b. Bilateral autosomal recessive polycystic renal disease in an 11-hour-old term male newborn. (a) US scan shows bilaterally enlarged and echogenic kidneys. (b) High-resolution US scan, obtained with a linear-array transducer, shows tubular cortical and medullary cysts, with a radial array of cysts in the medullary area (arrows). (c) US scan shows a subcapsular area spared of cysts (arrows).
Figure 7c. Bilateral autosomal recessive polycystic renal disease in an 11-hour-old term male newborn. (a) US scan shows bilaterally enlarged and echogenic kidneys. (b) High-resolution US scan, obtained with a linear-array transducer, shows tubular cortical and medullary cysts, with a radial array of cysts in the medullary area (arrows). (c) US scan shows a subcapsular area spared of cysts (arrows).
Figure 8a. Autosomal recessive polycystic renal disease in a 3-week-old boy, from whom the enlarged kidneys were removed to improve respiratory management. (a) Photograph shows gross specimen, approximately 17 cm long. (b) Photograph allows comparison of the size of the gross specimen with the affected neonate, immediately after surgery. (Case courtesy of Paul Austin, MD, Washington University, St Louis, Mo.)
Figure 8b. Autosomal recessive polycystic renal disease in a 3-week-old boy, from whom the enlarged kidneys were removed to improve respiratory management. (a) Photograph shows gross specimen, approximately 17 cm long. (b) Photograph allows comparison of the size of the gross specimen with the affected neonate, immediately after surgery. (Case courtesy of Paul Austin, MD, Washington University, St Louis, Mo.)
Figure 9a. Multicystic dysplastic kidney. (a) US scan shows a small right kidney with multiple cysts of different sizes arranged in no recognizable pattern. The presence of echogenic parenchyma is minimal. (b) US scan shows a different pattern with larger cysts and more echogenic, dysplastic parenchyma.
Figure 9b. Multicystic dysplastic kidney. (a) US scan shows a small right kidney with multiple cysts of different sizes arranged in no recognizable pattern. The presence of echogenic parenchyma is minimal. (b) US scan shows a different pattern with larger cysts and more echogenic, dysplastic parenchyma.
Figure 10a. Bilateral cystic renal dysplasia in a 1-day-old girl. US scans of the right (a) and left (b) kidneys show multiple cysts and echogenic, fibrotic parenchyma. The kidneys are small for gestational age and retain a reniform shape.
Figure 10b. Bilateral cystic renal dysplasia in a 1-day-old girl. US scans of the right (a) and left (b) kidneys show multiple cysts and echogenic, fibrotic parenchyma. The kidneys are small for gestational age and retain a reniform shape.
Figure 11a. Bilateral obstruction of the ureteropelvic junction in a 1-day-old boy. (a, b) US scans of the right (a) and left (b) kidneys show marked dilatation of the collecting system and diffuse renal dysplasia with increased parenchymal echogenicity and thinning. (c) US scans of the right kidney show parenchymal cysts.
Figure 11b. Bilateral obstruction of the ureteropelvic junction in a 1-day-old boy. (a, b) US scans of the right (a) and left (b) kidneys show marked dilatation of the collecting system and diffuse renal dysplasia with increased parenchymal echogenicity and thinning. (c) US scans of the right kidney show parenchymal cysts.
Figure 11c. Bilateral obstruction of the ureteropelvic junction in a 1-day-old boy. (a, b) US scans of the right (a) and left (b) kidneys show marked dilatation of the collecting system and diffuse renal dysplasia with increased parenchymal echogenicity and thinning. (c) US scans of the right kidney show parenchymal cysts.
Figure 12a. Posterior urethral valves in a 1-day-old boy. (a) US scan shows a markedly thickened bladder wall. (b) US scan shows a hydronephrotic kidney with associated dysplastic parenchymal changes of increased echogenicity and loss of corticomedullary differentiation. (c) Voiding cystourethrogram shows the posterior urethral valves (arrows) at both sides of an indwelling catheter. The bladder is heavily trabeculated.
Figure 12b. Posterior urethral valves in a 1-day-old boy. (a) US scan shows a markedly thickened bladder wall. (b) US scan shows a hydronephrotic kidney with associated dysplastic parenchymal changes of increased echogenicity and loss of corticomedullary differentiation. (c) Voiding cystourethrogram shows the posterior urethral valves (arrows) at both sides of an indwelling catheter. The bladder is heavily trabeculated.
Figure 12c. Posterior urethral valves in a 1-day-old boy. (a) US scan shows a markedly thickened bladder wall. (b) US scan shows a hydronephrotic kidney with associated dysplastic parenchymal changes of increased echogenicity and loss of corticomedullary differentiation. (c) Voiding cystourethrogram shows the posterior urethral valves (arrows) at both sides of an indwelling catheter. The bladder is heavily trabeculated.
Figure 13a. Candidal bezoars in a 4-week-old boy. (a) US scan shows an echogenic mass that fills the dilated renal pelvis (arrows) and obstructive dilatation of the pelvis and calices. (b) US scan shows diffusely increased echogenicity of the renal parenchyma, with heterogeneous loss of corticomedullary differentiation, in association with the renal pelvis bezoar (arrows). (c) US scan shows the rounded, echogenic mass in a dilated calix (arrow).
Figure 13b. Candidal bezoars in a 4-week-old boy. (a) US scan shows an echogenic mass that fills the dilated renal pelvis (arrows) and obstructive dilatation of the pelvis and calices. (b) US scan shows diffusely increased echogenicity of the renal parenchyma, with heterogeneous loss of corticomedullary differentiation, in association with the renal pelvis bezoar (arrows). (c) US scan shows the rounded, echogenic mass in a dilated calix (arrow).
Figure 13c. Candidal bezoars in a 4-week-old boy. (a) US scan shows an echogenic mass that fills the dilated renal pelvis (arrows) and obstructive dilatation of the pelvis and calices. (b) US scan shows diffusely increased echogenicity of the renal parenchyma, with heterogeneous loss of corticomedullary differentiation, in association with the renal pelvis bezoar (arrows). (c) US scan shows the rounded, echogenic mass in a dilated calix (arrow).
Figure 14. Renal agenesis in a 1-day-old boy. US scan shows that the right adrenal gland (arrow) is elongated in the right renal fossa. No renal tissue is identified bilaterally.
Abbreviation: ACE = angiotensin-converting enzyme
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