Hydramnion .
and fetal renal anomalies
M.
PERLMAN,
M.R.C.P.
G.
POTASHNIK,
M.B.,
S. WISE,
M.D.
Beer Sheva,
Israel
M.D.
Four instances of hydramnion associated with renal anomalies are reported: two had obstructuve uropathies and two had a neoplastic type of renal dysplasia. In infants water concentration tests revealed a defect in water-concentrating ability. postulated that the observed hydramnion resulted from fetal polyuria. In patients unexplained hydramnion a search for renal anomalies is indicated.
RENAL ANOMALIES are very rarely mentioned in surveys of hydramnion’+ in contrast to the wellestablished renal anomaly-oligohydramnios association.5-7 We report here four neonatal patients with renal anomalies who were delivered after pregnancies complicated by polyhydramnios. Clinicopathologic observations and postnatal renal function studies provide data which suggest that the hydramnion was caused by fetal polyuria.
water concentration test at the age of 5 weeks (‘Iable II) also showed a reversion to normal. Comment. This infant with a unilateral partial obstructive uropathy had impaired renal concentrating ability of water. There was no other obvious explanation for the hydramnion. Case 2. This male infant was the product of a healthy 24-year-old mother, gravida 1, para 1. The- pregnancy was normal. Parturition after 41 weeks’ gestation was complicated by polyhydramnios: 4.5 L. of fluid were measured. The umbilical cord was wound around the neck three times and the cord was elongated (130 cm.). There was a single umbilical artery. The Apgar score was 9 at 1 minute, the birth weight was 3,300 grams, and the head circumference was 32 cm. Physical examination revealed a distended, wrinkled, and toneless abdominal walI and macropenis. On palpation soft, elongated, tortuous masses were felt, mainly in the loins and lower abdomen. Constant dribbling micturition was observed postnatally. The bfood urea value was 10 mg. per 100 ml. on the first day and rose to 27 mg. per 100 ml. 3 days later. A urinary tract infection developed and the infant died at the age of 6 days with septicemia. Autopsy revealed stenosis of the penile urethra, dilatation and hypertrophy of the urinary bladder, and bilateral ureterohydronephrosis. There was no ascites. Additional findings included anorchidism and absence of abdominal muscles. Comment. This infant had a partial obstructive uropathy (prune-belly syndrome) and polyuria. There was no other obvious cause of polyhydramnios. Clse 3. This male neonate was the fifth affected child in a sibship of six with a unique syndrome of renal hamartomas, nephroblastomatosis, and gigantism.8 He was born, after an uncomplicated pregnancy of 40 weeks’ gestation, by breech delivery. The quantity of amniotic fluid was not measured as membrane rupture occurred before admission. There was a record of
Case reports Case 1. This male infant was born to a healthy woman, gravida 5, para 4. 22 years of age. The pregnancy was uncomplicated and delivery occurred after 41 weeks’ gestation. After rupture of the membrans, 6 L. of amniotic fluid were collected. Parturition was otherwise normal. The Apgar score was 9 at 1 minute, the birth weight was 4,060 grams, and the head circumference was 37 cm. The previous sibling, a female, weighed 3,490 grams after 39 weeks’ gestation. Routine physical examination on the first day revealed a mass in the left loin. Intravenous pyelography on the third day showed left hydronephrosis with moderate dilatation of the calyces and pelvis; the ureter was not dilated. On the eighth day a water concentration test was performed and the results are given in Table II. Blood urea and electrolyte values were normal and urinalysis was negative. Pyeloplasty was performed on postnatal day 20. The subsequent course was normal and repeat pyelography showed improvement in the hydronephrosis. The From
the Neonatal
Received
Unit, Soroka
for publication
Accepted Januaq
December
Medical
patients two It i.s with
Center.
30, 1975.
20, 1976.
Reprint requests: Dr. M. Perlmun, Neonatal Unit, Hadmsah University Hospital, P.O. Box 499, Jerusalem, Israel.
