Здравейте момичета!
Преди няколкo дни бях на фетална морфология и док установи в едно от бъбреците на бебето pyelectasia.Каза, че може да е маркер за синдром на Даун, но може и да не е серизоен проблем .Всички останали органи на плода са много добре разивити без никакви  отклонения.Имам правен БХС ,който отхвърля какъвто и да е риск за синдрома на Даун.Според док има много голяма вероятност ,всичко да се оправи вътреутробно и затова препоръча по -често наблюдение.Вие имате ли повече информация по този проблем , защото в нета не намерих много писано 

здравей Мери, търсих много в мрежата за тази диагноза, защото и при нас е същата. с тази разлика, че е и на двете бъбречета и бебето е момиче, което усложнява нещата. мога дамо да те успокоя, че наистина е възможно да се нормализира вътреутробно. не знам дали си струва честото наблюдение на УЗ, защото пренатално не би могло да се оправи. след раждането може да се действа. това, което си написала ме навежда на мисълта, че те е гледал Марков, но един единствен мек маркер не може да е категорично доказателство за синдром на Даун. ако бебето ти е момче пиелектазията би могла да се дължи на фимоза, която е често срещана при тях и затова пиелектазията се води физиологична, след раждането се оправя от самосебе си след забелването на главичката на пишока.

Благодаря ти за инфото Eternity, в Пловдив ме е гледал Даскалов.За Марков имам час на 03.09.-тогава ще видим какво ще каже той. И моето бебе е момиче , и засега има проблем само в единия бъбрек

Момичета, а колко големи в мм са ви находките?

ами евро, на първа ФМ бяха гранични (4.5 и 4.7), но за 10-ина минути се увеличиха. коментар от  доктора на въпроса ми: Как е възможно да се променят за толкова кратко време: първото мерене може да е било в спазъм на бъбреците. сега няма смисъл да го меря, с просто око се вижда , че са и по-големи. 2 седмици по-късно при друг лекар: 7.0 и 7.1 мм. надявам се кьм момента на раждане да не са по-големи от 10 мм.
едно уточнение: при мен количеството околоплодни води са в норма.

Аз не мога да разбера от снимката колко е голямо.Само знам че е в левия бъбрек.Eternity, а какво се предприема след раждане като лечение.
За околоплодните води , маойте малко са се увеличили и вече са над долна граница.Но аз имам малко повечко кг и това също може да е причина както и това с бъбрека .Док неможе да е категоричен.Мен повече ме притеснява доколко може да е свързано със синдрома на Даун.Все си мисля, че трябва и други признаци ,по които да съдим за даун

малко инфо на английски:

