Clinical
Findings
in Six Children With Edema,
Hypoproteinemia,
and Anemia
Patient/Sex/ Admission
Age,
wk
Admission diet
1/M/6 cow's milk
2/F/10
soy based
3/F/6
soy based
4/F/14
soy based
5/M/6
soy based
6/M/8
modified cow's milk
Protein content
gm/100
ml_3_3_2.5
Failure to thrive, < 3rd percentile
Abnormal stools Edema Total protein,
gm/100
3.1_2_5_3_1_1.7
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
ml_1_9_3.5 0.82_2.3
Albumin, gm/100 ml
3.05_3.25 1.45_203
+
+
—
3.9_3.1 2.5_2.0
Hemoglobin, gm/100 ml_8J?_10.4 9.5_6_4_9j>_6.2 SGOT (10-26) IU_52_-_66_3!}_49_Sweat chloride,
Nephroma kidney tumor, often con-
Congenital A
rare
Mesoblastic
and known by a variety of (mesoblastic nephroma,1 leiomyomatous hamartoma,2 fetal renal hamartoma,3 mesenchymal hamartoma of infancy4), has been confused with Wilms' tumor. On occasion, inap-
genital names
mEq/liter
edema_^9_)Và_91_73_54_18
With Without edema
12. Paxson CL Jr: Idiopathic hypoproteinemia in twins. JAMA 230:1257-1258, 1974. 13. Bass HN, Miller AA: Cystic fibrosis presenting with anemia and hypoproteinemia in identical twins. Pediatrics 59:126-127, 1977. 14. Sahidi NT, Diamond LK, Schwachman H: Anemia associated with protein deficiency: A study of two cases with cystic fibrosis. J Pediatr 59:533-541, 1961. 15. Roger R, Finegold MJ: Cholestasis in immature newborn infants: is parenteral nutrition responsible? J Pediatr 86:264-269, 1975.
108
134
infants in whom they were measured. This may be due to malnutrition15 as the values returned to normal when the serum proteins became normal. A positive sweat chloride test is required for the diagnosis of CF. Two of our patients had normal values for sweat chloride while edematous. In retrospect, the tests may not have been technically satisfactory. Retesting when the edema had resolved revealed elevated sweat chloride val¬ ues in both infants. The difficulty in obtaining a suffi¬ cient quantity of sweat (greater than 0.1 gm) makes the diagnosis of CF difficult in small infants. Only two of the six reports of falsely negative sweat tests in edematous infants state the amount of sweat collected and/or secretion rates.7-8 If a diagnosis of CF is not made initially, it should be kept in mind and the sweat test repeated after disap¬ pearance of the edema. The restitu¬ tion of serum proteins to normal generally requires the vigorous use of an elemental diet or total parenteral nutrition in small infants. In milder cases, the addition of pancreatic enzyme extract and cow's milk that has a high protein content may be sufficient. In summary, hypoproteinemia and edema may develop in infants with CF whatever their diet although prior ingestion of soy bean formula appears to be a predisposing factor, and a negative sweat chloride test may be present in a CF child during the hypoproteinemic phase of the illness. The diagnosis cannot be excluded until a
139
72
148
negative test with adequate secretion
of sweat is obtained after edema and hypoproteinemia have resolved. TANIA GUNN, MB, CHB Mimi M. BELMONTE, MD ELEANOR COLLE, MD CLAIRE DUPONT, MD, PHD Department of Pediatrics Montreal Children's Hospital Montreal, Quebec, Canada DS, DiGeorge AM, Barness LA, et Hypoproteinemia and edema in infants with cystic fibrosis of the pancreas. J Pediatr 64:341\x=req-\ 1. Fleisher
al:
348, 1964.