966
Volume
125
Number
7
Table
I. Clinical,
Hydramnion and fetal renal anomalies
laboratory,
and pathologic
correlates
Case 1: Unilateral hydronephrosis
Amniotic fluid volume (L.) Amniotic fluid dilution (mOsm./L.) Neonatal polyuria per cent weight loss (third day) Serum sodium (at 3 days) Renal concentration ability impaired Secondary bilateral hydronephrosis and ureter
6 0
of fetal renal anomalies case 2: Bilateral hydronephrosis
4.5 0
lo’
1:
155
156
967
and hydramnion
Case 3: Nephroblastomatosis
0 0 + 14 165
+
0
+
$
t
+
Case 4: Nephroblastomatosis
+++* 124 + lot 148
0 -
*+, Present; -, absent; 0, not examined. tDespite pushing fluids. SHydronephrosis and hydroureter were primary. polvhydramnios in one of the previous affected pregnancies and the mother described the delivery of her only normal child as “dry.” The physical and radiologic findings have been described in a previous puhlication.8 The findings relevant to renal function were as follows. (1) At the age of 2 hours the serum sodium was 145 mEq. per liter and the blood urea was 19 mg. per 100 ml. (2) There was a loss of 14 per cent of birth weight at 72 hours despite early feeding. (3) At 72 hours the serum osmolality was 324 mOsm. per liter, serum sodium 160 mEq. per liter, and blood urea nitrogen 65 mg. per 100 ml. The simultaneous urine osmolality was 298 mOsm. per liter. (4) The water concentration test at the age of 6 days (results in Table II) also indicated an impaired ability of the kidney to concentrate urine. The infant died at the age of 4 weeks. At autopsy nephromegaly with mild nonobstructive hydronephrosis and hydroureter were found. Microscopic examination of the kidneys revealed persistent nephrogenesis, hamartomas, and nephroblastomatosis. Other findings did not give a possible explanation of the polyhydramnios. Comment. An infant with dysplastic and enlarged kidneys had polyuria postnatally and rapidly developed hyperosmolar dehydration. The urine at that time was inappropriately dilute and further investigation revealed evidence of diabetes insipidus. Case 4. This younger female sibling of Case 3 was born by breech delivery after 40 postmenstrual weeks. The mother was admitted to the obstetric service before delivery on account of the bad obstetric history. Parturition commenced with spontaneous rupture of the membranes: hydramnion was noted but the volume of the amniotic fluid was not measured. The amniotic fluid osmolality was 124 mOsm. per liter. The birth weight was 3,850 grams. The infant had clinical findings similar to those of the previous siblings. In view of the experience with the previous sibling, special attention was paid to fluid balance. Polyuria (more than 250 ml. of urine per day with urine osmolarities ranging between 108 and 132 mOsm. per liter) was noted and appropriate fluid replacement was
made by gastric tube. Although the infant was maintained in fluid and electrolyte balance, she died on the fourth day of no apparent cause. Autopsy findings were similar to those of Case 3, with the addition of a nodular Wilms’ tumor at the upper pole of the left kidney. Comment. Like her previous siblings, this infant had hydramnion and postnatal impairment of renal retention of fluid. The amniotic fluid, as well as being increased in volume, was hypo-osmolar compared to normal values (23 1 to 26 1 mOsm. per liter for 38 to 4 1 week gestations).g
Comment The common denominators of the patients with renal anomalies described above are as follows: (1) hydramnion, (2) neonatal polyuria, and (3) laboratory evidence postnatally of impaired ability of the kidney to conserve water (Table I). Additional circumstantial evidence of fetal and neonatal renal dysfunction includes the findings of hypo-osmolar amniotic fluid in one instance, mild nonobstructive hydronephrosis and hydroureter in one patient, and the development of hyperosmolar dehydration in three infants (Table I). Particularly pertinent was the failure of renal concentration of water in case 3 in the first 72 postnatal hours, which occurred in the face of rising values of serum sodium and urea and the administration of fluids. Hansen and Smith” observed a rise of urine osmolality to 550 to 600 mOsm. per liter in normal neonates deprived of fluids for 72 hours from birth. Renal anomalies occupy a small place only in reported series of hydramnion.*-4 Incomplete documentation of those instances recorded does not permit their interpretation. Whereas hydramnion is relatively common in reports of bilateral nephroblastomatosis’* ‘* and of congenital mesoblastic nephroma,‘, i2. i3 we have found no reports of hydramnion in neonates with congenital hydronephrosis. Hydramnion has been hypothetically related to fetal
968
Perlman,
Table
Potashnik,
II. Six-hour
and Wise
water
deprivation
tests
acetaminophen
Case 1
Cuse 2
Case 3
8 2.5
35 1.0
6 5.0
284 299
282 281
298 312
the
in fetal
renal
tubules.