Prenatal Hydronephrosis:
The collecting system is the structure that gathers urine directly from the renal tissue and sends it to the bladder through the ureter. Prenatal hydronephrosis is the dilatation of the renal collecting system detected before birth.
Development of the Fetal Kidney & Production of Amniotic Liquid
The kidneys are formed by three separate, but interrelated, structures: the ureteric bud, the metanephric blastema and the cloaca. By 20 weeks of pregnancy, the excretory system is already completely formed, including the ureter, renal pelvis, calyxes, and papillary and collecting ducts. However, by this time, when the collecting system has finished its formation, only a third of the total number of nephrons is present; nephrogenesis continues until 36 weeks of gestation.[1]
Fetal urine contributes to the quantity and quality of the amniotic fluid depending on the gestational time. At the beginning of pregnancy, the amniotic liquid is a transudate of maternal plasma, and as the fetus grows, the amniotic liquid becomes similar to the fetal plasma, which is thought to be due to diffusion through the fetal skin. Production of fetal urine begins after the ninth week of pregnancy, and the kidneys are capable of excreting sodium and concentrating urea between 12 and 14 weeks of gestation. After 18 weeks, and especially after 20 or 22 weeks, all the amniotic liquid is constituted by fetal urine.[1,2]
For that reason, before 16 weeks of gestation, although there are no functional kidneys, the amniotic liquid can be normal because it is produced by other non-renal pathways. After 16 or 18 weeks of pregnancy and especially past 20 weeks, bilateral kidney agenesis is always associated with severe and progressive oligohydramnion.
Fetal Ultrasonographic Exploration
Maternal-fetal ultrasound has posed questions and challenges in the management of problems that were unknown a few years ago. However, it has also provided a new and splendid way of introducing ourselves in human renal pathophysiology.[3]
The first urinary tract structure that can be detected by ultrasound is the bladder, visualized between the ninth and tenth weeks of pregnancy, just after the start of urine production. The fetal bladder appears as a round or oval, echolucid, structure emerging from the fetal pelvis. It fills up and empties every 20 to 30 minutes, so that if is not visible at the beginning of the study, it is generally full by the end and may easily be detected.[1] If it is not possible to detect the bladder in several studies, vesical extrophy should be suspected.[2]
The fetal kidney may be visualized after about 14 weeks of pregnancy, but it is not routinely observed until after 16 or 18 weeks. Initially the kidneys appear as two hypoechogenic masses adjacent to the lumbar spine of the fetus and may be difficult to define, but as pregnancy progresses, they are easy to detect since retroperitoneal fat deposits around them and they are more clearly defined. Some of the internal structures of the kidneys, such as the fat of the renal sinuses and the medullar pyramids are not well defined until 20 weeks of gestation.[1]
Generalized use of maternal-fetal ultrasound has shown that, in addition to hydronephrosis, renal cystic diseases and even calculi and tumors[4] can be detected. But it has also been shown that pelvic dilatation or hydronephrosis is the most frequently found condition.[4-7]
Examination of the fetal urinary tract should include the volume of amniotic liquid, shape, echogenicity and position of the kidneys, presence or absence of renal cysts, good or poor delimitation between the cortex and the medulla, and the presence of cortex thinning.[1,8,9]
Most fetal ultrasound studies are performed before 24 weeks of gestation because the obstetric management may be changed if desired. However, since anomalies of the urinary tract are generally progressive lesions, alterations that were not detectable between 20 and 24 weeks may appear. Maternal-fetal ultrasound should be performed after 28 weeks of pregnancy to detect alterations of the urinary tract.[1,10] Many obstructive, as well as cystic, abnormalities can be detected and this is very important for giving counsel to the family,[1] and for the study and follow-up of the newborn.
Prenatal ultrasound has given rise to new situations in nephrourology that require adequate management. Many of these children may benefit from early diagnosis and prevention of secondary complications, mainly infections.[2]
Hydronephrosis
As already mentioned, pelvic dilatation or hydronephrosis is the alteration of the urinary tract most frequently detected by maternal-fetal ultrasound.[2,4-7]
Hydronephrosis is not a diagnosis; it is an image finding. The diagnosis is the cause that produces it.[2]
Since pelvic dilatation is relatively frequent in the normal fetus, and the definition and diagnosis of hydronephrosis are difficult, once it is detected, adequate follow-up is required. Postnatal study has shown that mild dilatation of the higher urinary tract does not indicate an obstruction; mild hydronephrosis may be transient; and spontaneous improvement can occur.[11,12] The idea of considering every dilatation of the urinary system as a disorder for which surgery is the solution, is no longer an axiom.[13]
Prenatal pelvic dilatation that is not found after birth or disappears quickly has been explained as a process of embryonic development of the ureter. The developing ureter undergoes an obstruction and re-channeling process at the middle level; some researchers have speculated that this obstruction may occur due to an incomplete re-channeling of the cephalic and caudal ends of the developing ureter, which is later resolved. If the ureter is not permeable when urine production begins, the pelvis may suffer a transient dilatation. Fetal ureters are redundant and tortuous, but they stretch out afterwards during the longitudinal growth of the body and the ascent of the kidneys to an upper retroperitoneal position. This could be an alternative explanation for transient dilatation.[14]
Different criteria have been used to classify the degrees of prenatal hydronephrosis based on the measurement of the anteroposterior diameter of the pelvis.
In our studies we have followed the criteria of Blachar and Blachar,[11,12] while others have followed very similar criteria[16] ( Table 1 ). Some authors[17] have used the criterion of the larger pelvic diameter measuring over 4mm before 33 weeks and 7mm after 33 weeks of gestation to suggest dilatation. Others consider that the anteroposterior diameter of the pelvis should be less that 6mm before 20 weeks of gestation; less than 8mm between 20 and 30 weeks and less than 10mm after 30 weeks.[18] The Society for Fetal Urology has proposed a classification in four groups or categories ( Table 2 ).[9,19,20] Although different criteria have been used, it is generally accepted that a renal pelvis of 10mm or more, during the second quarter of pregnancy, is an indication of hydronephrosis.
Table 1: Classifications Used for Grading Prenatal Hydronephrosis According to the Anteroposterior Diameter of the Pelvis
Degree    Blachar y Blachar[11,12]    Barker et al.[16]
Normal    0 - 4mm    0 - 5mm
Mild dilatation    5 - 9mm    6 - 10mm
Moderate dilatation    10 - 14mm    11 - 14mm
Severe dilatation    15mm or more    15mm or more
Table 2: Degrees of Ultrasonographic Hydronephrosis According to the Society for Fetal Urology[9]
Degree    Ultrasound findings
1    Visualization of the pelvis
2    Dilated pelvis and there could be a dilated calyx
3    Dilated pelvis and calyxes
4    Dilated pelvis and calyxes with thinning of the parenchyma
Of the parameters used for diagnosing hydronephrosis, the most useful seem to be those used by the Society for Fetal Urology. However, degrees 1 and 2 do not represent true hydronephrosis, but a mild or moderate degree of pyeloectasia.[20,21] Real hydronephrosis always includes significant pelvic dilatation of the pelvis and calyxes. Classifications based solely on pelvic diameter can be misleading since pyeloectasia without calyx dilatation is generally not a sign of significant obstruction.[21]
Congenital obstructions of the utero-pelvic union have historically been classified as intrinsic and extrinsic. The intrinsic ones are attributed to changes in the quantity and orientation of the muscular fibers of the utero-pelvic union, collagen increase, and alterations of peristalsis. Extrinsic obstructions are attributed to anomalous, ectopic or aberrant, vessels, when a branch of the renal artery that compresses the ureter irrigates the lower pole of the kidney. Fibroepithelial polyps and ureteral valves are rare causes of obstruction.[21] Pelvic dilatations of fewer than 10mm in the third quarter of gestation are more frequently due to non-obstructive vesicourethral reflux or pyeloectasia, both conditions being more frequent in male infants.[6,7,15]
 