2. Mulne A, McClung HJ, Tokarski P: Anti\x=req-\ trypsin activity in soy formulas. Pediatr Res 10:358, 1976. 3. Billee BS, Vahlquist B: Idiopathic hypoproteinemia versus hypoproteinemia due to pancreatic dysfunction. Acta Pediatr 44:435-443,
propriately aggressive therapy
has
been instituted. An
autopsy was recently performed
infant with this tumor. Wilms' was the primary diagnosis before death. The need to convey the benign nature of this mimic of Wilms' tumor prompted this case report.
on an
tumor
Report of a Case.\p=m-\Apremature boy was vaginally following 36 weeks gestation. Polyhydramnios complicated the delivered
otherwise uneventful pregnancy. Amniotic fluid, 5,000 ml, escaped when the membranes ruptured during an attempted amniocentesis, followed promptly by labor and delivery. The infant's cry and grasp were good, but the initial Apgar score of 3 rose only to
1955. 4. Goldman
AS, Travis LB, Dodge WF, et al: Falsely negative skin tests in children with cystic fibrosis complicated by hypoproteinemic oedema. J Pediatr 59:301, 1961. 5. Anderson C: Fibrocystic disease of the pancreas presenting with oedema and hypoproteinemia. Med J Aust 2:195-196, 1966. 6. Masi M, Lazzari R: Forma anemico edematosa della mucoviscidosi. Clin Pediatr 53:55-72, 1971. 7. MacLean WC Jr, Tripp RW: Cystic fibrosis with edema and falsely negative sweat tests. J Pediatr 83:86-88, 1973. 8. Lee PA, Roloff DW, Howatt MD: Hypoproteinemia and anemia in infants with cystic fibrosis: A presenting symptom complex often misdiagnosed. JAMA 228:585-588, 1974. 9. Vlachos P: Cystic fibrosis with edema and falsely negative sweat test. J Pediatr 84:926, 1974. 10. Dolan TF, Rowe DS, Gibson LE: Edema and hypoproteinemia in infants with cystic fibrosis: The hypoalbuminemia sometimes seen is presumably due to malabsorption. Clin Pediatr 9:295-297, 1970. 11. Lock J: Breast milk-induced hypoproteinemic shock, coagulopathy, and siderocystic anemia in cystic fibrosis. J Pediatr 84:912, 1974.
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Iowa User on 06/11/2015
1.—Tumor has almost replaced entire left kidney leaving only a thin rim of renal tissue (arrow).
Fig
A normal right kidney weighed 11.5 gm. The left kidney (75 gm) weighed nearly seven times as much as its partner and contained a firm, tan tumor, which, when bisected, resembled the whorled, trabeculated surface of a uterine leiomyoma (Fig 1). The poorly-demarcated tumor margins blended with a small amount of normal kidney in the lower pole.
Microscopic Pattern.-The kidney tumor composed of many uniform, elongated cells with fusiform nuclei (Fig 2). These was
cells, devoid of cross striations, most closely resembled those of primitive smooth mus¬ cle. Normal mitoses indicated active growth. Tubular structures, resembling normal and compressed kidney tubules, were prominently intermixed with the tumor immediately adjacent to the normal kidney. On the edges, fingers of tumor extended into normal kidney merging with the renal interstitium. The tumor did not invade vessels or implant in the perirenal fat. One single small island of hyaline Fig 2.\p=m-\Elongated,uniform, spindled,
tu-
separate normal kidney tubules and a glomerulus. These structures appear to be entrapped within tumor parenchyma. Similarity of tumor cells to smooth muscle is apparent (hematoxylineosin stain, original magnification mor
cells
X125).
5 after three minutes. Apnea occurred a few minutes later. Oxygen therapy and
resuscitation restored spontaneous breath¬ ing, but the infant remained limp. The pulse rate, normal at birth, fell to 40 beats per minute. Findings from the physical examination disclosed poor color, limited air exchange, and sternal and intercostal retraction. The left hemiabdomen contained a palpable mass. The infant was transferred to the newborn intensive care nursery with admitting diagnoses of (1) respiratorydistress syndrome with early hyaline mem¬ brane disease: (2) abdominal mass; ? Wilms' tumor; ? neuroblastoma. The chest roentgenogram and laboratory studies confirmed the clinical diagnosis of hyaline membrane disease. Abdominal roentgenograms showed a left hemiabdominal mass displacing the small bowel toward the midline and displacing the large bowel upward and laterally. The left kidney margins were indistinct. The diagnosis was tumor of the left kidney. Continued respiratory problems pre¬ cluded further diagnostic studies. Aggres¬ sive therapy directed at the hyaline membrane disease was unsuccessful. The infant died at 48 hours of age of respira¬ tory failure. At autopsy this normal-appearing male infant weighed 2,400 gm. The red-purple, heavy lungs showed the characteristic microscopic picture of advanced hyaline membrane disease.