concentration Age at examination (days) Weight loss (per cent) Plasma osnzolali~: Start Finish Urine osmolalily: Start Finish
190 193
194 208
dramnion. nephrogenic
In
the
parabiotic
recipient
twin’s
attributed of
This
The
of neonatal
obstruction
was due
invoked
as an explanation
A similar renal
tubules
to a lack
upon
these
and with
considered
possibly
with
been
resultant
the
and
in
has been
reported
above
of renal
to one
half
together
to indicate
fetal
polyuria,
in the
production
causing
fetal
hydramnion.
hydramnion in an infant
is that and
dilated
exposed
should to
REFERENCES
1. Jacoby, H. E., and Charles, B.: Clinical conditions associated with hydramnios, AM. J. OBSTET. GYNECOL. 94: 910, 1966. 2. Lee, K. H.: Hydramnios in the Chinese: A clinical study of 256 cases, J. Obstet. Gynecol. Br. Commonw. 74: 868, 1967. 3. Kramer, E. E.: Hydramnios, oligohydramnios and fetal malformations, Clin. Obstet. Gynecol. 9: 508, 1966. 4. Wagner, M. L., Rudolph, A. J., and Singleton, E. B.: Neonatal defects associated with abnormalities of the amnion and amniotic fluid, Radiol. Clin. North Am. 6: 279, 1968. 5. Blanc, W. A., Apperson, J. W., and McNally, J.: Pathology of the newborn and of the placenta in olygohydramnios, Bull. Sloane Hosp. Women 8: 51, 1962. 6. Perlman, M., and Levin, M.! Fetal pulmonary hypoplasia, anuria, and oligohydramnios: Clinico-pathologic observations and review of the literature, AM. J. OBSTET. GYNECOL. 118: 1119, 1974. 7. Thomas, I. T., and Smith, D. W.: Oligohydramnios, cause of the nonrenal features of Potter’s syndrome, including pulmonary hypoplasia, J. Pediatr. 84: 811, 1974. 8. Perlman, M., Goldberg, G. M., Bar-Ziv, J., and Danovitch, G.: Renal hamartomas and nephroblastomatosis with fetal gigantism: a familial syndrome, J. Pediatr. 83: 414, 1973. 9. Gillibrand, P. N.: Changes in the electrolytes, urea and osmolality of the amniotic fluid with advancing pregnancy, J. Obstet. Gynaecol. Br. Commonw. 76: 898, 1969.
renal
also II)
in The
i*~c~m~plrtc of impaired
in cl~ildt~ootl.l*~
suggest the
a causative
etiology
pathogenesis
the lead
renal
in
cause
of abilito
1.5
The
review
of
of‘
the
the
irn-
in c;tse
may
of some
instances
The
finding
of
to a careful in the
pet
patients have
:i
unexplainecl infants
of one
presented literature
a causative
role
of hydramnion
implication
prospective
cent
in about
pertinent
anomalies
polyuria.
dysfunction
about
is undiagnosed
of them.3
with
that
was
Tcr cause
kidney,
1 (Table
occurs the
suggest
and
h! -
water-concentrating
and
tubules.”