Тук има една схема, която няма как да копирам в отговора.

продължение на горното и в отговр на съпроса ти, Мари:
STUDY AND FOLLOW-UP
When maternal-fetal ultrasound detects a dilatation of the renal pelvis or hydronephrosis during any period of pregnancy, the neonate must be studied by renal ultrasonography in the first week of extrauterine life. The need to act fast may vary depending on the degree of dilatation or prenatal hydronephrosis; whether it is unilateral or bilateral; whether there is a palpable renal mass; or the presence of only one kidney or a urinary infection in the neonatal period.
Considering these particularities in each case, the general follow-up proposal, shown in Figure 1 , may be modified. Some recommend that if hydronephrosis is moderate or severe the study must be carried out according to our proposal, but if the degree of hydronephrosis is less (mild), they prefer waiting for a few days to ensure an adequate hydration and to minimize the incidence of false negative ultrasonographic studies.[22]
Between the third and seventh days of life an ultrasound must be performed to determine precisely whether there is dilatation or not, and to measure the pelvis, calyxes and renal parenchyma. It will also enable adequate evaluation of the contra lateral kidney (when hydronephrosis is unilateral), to look for ureteric dilatation and visualize the bladder, and to rule out the possibility of ureterocele as the cause of dilatation of the upper urinary tract. It is also important to measure the size of the kidney, which grows 1mm in height every week of the gestational period.[22]
In the first three days of life, renal ultrasound should not be performed, except in very special situations, since at this stage oliguria and hypohydration may conceal pelvic dilatation.
If, during the first week of life, the renal ultrasound shows no evidence of pelvic dilatation and the kidney size is normal, the parents must be given reassuring information, but the child has to be reevaluated ultrasonographically between 3 and 6 months of age. If this second kidney ultrasound is normal, it is not necessary to continue the follow-up, if the baby remains asymptomatic. If during the second study pelvic dilatation is found, even if it is mild, micturitional ureterocystography must be performed to rule out vesicoureteral reflux. Mild dilatations (less than 10mm in diameter) are frequently due to vesicoureteral reflux,[23, 24] and it has been proven in children without postnatal dilatation detectable by ultrasound.[15,24,25] A valuable sign for suspecting vesicoureteral reflux and performing a micturitional ureterocystography is the cyclic dilatation of the pelvis during the ultrasonographic study.[26]
In all cases with dilated pelvis, micturitional ureterocystography should be performed. If the dilatation is severe or moderate, antibiotic prophylaxis should be used to try to avoid urinary infection. In the neonatal period, preferred antibiotics and chemotherapy are cephalexin (2-3 mg/kg/day). Nitrofurantoin (1-2 mg/kg/day) is used after the first month of life, and trimethropin-sulphamethoxazole (sulphaprim at 1-2 mg/kg/day of trimethoprim) after two months of age.[27] In case vesicoureteral reflux is detected, the conduct advocated for this condition shall be followed[28] and congenital or prenatal kidney damage must be ruled out by static gammagraphy.
If vesicoureteral reflux is not found and hydronephrosis is of grade 1 or 2, renal ultrasound follow-up shall be carried out every 6 months. If hydronephrosis progresses, the conduct proposed for higher degrees will be followed. In hydronephrosis of grades 3 and 4, dynamic gammagraphic studies (MAG 3 + furosemide) should be performed. If a non-obstructive renographic pattern appears, ultrasound will be performed every 6 months, carefully measuring the pelvis, calyxes and the renal parenchyma. If the result of the gammagraphic pattern is uncertain, it will be repeated after 3 months, and if the pattern is obstructive it should be repeated after 4 or 6 weeks. In any of these two situations (obstructive or uncertain pattern), if the differential kidney function decreases, especially more than 10% (40% or less) and the pelvic diameter or the calyx dilatation in the ultrasound increase, surgery must be considered (pyeloplasty).