cartilage lay
within the tumor. In the brain a subependymal hemor¬ rhage in the right thalamus extended into the right lateral ventricle. The final anatomic diagnoses were: (1) Subependymal hemorrhage, right thala¬ mus, with extension into right lateral ventricle. (2) Hyaline membrane disease, lungs, severe. (3) Mesoblastic nephroma, left kidney.
event, the patient then becomes candidate for more intensive ther¬ apy. Deaths associated with meso¬ blastic nephroma follow complications resulting from the combined therapy of surgery, irradiation and chemo¬ therapy, commenced with the mistak¬ en belief that the patient harbored a highly malignant Wilms' tumor.210 With mesoblastic nephroma, benign behavior, or at worst, local recurrence after surgery,11 is to be expected. Unlike Wilms' tumor, postoperative irradiation and/or chemotherapy does not improve the outlook for these patients. In fact, such therapeutic measures increase the complication rate, and almost certainly lessen the chances for survival. Treatment should be simple nephrectomy with complete excision of the tumor, since the majority of patients with this treatment go on to lead normal, healthy lives. The one exception reported to this date12 should not modify this conservative approach. This practical point remains: any kidney tumor should be completely removed. When the diagnosis is meso¬ blastic nephroma, no additional treat¬ ment is indicated. A good prognosis is the rule. a rare a
LARSON, MD Department of Pathology University of Minnesota, Duluth DONALD M.
Comment.—More than 50 cases of mesoblastic nephroma have now been
School of Medicine 2205 E 5th St Duluth, MN 55812
reported, primarily in the pathology and urology literature. Some of the
detected at birth or in the first few days of life, were incorrectly considered to be congenital Wilms' cases,
tumors.:,s
Wilms' tumor is an extremely rare condition, and Wilms' tumor in its classic form is also rare during the first six months of life. After the first year, Wilms' tumor is the most common kidney tumor of childhood. At birth, and for the first few neonatal months, mesoblastic nephroma is the most common kidney tumor.' This differing age incidence should permit segregation of the tumors on clinical grounds with rea¬ sonable certainty. Whether mesoblas¬ tic nephroma represents a "maturing form of Wilms' tumor," as Bolande and others have suggested,'-'' remains unresolved. Combined therapy (surgery, chemo¬ therapy and irradiation) is recom¬ mended for treatment of Wilms' tumor, but with congenital mesoblas¬ tic nephroma, tumor-free survival fol¬ lows simple nephrectomy in nearly every patient. Should the tumor recur,
Congenital
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Iowa User on 06/11/2015
Congenital mesoblastic nephroinfancy. Perspect Pediatr Pathol 1:227-250,
1. Bolande RP:
of 1973. ma
2. Kay S, Pratt CB, Salzberg AM: Hamartoma (leiomyomatous type) of the kidney. Cancer
19:1825-1841, 1966.
3. Dehner LP: Pediatric Surgical Pathology. St
Louis, CV Mosby Co, 1973, p 505.
4. Wigger HJ: Fetal mesenchymal hamartoma of infancy: A tumor of secondary mesenchyme. Cancer 36:1002-1008, 1975. 5. Annamunthodo H, Hutchings RF: Nephroblastoma (Wilms' tumor): Case report. J Urol 78:197-204, 1957. 6. Deming CL: Congenital sarcoma of the kidney in a child of 29 days. JAMA 80:902-905, 1923. 7. Wright ES: Congenital Wilms' tumor. Br J Urol 42:270-272, 1970. 8. Latimer JK, Melicou MM, Uson AC: Wilms' tumor: A report of 71 cases. J Urol 80:401-416, 1958. 9. Beckwith JB: Mesenchymal renal neoplasm of infancy. J Pediatr Surg 5:405-406, 1970. 10. Bolande RP, Brough AJ, Isanti RJ: Congenital mesoblastic nephroma of infancy. Pediatrics 40:272-278, 1967. 11. Fu YS, Kay S: Congenital mesoblastic nephroma and its recurrence. Arch Pathol 96:66\x=req-\ 70, 1973. 12. Walker D, Richard GA: Fetal hamartoma of the kidney: Recurrence and death of patient. J Urol 110:352-354, 1973.