hormone(s),
to
observed
clear.
renal
of the of
in case hydronephrosis
dilated
of pituitary
concurrence
agenesis,
considered
the
due
by the
the
deliveries” quarter
pituitary
II)
renal
the mothers ot children with insipidus occasionally have cx-
findings
pairment
TO IX toxic impaired
was of
is an established
Hydramnion the
postnatally
hydramnion.
is not
observa-
infants
of
observed
polyuria.
infants
is associated
latter
in
has
flow
role
polycythemic
hydramnion
is based
tubules
conditions.
the
blood
hypothesis
anencephalic
hydramnion
to renal
renal
finding
of different
syndrome,
propensity
dilated
postnatal In
twin
to increased
polyuria.14 tion
in a number
of
hydronephrosis
concentration
Is The dysfunction
known
fluid.”
Obstructive ureteric
a drug finding
explanation
Furthermore, diabetes
cess amniotic
123 119
water
a possible
water renal
of
provide
life,
I6 The
for
the
1,) clinician
polvhv~lramnios search
for
(:aLtses of‘
concernrtl.
10. Hansen, J. D. L., and Smith, C. A.: Effects of’withholding Huids in the immediate neonatal period, Pediatrics 12: 99. 1953. 11. Hustin, J., and Chef. R.: Nephroblastomatose diffuse bilatcrai-reflexions sur un nouveau cas, J. Gynecol. Obstet. Biol. Reprod. (Paris) 1: 373, 1972. 12. Hartenstien, H.: Wilms’ tumor in a newborn infant, ,J. Pediatr. 35: 381, 1949. 13. Favara, B., Johnson, W., and Ito, J.: Renal t.umors in rhe neonatal period, Cancer 22: 845, 1968. 14. Naeye, R. L.: Human intrauterine parabiotic syndrome and its complications, N. Engl. J. Med. 268: 804, 1963. 15. Naeye, R. L.. Blanc, W.. and Milic. A. M.: Renal development in dysplasia of the fetal pituitary. Prdiatr. Res. 4: 257, 1970. 16. Char, V. C., Chandra, R., Fletcher, A. B.. and -4very. G. B.: Polyuria and neonatal renal failure-a possible association with maternal acetominophen ingestion. J. Pediatr. Stand. 86: 638. 1975. 17. Barratt, T. M.: In Williams, D. l., editor: Urology in Childhood, Berlin, 1974, Springer Verlag, p. 2. 18. Ericsson, N. O., Winberg, J., and Zetterstrom. R.: Renal function in infantile obstructive uropathy, Acta Paediatr. 44: 444, 1955. 19. Earley, L. E.: Extreme polyuria in obstructive uropathy. N. Engl. J. Med. 255: 600, 1956. 20. Niswander, K. R., and Gordon, M.: The Women and their pregnancies. Philadelphia, 1972, W. B. Saunders Company.
and fetal renal anomalies
M.
PERLMAN,
M.R.C.P.
G.
POTASHNIK,
M.B.,
S. WISE,
M.D.
Beer Sheva,
Israel
M.D.
Four instances of hydramnion associated with renal anomalies are reported: two had obstructuve uropathies and two had a neoplastic type of renal dysplasia. In infants water concentration tests revealed a defect in water-concentrating ability. postulated that the observed hydramnion resulted from fetal polyuria. In patients unexplained hydramnion a search for renal anomalies is indicated.