ANALYSIS OF MANAGEMENT PROPOSED
Micturitional ureterocystography should be performed on every newborn in which prenatal renal pelvic dilatation is detected and confirmed after birth, even if the dilatation is mild. This is due to the frequency of renal pelvic dilatations secondary to vesicoureteral reflux.[15] Also because there is no correlation between the degree of dilatation detected by ultrasound and the degree of vesicoureteral reflux.[29] This general indication is more specifically for male infants, since it has been demonstrated that vesicoureteral reflux is up to six times more frequent in males than in females.[30] It is even more necessary in male infants with bilateral dilatation due to the possibility of valve obstruction of the posterior urethra.[31]
In practice, the presence of vesicoureteral reflux determines the need for and duration of antibiotic prophylaxis[21] that we use in severe and moderate dilatations, and should be used in those cases classified as mild, if they are secondary to vesicoureteral reflux. If vesicoureteral reflux is detected, a static gammagraphic study should be carried out because of the possibility of congenital renal damage.[29,30,33]
In every child with grade 3 or 4 hydronephrosis, a dynamic gammagraphic study should also be carried out to provide information on the differential renal function and the clearance rate of the renal pelvis. For this study, two substances shall mainly be used: mercaptoacethylglicine (MAG 3) and dimethyltriaminopentacetic acid (DTPA) both labeled with 99m technetium (99m Tc-MAG 3 and 99m Tc-DTPA).
Ninety percent of MAG 3 combines with plasma proteins and is mainly excreted by tubular secretion with an alternative hepatobiliary excretion pathway. DTPA scarcely combines with plasma proteins and is excreted by glomerular filtration, so it should not be used when there is an immature kidney. Due to these characteristics MAG 3 is better for this study,[32] especially in nursing babies.
Furosemide is used for the diuretic gammagraphy, since it produces an abrupt increase in urine flow, reaching a maximum effect between 15 and 18 minutes after intravenous administration. The dose recommended for this purpose is 1 mg/kg of body weight in nursing babies, 0.5 mg/kg between 1 and 16 years of age and 40 mg as the maximum dose.[32]
Surgical recommendations have been controversial and they remain unchanged for asymptomatic patients.[34] The decision becomes difficult in some cases.
Eighty-five percent of the children with a prenatal diagnosis of hydronephrosis do not have a real obstruction and so they do not require surgery and will improve spontaneously. But the true ureteropelvic obstruction should be operated on as soon as possible to avoid kidney damage. The difficulty of the decision can be minimized with a very strict protocol.[35] The degree and severity of prenatal hydronephrosis is determined after birth by evaluating the general condition of the child, the degree of dilatation by echography, and the radioisotope excretion curve after administering furosemide. Dilatation alone does not imply obstruction. However, if all the remaining parameters indicate the presence of obstruction, early surgical treatment is recommended.[36] Surgical criteria used by the Society for Fetal Urology are concurrence of the increase of the hydronephrosis and a worsening of the radioisotopic clearance of over 10% between studies.[37] Obstruction has been defined as such a state of urinary drainage that if not corrected, it will limit the final functional potential of the developing kidney.[38] Early repair is recommended if obstruction is demonstrated,[39] because the delay in alleviating the obstruction may allow rupture of the basal tubular membrane and promote the transition of the epithelium to myofibroblasts, a process that is probably irreversible.[39,40] Surveillance and control of the patient before a decision is made must be very strict in some cases.