Findings
in Six Children With Edema,
Hypoproteinemia,
and Anemia
Patient/Sex/ Admission
Age,
wk
Admission diet
1/M/6 cow's milk
2/F/10
soy based
3/F/6
soy based
4/F/14
soy based
5/M/6
soy based
6/M/8
modified cow's milk
Protein content
gm/100
ml_3_3_2.5
Failure to thrive, < 3rd percentile
Abnormal stools Edema Total protein,
gm/100
3.1_2_5_3_1_1.7
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
ml_1_9_3.5 0.82_2.3
Albumin, gm/100 ml
3.05_3.25 1.45_203
+
+
—
3.9_3.1 2.5_2.0
Hemoglobin, gm/100 ml_8J?_10.4 9.5_6_4_9j>_6.2 SGOT (10-26) IU_52_-_66_3!}_49_Sweat chloride,
Nephroma kidney tumor, often con-
Congenital A
rare
Mesoblastic
and known by a variety of (mesoblastic nephroma,1 leiomyomatous hamartoma,2 fetal renal hamartoma,3 mesenchymal hamartoma of infancy4), has been confused with Wilms' tumor. On occasion, inap-
genital names
mEq/liter
edema_^9_)Và_91_73_54_18
With Without edema
12. Paxson CL Jr: Idiopathic hypoproteinemia in twins. JAMA 230:1257-1258, 1974. 13. Bass HN, Miller AA: Cystic fibrosis presenting with anemia and hypoproteinemia in identical twins. Pediatrics 59:126-127, 1977. 14. Sahidi NT, Diamond LK, Schwachman H: Anemia associated with protein deficiency: A study of two cases with cystic fibrosis. J Pediatr 59:533-541, 1961. 15. Roger R, Finegold MJ: Cholestasis in immature newborn infants: is parenteral nutrition responsible? J Pediatr 86:264-269, 1975.
108
134
infants in whom they were measured. This may be due to malnutrition15 as the values returned to normal when the serum proteins became normal. A positive sweat chloride test is required for the diagnosis of CF. Two of our patients had normal values for sweat chloride while edematous. In retrospect, the tests may not have been technically satisfactory. Retesting when the edema had resolved revealed elevated sweat chloride val¬ ues in both infants. The difficulty in obtaining a suffi¬ cient quantity of sweat (greater than 0.1 gm) makes the diagnosis of CF difficult in small infants. Only two of the six reports of falsely negative sweat tests in edematous infants state the amount of sweat collected and/or secretion rates.7-8 If a diagnosis of CF is not made initially, it should be kept in mind and the sweat test repeated after disap¬ pearance of the edema. The restitu¬ tion of serum proteins to normal generally requires the vigorous use of an elemental diet or total parenteral nutrition in small infants. In milder cases, the addition of pancreatic enzyme extract and cow's milk that has a high protein content may be sufficient. In summary, hypoproteinemia and edema may develop in infants with CF whatever their diet although prior ingestion of soy bean formula appears to be a predisposing factor, and a negative sweat chloride test may be present in a CF child during the hypoproteinemic phase of the illness. The diagnosis cannot be excluded until a
139
72
148
negative test with adequate secretion
of sweat is obtained after edema and hypoproteinemia have resolved. TANIA GUNN, MB, CHB Mimi M. BELMONTE, MD ELEANOR COLLE, MD CLAIRE DUPONT, MD, PHD Department of Pediatrics Montreal Children's Hospital Montreal, Quebec, Canada DS, DiGeorge AM, Barness LA, et Hypoproteinemia and edema in infants with cystic fibrosis of the pancreas. J Pediatr 64:341\x=req-\ 1. Fleisher
al:
348, 1964.