RENAL ANOMALIES are very rarely mentioned in surveys of hydramnion’+ in contrast to the wellestablished renal anomaly-oligohydramnios association.5-7 We report here four neonatal patients with renal anomalies who were delivered after pregnancies complicated by polyhydramnios. Clinicopathologic observations and postnatal renal function studies provide data which suggest that the hydramnion was caused by fetal polyuria.
water concentration test at the age of 5 weeks (‘Iable II) also showed a reversion to normal. Comment. This infant with a unilateral partial obstructive uropathy had impaired renal concentrating ability of water. There was no other obvious explanation for the hydramnion. Case 2. This male infant was the product of a healthy 24-year-old mother, gravida 1, para 1. The- pregnancy was normal. Parturition after 41 weeks’ gestation was complicated by polyhydramnios: 4.5 L. of fluid were measured. The umbilical cord was wound around the neck three times and the cord was elongated (130 cm.). There was a single umbilical artery. The Apgar score was 9 at 1 minute, the birth weight was 3,300 grams, and the head circumference was 32 cm. Physical examination revealed a distended, wrinkled, and toneless abdominal walI and macropenis. On palpation soft, elongated, tortuous masses were felt, mainly in the loins and lower abdomen. Constant dribbling micturition was observed postnatally. The bfood urea value was 10 mg. per 100 ml. on the first day and rose to 27 mg. per 100 ml. 3 days later. A urinary tract infection developed and the infant died at the age of 6 days with septicemia. Autopsy revealed stenosis of the penile urethra, dilatation and hypertrophy of the urinary bladder, and bilateral ureterohydronephrosis. There was no ascites. Additional findings included anorchidism and absence of abdominal muscles. Comment. This infant had a partial obstructive uropathy (prune-belly syndrome) and polyuria. There was no other obvious cause of polyhydramnios. Clse 3. This male neonate was the fifth affected child in a sibship of six with a unique syndrome of renal hamartomas, nephroblastomatosis, and gigantism.8 He was born, after an uncomplicated pregnancy of 40 weeks’ gestation, by breech delivery. The quantity of amniotic fluid was not measured as membrane rupture occurred before admission. There was a record of
Case reports Case 1. This male infant was born to a healthy woman, gravida 5, para 4. 22 years of age. The pregnancy was uncomplicated and delivery occurred after 41 weeks’ gestation. After rupture of the membrans, 6 L. of amniotic fluid were collected. Parturition was otherwise normal. The Apgar score was 9 at 1 minute, the birth weight was 4,060 grams, and the head circumference was 37 cm. The previous sibling, a female, weighed 3,490 grams after 39 weeks’ gestation. Routine physical examination on the first day revealed a mass in the left loin. Intravenous pyelography on the third day showed left hydronephrosis with moderate dilatation of the calyces and pelvis; the ureter was not dilated. On the eighth day a water concentration test was performed and the results are given in Table II. Blood urea and electrolyte values were normal and urinalysis was negative. Pyeloplasty was performed on postnatal day 20. The subsequent course was normal and repeat pyelography showed improvement in the hydronephrosis. The From
the Neonatal
Received
Unit, Soroka
for publication
Accepted Januaq
December
Medical
patients two It i.s with
Center.
30, 1975.
20, 1976.
Reprint requests: Dr. M. Perlmun, Neonatal Unit, Hadmsah University Hospital, P.O. Box 499, Jerusalem, Israel.