Based on different criteria found in the literature and on the clinical evolution of our patients, we think that surgery (pyeloplasty) is indicated if the renographic pattern is obstructive or uncertain, the relative function falls below 40% or hydronephrotic dilatation increases in follow-up ultrasound studies. The obstructive cases that do not receive the benefits of timely pyeloplasty may progress to a renal function deterioration, which may become irreversible, requiring the substitution of reconstructive surgery (pyeloplasty) by mutilating surgery (nephrectomy).
Whichever the treatment used (expectant or reconstructive), hydronephrosis must be followed-up for years to evaluate the growth and functioning of the kidneys. Another important element is the control of arterial hypertension.[22] In surgically treated cases, non-steroid anti-inflammatory drugs should not be administered, and if hypertension or significant proteinuria appear, they must be treated resolutely.[39]
REFERENCES
1.   Resnik, VM, Budorick, NE. "Prenatal Diagnosis of Congenital Renal Disease." Urol Clin North Amer 1995, 22:21-30.
2.   Peters, CA. "Perinatal Urology." In: Campbell's Urology . Wahls; Retik; Vaughan; Wein (Eds) 8 th Edition, Volume III, Chapter 51 Philadelphia: Saunders, 2003 (electronic version).
3.   Peters, CA. "Obstruction of the Urinary Tract." J Amer Soc Nephrol 1997, 8:653-663.
4.   Diamond, DA, Peters CA,: "Perinatal Urology." In: Pediatric Nephrology . Barratt, TM; Avner, ED; Harmon, WE, (Eds), 4 th Edition, 897-912 Baltimore: Lippincott, Williams and Wilkins, 1999.
5.   Helin, I; Persson, PH. "Prenatal Diagnosis of Urinary Abnormalities by Ultrasound." Pediatrics 1986, 78:879-883.
6.   Durán Álvarez, S., Jústiz Hernández, L., Álvarez Díaz, S., Vázquez Ríos, B., Betancourt González, U., Calviac Mendoza, R. "Diagnóstico Prenatal de Hidronefrosis Detectadas por Ultrasonido Materno-Fetal." Rev Esp Pediatr 2003, 59:146-150.
7.   Durán Álvarez, S., Betancourt González, U; Hernández Hernández, JS; Campañá Cobas, NG; González Pérez, O. "Diagnósticos Postnatales de Anomalías del Tracto Urinario Detectadas por Ultrasonido Materno-Fetal." Rev Cub Pediatr Oct-Dec, 2004, 76(4); http//bus.sld.cu/revistas/indice.htm/.
8.   Avni, EF; Ayadi, K., Rypens, F., Hall, M., Schulman, CC. "Can Careful Examinations of the Urinary Tract Exclude Vesicoureteral Reflux in the Neonate?" Br J Radiol 1997, 70:977-982.
9.   Fernbach, SK; Maizels, M., Conway, JJ. "Ultrasound Grading of Hydronephrosis: Introduction to the System Used by the Society for Fetal Urology." Pediatr Radiol 1993, 23:478-480.
10.   Rickwood, AMK; Harney, JV; Jones, MO; Oak, S. ""Congenital" Hydronephrosis: Limitations of Diagnosis by Fetal Ultrasonography." Brit J Urol 1995, 75:529-530.
11.   Blachar, A., Blachar, Y." Congenital Hydronephrosis: Evaluation, Follow-up and Clinical Outcome." In: Pediatric Nephrology . Dukker, A., Gruskin, AB (Eds) Vol 5, 141-153 Basel: Pediatr Adolesc Med, 1994.
12.   Blachar, A., Blachar, Y., Levine, PM, Surkouski, L., Pelet, D., Mogilner B. "Clinical Outcome and Follow-up of Prenatal Hydronephrosis" Pediatr Nephrol 1994, 8: 30-35.
13.   Eraña Guerra, LH, Gordillo Paniagua, G. "Uropatía Obstructiva." In: Nefrología Pediátrica. Gordillo Paniagua, G (Ed), 139-147 Spain: Mosby-Doyma Libros, 1995.
14.   Park, JM, Bloom, DA. "The Pathophysiology of UPJ Obstruction: Current Concepts." Urol Clin North Amer 1998, 25:161-169.
15.   Durán Álvarez, S., Jústiz Hernández, L., Álvarez Díaz, S., Vázquez Ríos, B., Rivas Cristo, I. "Hidronefrosis Prenatal Secundaria a Reflujo Vesicoureteral." Rev Cub Pediatr Jul-Sept, 2003, 75 (3); http//bus.sld.cu./revistas/indice/htm/.