2. Mulne A, McClung HJ, Tokarski P: Anti\x=req-\ trypsin activity in soy formulas. Pediatr Res 10:358, 1976. 3. Billee BS, Vahlquist B: Idiopathic hypoproteinemia versus hypoproteinemia due to pancreatic dysfunction. Acta Pediatr 44:435-443,
propriately aggressive therapy
has
been instituted. An
autopsy was recently performed
infant with this tumor. Wilms' was the primary diagnosis before death. The need to convey the benign nature of this mimic of Wilms' tumor prompted this case report.
on an
tumor
Report of a Case.\p=m-\Apremature boy was vaginally following 36 weeks gestation. Polyhydramnios complicated the delivered
otherwise uneventful pregnancy. Amniotic fluid, 5,000 ml, escaped when the membranes ruptured during an attempted amniocentesis, followed promptly by labor and delivery. The infant's cry and grasp were good, but the initial Apgar score of 3 rose only to
1955. 4. Goldman
AS, Travis LB, Dodge WF, et al: Falsely negative skin tests in children with cystic fibrosis complicated by hypoproteinemic oedema. J Pediatr 59:301, 1961. 5. Anderson C: Fibrocystic disease of the pancreas presenting with oedema and hypoproteinemia. Med J Aust 2:195-196, 1966. 6. Masi M, Lazzari R: Forma anemico edematosa della mucoviscidosi. Clin Pediatr 53:55-72, 1971. 7. MacLean WC Jr, Tripp RW: Cystic fibrosis with edema and falsely negative sweat tests. J Pediatr 83:86-88, 1973. 8. Lee PA, Roloff DW, Howatt MD: Hypoproteinemia and anemia in infants with cystic fibrosis: A presenting symptom complex often misdiagnosed. JAMA 228:585-588, 1974. 9. Vlachos P: Cystic fibrosis with edema and falsely negative sweat test. J Pediatr 84:926, 1974. 10. Dolan TF, Rowe DS, Gibson LE: Edema and hypoproteinemia in infants with cystic fibrosis: The hypoalbuminemia sometimes seen is presumably due to malabsorption. Clin Pediatr 9:295-297, 1970. 11. Lock J: Breast milk-induced hypoproteinemic shock, coagulopathy, and siderocystic anemia in cystic fibrosis. J Pediatr 84:912, 1974.
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Iowa User on 06/11/2015
1.—Tumor has almost replaced entire left kidney leaving only a thin rim of renal tissue (arrow).
Fig
A normal right kidney weighed 11.5 gm. The left kidney (75 gm) weighed nearly seven times as much as its partner and contained a firm, tan tumor, which, when bisected, resembled the whorled, trabeculated surface of a uterine leiomyoma (Fig 1). The poorly-demarcated tumor margins blended with a small amount of normal kidney in the lower pole.
Microscopic Pattern.-The kidney tumor composed of many uniform, elongated cells with fusiform nuclei (Fig 2). These was
cells, devoid of cross striations, most closely resembled those of primitive smooth mus¬ cle. Normal mitoses indicated active growth. Tubular structures, resembling normal and compressed kidney tubules, were prominently intermixed with the tumor immediately adjacent to the normal kidney. On the edges, fingers of tumor extended into normal kidney merging with the renal interstitium. The tumor did not invade vessels or implant in the perirenal fat. One single small island of hyaline Fig 2.\p=m-\Elongated,uniform, spindled,
tu-
separate normal kidney tubules and a glomerulus. These structures appear to be entrapped within tumor parenchyma. Similarity of tumor cells to smooth muscle is apparent (hematoxylineosin stain, original magnification mor
cells
X125).
5 after three minutes. Apnea occurred a few minutes later. Oxygen therapy and
resuscitation restored spontaneous breath¬ ing, but the infant remained limp. The pulse rate, normal at birth, fell to 40 beats per minute. Findings from the physical examination disclosed poor color, limited air exchange, and sternal and intercostal retraction. The left hemiabdomen contained a palpable mass. The infant was transferred to the newborn intensive care nursery with admitting diagnoses of (1) respiratorydistress syndrome with early hyaline mem¬ brane disease: (2) abdominal mass; ? Wilms' tumor; ? neuroblastoma. The chest roentgenogram and laboratory studies confirmed the clinical diagnosis of hyaline membrane disease. Abdominal roentgenograms showed a left hemiabdominal mass displacing the small bowel toward the midline and displacing the large bowel upward and laterally. The left kidney margins were indistinct. The diagnosis was tumor of the left kidney. Continued respiratory problems pre¬ cluded further diagnostic studies. Aggres¬ sive therapy directed at the hyaline membrane disease was unsuccessful. The infant died at 48 hours of age of respira¬ tory failure. At autopsy this normal-appearing male infant weighed 2,400 gm. The red-purple, heavy lungs showed the characteristic microscopic picture of advanced hyaline membrane disease.