966
Volume
125
Number
7
Table
I. Clinical,
Hydramnion and fetal renal anomalies
laboratory,
and pathologic
correlates
Case 1: Unilateral hydronephrosis
Amniotic fluid volume (L.) Amniotic fluid dilution (mOsm./L.) Neonatal polyuria per cent weight loss (third day) Serum sodium (at 3 days) Renal concentration ability impaired Secondary bilateral hydronephrosis and ureter
6 0
of fetal renal anomalies case 2: Bilateral hydronephrosis
4.5 0
lo’
1:
155
156
967
and hydramnion
Case 3: Nephroblastomatosis
0 0 + 14 165
+
0
+
$
t
+
Case 4: Nephroblastomatosis
+++* 124 + lot 148
0 -
*+, Present; -, absent; 0, not examined. tDespite pushing fluids. SHydronephrosis and hydroureter were primary. polvhydramnios in one of the previous affected pregnancies and the mother described the delivery of her only normal child as “dry.” The physical and radiologic findings have been described in a previous puhlication.8 The findings relevant to renal function were as follows. (1) At the age of 2 hours the serum sodium was 145 mEq. per liter and the blood urea was 19 mg. per 100 ml. (2) There was a loss of 14 per cent of birth weight at 72 hours despite early feeding. (3) At 72 hours the serum osmolality was 324 mOsm. per liter, serum sodium 160 mEq. per liter, and blood urea nitrogen 65 mg. per 100 ml. The simultaneous urine osmolality was 298 mOsm. per liter. (4) The water concentration test at the age of 6 days (results in Table II) also indicated an impaired ability of the kidney to concentrate urine. The infant died at the age of 4 weeks. At autopsy nephromegaly with mild nonobstructive hydronephrosis and hydroureter were found. Microscopic examination of the kidneys revealed persistent nephrogenesis, hamartomas, and nephroblastomatosis. Other findings did not give a possible explanation of the polyhydramnios. Comment. An infant with dysplastic and enlarged kidneys had polyuria postnatally and rapidly developed hyperosmolar dehydration. The urine at that time was inappropriately dilute and further investigation revealed evidence of diabetes insipidus. Case 4. This younger female sibling of Case 3 was born by breech delivery after 40 postmenstrual weeks. The mother was admitted to the obstetric service before delivery on account of the bad obstetric history. Parturition commenced with spontaneous rupture of the membranes: hydramnion was noted but the volume of the amniotic fluid was not measured. The amniotic fluid osmolality was 124 mOsm. per liter. The birth weight was 3,850 grams. The infant had clinical findings similar to those of the previous siblings. In view of the experience with the previous sibling, special attention was paid to fluid balance. Polyuria (more than 250 ml. of urine per day with urine osmolarities ranging between 108 and 132 mOsm. per liter) was noted and appropriate fluid replacement was
made by gastric tube. Although the infant was maintained in fluid and electrolyte balance, she died on the fourth day of no apparent cause. Autopsy findings were similar to those of Case 3, with the addition of a nodular Wilms’ tumor at the upper pole of the left kidney. Comment. Like her previous siblings, this infant had hydramnion and postnatal impairment of renal retention of fluid. The amniotic fluid, as well as being increased in volume, was hypo-osmolar compared to normal values (23 1 to 26 1 mOsm. per liter for 38 to 4 1 week gestations).g
Comment The common denominators of the patients with renal anomalies described above are as follows: (1) hydramnion, (2) neonatal polyuria, and (3) laboratory evidence postnatally of impaired ability of the kidney to conserve water (Table I). Additional circumstantial evidence of fetal and neonatal renal dysfunction includes the findings of hypo-osmolar amniotic fluid in one instance, mild nonobstructive hydronephrosis and hydroureter in one patient, and the development of hyperosmolar dehydration in three infants (Table I). Particularly pertinent was the failure of renal concentration of water in case 3 in the first 72 postnatal hours, which occurred in the face of rising values of serum sodium and urea and the administration of fluids. Hansen and Smith” observed a rise of urine osmolality to 550 to 600 mOsm. per liter in normal neonates deprived of fluids for 72 hours from birth. Renal anomalies occupy a small place only in reported series of hydramnion.*-4 Incomplete documentation of those instances recorded does not permit their interpretation. Whereas hydramnion is relatively common in reports of bilateral nephroblastomatosis’* ‘* and of congenital mesoblastic nephroma,‘, i2. i3 we have found no reports of hydramnion in neonates with congenital hydronephrosis. Hydramnion has been hypothetically related to fetal
968
Perlman,
Table
Potashnik,
II. Six-hour
and Wise
water
deprivation
tests
acetaminophen
Case 1
Cuse 2
Case 3
8 2.5
35 1.0
6 5.0
284 299
282 281
298 312
the
in fetal
renal
tubules.