16.   Barker, AP; Cave, MM; Thomas, DFM; Lilford, RJ; Irving, HC; Arthur, RJ; et al. "Fetal PUJ Obstruction: Predictors of Outcome." Pediatr Nephrol 1994, 8(5):C12 (Abstract).
17.   Ismaili, K., Avni, FE, Guissar, DG, Gassart, M., Massez, A., Vermeylen, D. "Systematic Cystourethrography in Antenatally Diagnosed Renal Pelvis Dilatation." Pediatr Nephrol 2001, 18 (:084, p28 (Abstract).
18.   Siemmens, D., Prouse, K., MacNiely, A. "Antenatal Hydronephrosis: Thresholds of Renal Pelvic Diameter to Predict Insignificant Postnatal Pelviectasis." Tech Urol 1998, 4:198-201.
19.   Gómez Fraile, A. "Hidronefrosis en la Infancia: Estado Actual." Rev Esp Pediatr 1999, 55:86-90.
20.   Kletsher, B., de Badiola, FIP, González, R. "Outcome of Prenatally Diagnosed Hydronephrosis." J Pediatr Surg 1991, 26:455 (Cited in 20).
21.   González, R, Schimke, CM; "Ureteropelvic Junction Obstruction in Infants and Children." Pediatr Clin North Amer 2001, 48:1505-1518.
22.   Cornell University. "Prenatal Hydronephrosis." 2001; http://www.Cornell/pediatric/prenatal/shtm/ .
23.   Marra, G., Secco, G., Melzi, ML, Guez, S., Tadini, B., Barbieri, G, et al. "Clinical Outcome of Mild Hydronephrosis: A Follow-up Study in 79 Cases." Pediatr Nephrol 1996, 10:C143, p79 (Abstract).
24.   Fenton, THM, McGraw, ME, Haworth, JH, Smith, P., Tizard, EJ; "Outcome of Antenatal Hydronephrosis." Pediatr Nephrol 1993, 7:C44, p79 (Abstract).
25.   Dönmez, O., Nemesa, A., Köksal, N., Balkan, E., Alper, E., Kimya, Y. "Clinical Outcome of the Newborns with Prenatal Renal Pelvic Dilatation." Pediatr Nephrol 2001, 16 (:C65, p32 (Abstract).
26.   Nakamura, M., Itoh, IK. "Wax-and-Wane Hydronephrosis: Sonographic Finding in Vesicoureteral Reflux." J Clin Ultrasound 1997, 25:27-28.
27.   Chon, CH, Lai, FC, Shortliffe, LMD. "Pediatric Urinary Tract Infections." Pediatr Clin North Amer 2001, 48:1441-1460.
28.   Durán Álvarez, S. "Reflujo Vesicoureteral: Conceptos Actuales." Rev Cub Pediatr 2000; 72:132-143.
29.   Jaswon, MS, Dibble, L., Puri, S., Davis, J., Young, J., Dave, R, et al. "Prospective Study Outcome in Antenatally Diagnosed Renal Pelvis Dilatation." Arch Dis Child Fetal Neonatol Ed, 1999; 80: F135-F138.
30.   Marra, G., Barbieri, G., Dell'Agnola, CA, Caccamo, M., Castellani, A., Assael, BM. "Congenital Renal Damage Associated with Primary Vesicoureteral Reflux Detected Prenatally in Male Infants." J Pediatr 1994, 124:726-730.
31.   Abbott, JF, Levine, D., Wapner, R. "Posterior Urethral Valves: Inaccuracy of Prenatal Diagnosis." Fetal Diagn Thr 1998, 13:179-183.
32.   Alconcher. L., Tombesi, M. "Primary Vesicoureteral Reflux Detected Prenatally and Congenital Renal Damage Associated." Pediatr Nephrol 2000, 16 (:C102, p177 (Abstract).
33.   Roarke, MC, Sandler, CM. "Provocative Imaging Diuretic Renography." Urol Clin North Amer 1998, 23:227-249.
34.   Zhang, PL, Peters, CA, Rosen, S. "Ureteropelvic Junction Obstruction: Morphological and Clinical Studies." Pediatr Nephrol 2000, 14:820-826.
35.   Koff, SA. "Diagnóstico Prenatal de la Hidronefrosis ¿Cuándo y por qué no Operar?" Arch Esp Urol 1998, 51:569-574.
36.   González, R., Schimke, CM. "Diagnóstico Prenatal de la Hidronefrosis ¿Cuándo y por qué Operar?" Arch Esp Urol 1998, 51: 575-579.
37.   Palmer, LS, Maizels, M., Cartwright, PC, Fernbach, SK, Conway, JJ. "Surgery versus Observation for Imaging in Obstructive Grade 3 to 4 Unilateral Hydronephrosis: A Report from the Society for Fetal Urology." J Urol 1998, 159:222-228.
38.   Peters, CA. "Urinary Tract Obstruction in Children." J Urol 1995, 154:1874-1883.
39.   Chevalier, RL. "Nefropatía Obstructiva Congénita." Arch Latino Nefr Ped 2003, 3: 66-72.
40.   Yang, JW, Shultz, RW, Mars, WM, Wegner, RE, Li, YJ, Dai, CS, et al. "Disruption of Tissue-Type Plasminogen Activator Gene in Mice Reduces Renal Interstitial Fibrosis in Obstructive Nephropathy." J Clin Invest 2002, 110:1525-1538.