cartilage lay
within the tumor. In the brain a subependymal hemor¬ rhage in the right thalamus extended into the right lateral ventricle. The final anatomic diagnoses were: (1) Subependymal hemorrhage, right thala¬ mus, with extension into right lateral ventricle. (2) Hyaline membrane disease, lungs, severe. (3) Mesoblastic nephroma, left kidney.
event, the patient then becomes candidate for more intensive ther¬ apy. Deaths associated with meso¬ blastic nephroma follow complications resulting from the combined therapy of surgery, irradiation and chemo¬ therapy, commenced with the mistak¬ en belief that the patient harbored a highly malignant Wilms' tumor.210 With mesoblastic nephroma, benign behavior, or at worst, local recurrence after surgery,11 is to be expected. Unlike Wilms' tumor, postoperative irradiation and/or chemotherapy does not improve the outlook for these patients. In fact, such therapeutic measures increase the complication rate, and almost certainly lessen the chances for survival. Treatment should be simple nephrectomy with complete excision of the tumor, since the majority of patients with this treatment go on to lead normal, healthy lives. The one exception reported to this date12 should not modify this conservative approach. This practical point remains: any kidney tumor should be completely removed. When the diagnosis is meso¬ blastic nephroma, no additional treat¬ ment is indicated. A good prognosis is the rule. a rare a
LARSON, MD Department of Pathology University of Minnesota, Duluth DONALD M.
Comment.—More than 50 cases of mesoblastic nephroma have now been
School of Medicine 2205 E 5th St Duluth, MN 55812
reported, primarily in the pathology and urology literature. Some of the
detected at birth or in the first few days of life, were incorrectly considered to be congenital Wilms' cases,
tumors.:,s
Wilms' tumor is an extremely rare condition, and Wilms' tumor in its classic form is also rare during the first six months of life. After the first year, Wilms' tumor is the most common kidney tumor of childhood. At birth, and for the first few neonatal months, mesoblastic nephroma is the most common kidney tumor.' This differing age incidence should permit segregation of the tumors on clinical grounds with rea¬ sonable certainty. Whether mesoblas¬ tic nephroma represents a "maturing form of Wilms' tumor," as Bolande and others have suggested,'-'' remains unresolved. Combined therapy (surgery, chemo¬ therapy and irradiation) is recom¬ mended for treatment of Wilms' tumor, but with congenital mesoblas¬ tic nephroma, tumor-free survival fol¬ lows simple nephrectomy in nearly every patient. Should the tumor recur,
Congenital
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Iowa User on 06/11/2015
Congenital mesoblastic nephroinfancy. Perspect Pediatr Pathol 1:227-250,
1. Bolande RP:
of 1973. ma
2. Kay S, Pratt CB, Salzberg AM: Hamartoma (leiomyomatous type) of the kidney. Cancer
19:1825-1841, 1966.
3. Dehner LP: Pediatric Surgical Pathology. St
Louis, CV Mosby Co, 1973, p 505.
4. Wigger HJ: Fetal mesenchymal hamartoma of infancy: A tumor of secondary mesenchyme. Cancer 36:1002-1008, 1975. 5. Annamunthodo H, Hutchings RF: Nephroblastoma (Wilms' tumor): Case report. J Urol 78:197-204, 1957. 6. Deming CL: Congenital sarcoma of the kidney in a child of 29 days. JAMA 80:902-905, 1923. 7. Wright ES: Congenital Wilms' tumor. Br J Urol 42:270-272, 1970. 8. Latimer JK, Melicou MM, Uson AC: Wilms' tumor: A report of 71 cases. J Urol 80:401-416, 1958. 9. Beckwith JB: Mesenchymal renal neoplasm of infancy. J Pediatr Surg 5:405-406, 1970. 10. Bolande RP, Brough AJ, Isanti RJ: Congenital mesoblastic nephroma of infancy. Pediatrics 40:272-278, 1967. 11. Fu YS, Kay S: Congenital mesoblastic nephroma and its recurrence. Arch Pathol 96:66\x=req-\ 70, 1973. 12. Walker D, Richard GA: Fetal hamartoma of the kidney: Recurrence and death of patient. J Urol 110:352-354, 1973.