concentration Age at examination (days) Weight loss (per cent) Plasma osnzolali~: Start Finish Urine osmolalily: Start Finish
190 193
194 208
dramnion. nephrogenic
In
the
parabiotic
recipient
twin’s
attributed of
This
The
of neonatal
obstruction
was due
invoked
as an explanation
A similar renal
tubules
to a lack
upon
these
and with
considered
possibly
with
been
resultant
the
and
in
has been
reported
above
of renal
to one
half
together
to indicate
fetal
polyuria,
in the
production
causing
fetal
hydramnion.
hydramnion in an infant
is that and
dilated
exposed
should to
REFERENCES
1. Jacoby, H. E., and Charles, B.: Clinical conditions associated with hydramnios, AM. J. OBSTET. GYNECOL. 94: 910, 1966. 2. Lee, K. H.: Hydramnios in the Chinese: A clinical study of 256 cases, J. Obstet. Gynecol. Br. Commonw. 74: 868, 1967. 3. Kramer, E. E.: Hydramnios, oligohydramnios and fetal malformations, Clin. Obstet. Gynecol. 9: 508, 1966. 4. Wagner, M. L., Rudolph, A. J., and Singleton, E. B.: Neonatal defects associated with abnormalities of the amnion and amniotic fluid, Radiol. Clin. North Am. 6: 279, 1968. 5. Blanc, W. A., Apperson, J. W., and McNally, J.: Pathology of the newborn and of the placenta in olygohydramnios, Bull. Sloane Hosp. Women 8: 51, 1962. 6. Perlman, M., and Levin, M.! Fetal pulmonary hypoplasia, anuria, and oligohydramnios: Clinico-pathologic observations and review of the literature, AM. J. OBSTET. GYNECOL. 118: 1119, 1974. 7. Thomas, I. T., and Smith, D. W.: Oligohydramnios, cause of the nonrenal features of Potter’s syndrome, including pulmonary hypoplasia, J. Pediatr. 84: 811, 1974. 8. Perlman, M., Goldberg, G. M., Bar-Ziv, J., and Danovitch, G.: Renal hamartomas and nephroblastomatosis with fetal gigantism: a familial syndrome, J. Pediatr. 83: 414, 1973. 9. Gillibrand, P. N.: Changes in the electrolytes, urea and osmolality of the amniotic fluid with advancing pregnancy, J. Obstet. Gynaecol. Br. Commonw. 76: 898, 1969.
renal
also II)
in The
i*~c~m~plrtc of impaired
in cl~ildt~ootl.l*~
suggest the
a causative
etiology
pathogenesis
the lead
renal
in
cause
of abilito
1.5
The
review
of
of‘
the
the
irn-
in c;tse
may
of some
instances
The
finding
of
to a careful in the
pet
patients have
:i
unexplainecl infants
of one
presented literature
a causative
role
of hydramnion
implication
prospective
cent
in about
pertinent
anomalies
polyuria.
dysfunction
about
is undiagnosed
of them.3
with
that
was
Tcr cause
kidney,
1 (Table
occurs the
suggest
and
h! -
water-concentrating
and
tubules.”
hormone(s),
to
observed
clear.
renal
of the of
in case hydronephrosis
dilated
of pituitary
concurrence
agenesis,
considered
the
due
by the
the
deliveries” quarter
pituitary
II)
renal
the mothers ot children with insipidus occasionally have cx-
findings
pairment
TO IX toxic impaired
was of
is an established
Hydramnion the
postnatally
hydramnion.
is not
observa-
infants
of
observed
polyuria.
infants
is associated
latter
in
has
flow
role
polycythemic
hydramnion
is based
tubules
conditions.
the
blood
hypothesis
anencephalic
hydramnion
to renal
renal
finding
of different
syndrome,
propensity
dilated
postnatal In
twin
to increased
polyuria.14 tion
in a number
of
hydronephrosis
concentration
Is The dysfunction
known
fluid.”
Obstructive ureteric
a drug finding
explanation
Furthermore, diabetes
cess amniotic
123 119
water
a possible
water renal
of
provide
life,
I6 The
for
the
1,) clinician
polvhv~lramnios search
for
(:aLtses of‘
concernrtl.
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