и още нещо във връзка с меките маркери на Даун (един от който е пиелектазията):

Ultrasonographic "soft markers" of fetal chromosomal defects
Detecting them may do more harm than good
Most women in Britain have at least one ultrasound scan during their pregnancy. Aside from confirming viability and establishing gestational age, ultrasound may also indicate the possibility of an abnormality. An obvious structural problem, such as anencephaly, will have predictable consequences that can be discussed with the patient with some confidence. Less straightforward is the case in which a scan identifies a so called "soft marker"–a minor, usually transient, structural change which may indicate a risk of serious fetal anomaly but which in itself is probably inconsequential.
Ultrasound imaging has improved vastly in quality, and for this reason, and because first trimester scans are now performed more often, the frequency with which "markers" are observed has risen correspondingly. Some markers may well have disappeared by the time of the "routine" scan at 18-20 weeks.
Of those markers indicating pathology, most are associated with an abnormal karyotype. The presence of two or more markers makes this much more likely, although some markers, such as nuchal translucency, have a significant association with chromosomal anomalies even when they occur alone.
Measurement of nuchal translucency has now been refined to the point where risk can be calculated with some precision.1 When the test is performed between 10 and 14 weeks, one study suggests that about 6% of low risk and 16% of high risk women will be positive and merit further investigation by invasive prenatal diagnosis.2 The sensitivity for aneuploidy is about 85%.2 However, about half of those with a chromosomal disorder are likely to undergo spontaneous abortion,3 which throws uncertainty over the precise value of the test. It may be less appropriate for widespread clinical use than was first anticipated, and certainly, other groups have found nuchal translucency screening to be less effective.4
Choroid plexus cysts have also caused controversy. Found in about 1% of fetuses examined before 20 weeks, these structures may, when found in isolation, indicate an overall risk of trisomy of about 1 in 150.5 But their most common association is with trisomy 18, which is almost universally fatal. The residual risk of Down's syndrome is therefore about 1 in 880, so the need for confirmation by invasive prenatal testing cannot be an automatic assumption; maternal age, together with the presence of other risk factors, must be taken into account.
Another marker, minor dilatation of the fetal renal pelvis (pyelectasia), has a background incidence of about 1% and was originally thought to be fairly strongly associated with Down's syndrome.6 Although this association holds when pyelectasia is found with other markers,7 the risk in isolation may be small. However, identification of this marker may confer other long term advantages, since its presence may indicate a baby at subsequent risk of urinary tract abnormalities.8
Ultrasonically echoreflective bowel (bright gut), short femurs, clinodactyly of the fifth digit, and oddly shaped heads have all been identified as soft markers associated with an increased risk of trisomy. The risk associated with any one of these may be little greater than that conferred by maternal age, but if other markers are also present the likelihood of a karyotypic problem rises dramatically.
The problem with soft markers is that, even when karyotypic abnormalities are excluded, the mother and her obstetrician will remain in doubt as to their significance–a cause of considerable anxiety.
Information about ultrasonographic markers is relatively new. Many of the background data come from referral units and are therefore biased. These markers promise to be useful in screening for chromosomal abnormalities when considered alongside maternal age. But such screening may not be feasible when searching for soft markers requires more time and probably better equipment and training than a standard scan; and it may not be ethically acceptable when identifying these markers increases anxiety, usually unnecessarily and often without prior counselling.
The role of ultrasonographic soft markers and their relation to serum screening is therefore unclear. If markers are to form part of the routine ultrasound examination three criteria must be fulfilled: the complexity of diagnosis must be matched by technical skills and equipment; the counselling offered must be detailed and of high quality; and the costs must be justified by the benefits to women.

Момичета новините от нас днес са добри!
Разширените бъбречни легенчета вече са в норма, според днешната ФМ!
Слава на Бог!

Явно наистина с напредване на технологията и квалифицирането на докторите, дилатациите на бъбречните легенчета се оказват честа находка до 27-28 г.с., която в повечето случаи се израства вътреутробно. Въпреки това пожелавам на всички да не се минават и през това изпитание.

Пожелавам всяко бебе да се пребори и да се роди живо и здраво!
Поздрави и успех!

чудесна новина, evro! дано същото да ни докладват скоро и останалите момичета!

Това е чудесна новина Евро, аз бях при Марков на ФМ в 24 седмица и той каза, че всичко е в норма и при нас.Дай боже наистина да е така .Успокоявам , се че вече и околоплодните ми води се нормализираха 

За следящите по темата: днес при прегледа на Мария легенчетата са с гранична ширина - 4 мм, нормална за двумесечни бебета. Благодаря на Бог!
Препоръката е контрола при навършване на една годинка.
Късмет на всички!

Продължавам да споделям горчивя ни опит, въпреки че развитието при нас не е за този подфорум, но се надявам да е обица на ухото за тези с установени вътеутробни аномалии.
Преди 15-тина дни за 3 дни вдигна 37.7-8, седмица след това нищо и след това вдигна до ~40, приеха ни в Детска клиника във ВМИ в Пд, CRP - 162, левкоцити 27, СУЕ - 35, урокултура - стерилна, в урината 25-30 левкоцита и следи от белтък, включиха ни амикацин и роцефин, УЗИ - десен бъбрек първа степен задръжка, уретри не се визуализират, след 3-4 дни излезе копрокултурата (от акито) - Е. коли 0/25 (така пише). Последва настаняване в инфекциозна и смяна на АБ на миронем (колито бе мн. резистентно) и така 7 дни, няколко урокултури - стерилни, копрокултури - стерилни, утайката 15, левкоцити 4.4, CRP - 16, консултира ни Проф. Бойкинов - евентуален пиелонефрит и цистография за отхвърляне на релукс.
Пием много вода (чай) ~300 мл. на 24 часа, но ми се струва че пампитата не преливат в сръвнение с връстниците ни, които не пият и 100 мл вода (сменям 7-8 бр). Нямахме апетит по болниците, сега се връщаме към нормалните дози за възрастта и, избрах късното захранване и сега съм много деликатна във въвеждането на храни.

Сега сме 15 дни на бисиптол и следват снимките. Със изследванията се грабваме и идваме в Сф.

Та извода ми е:
1. Джи-питата стават само за мерки и теглилки, дори ваксините ги бият сестире им!
2. Нормална температура - НЯМА! При установени проблеми е престъпление да не се пусне една ПКК и урина.
3. След раждането на дете с подобни аномалии е необходим преглед при съответен специалист на всеки 1-2 месеца.

Толкова съжалявам че не послушах приятелките си за нуждата от клиничен лекар, който да следи дъщеря ни!

Моля те Господи, пази рожбите ни живи и здрави!