 Good evening. So, in the fetal urinary system part 1, we will include venal anomalies while in part 2 we will include the bladder, adrenal and the other anomalies. So, traditionally the screening for the congenital anomalies of the kidney and the urinary tract called as Cacute is done at our routine anomalies scan between 19 to 21 weeks. We should remember that these anomalies are the evolving anomalies and that the in the later gestation the detection rate is quite higher that means in the second and the third trimester the anomalies are quite evident. But with the inversion of the pyramid of the fetal care, we need to evaluate the GUT in the first trimester also though we must remember that the detection rate of the Cacute is lowest in the first trimester. The ISUT guidelines say that in the first trimester the evaluation of the bladder and the kidneys is optional while second trimester onwards we should see for the kidneys as well as the bladder. The kidneys are evaluated in the axial parasitic plane and the coronal plane. In the axial view we take the renal pelvic diameter, in the parasitic view the renal length is measured, the kidney length is measured from the upper to the lower prole and then there are different nomograms available regarding the length and the weeks of gestation and in the coronal view basically we evaluate the renal arteries and there is a ratio between the renal circumference to the abdominal circumference which is 0.27 to 0.03 which is constant throughout the pregnancy. Now how do the kidneys look on ultrasound? In the first trimester with the high resolution TA or the TBS the kidneys are seen as rounded structures which are bright, there is an anechoic center which is nothing but the renal pelvis and the optimal visualization in the first trimester is basically in the coronal plane. Well in the second and the third trimester we see the typical oval shape of the kidneys and the ectogenicity of the kidneys then decreases and it is less than the liver and that of the spleen. The cortico-modulary differentiation is seen better in the late second trimester and the third trimester and how do we identify the cortex and the medulla that the outer hyperechoic is the renal cortex while the hypoechoic center is the renal medulla. The urinary bladder is seen from the 10-week onwards. It is seen as a rounded and anechoic structure with ecogenic walls and in the first trimester the longitudinal length of the bladder should be less than 7 millimeters then the ball thickness should be less than 2 millimeters. Bladder is identified by the peri-bicycle arteries on the color Doppler. When we begin our ultrasound scan in the first trimester first thing we should do is to assess the bladder because if we don't see the bladder we get at least some time to assess the bladder without visualizing the bladder in the first trimester the anti-scan is not complete. The urethra and the urecra is not visible prenatally unless they are deceased. Sonographically the caciot may present as urinary tract dilatation, pathologies of the location and number, ulter-trenal ecogenicity, bladder pathology and all of this affecting the amniotic fluid. So, how will we proceed when we see a case of hydronephrosis? So, we should follow this algorithm. When we see hydronephrosis first see if the urethras are dilated or not. If the urethras are not dilated then it is probably a PUG obstruction. If the urethras are dilated look for the bladder. How is the bladder? If the bladder is not dilated, if the bladder is normal it could be PUG obstruction or it can be unilaterally UV reflux and if the bladder is dilated see the severity of the bladder. If the bladder is severely dilated then it can be posterior urethral valve or urethral atresia while if the bladder is moderated dilated it can be bilateral UV reflux. Grading of hydronephrosis. Why should we grade the hydronephrosis? We should grade it because it is an important prognostic sonographic finding. Accordingly we can plan and it will follow up to see if the pathology is worsening or regressing and then it also help us for the proper counseling of the parents. Also, grading is important for planning antinatal and the post-natal therapies. Hydronephrosis used to be grade subjectively into mild, moderate and severe but subjective evaluation is always confusing. Hence, anterior posterior renal pelvic diameter measurement is used to grade the hydronephrosis. The RPT is measured in the transverse of the axial section where the spine can be at 12 o'clock or 6 o'clock position and the anterior posterior diameter of the intra-renal part of the pelvis is measured. And the RPD of more than or equal to 4 millimeters before 32 weeks and more than or equal to 7 millimeters from 32 weeks onwards is considered as pathological. And when the RPD is between 4 to 10 millimeters it is mild hydronephrosis, 10.25 is moderate hydronephrosis and more than 15 is severe hydronephrosis. But the grading of hydronephrosis depending on RPD doesn't tell anything about the renal parenchyma or the calyxial dilatation. So for that, the Society of Fetal Urology proposed a grading system where along with the dilation of the renal pelvis, calyxial dilation and the parenchyma thinning were also included. So there are five grades from zero to four depending on the splitting of the pelvis dilation of the calyxes and then the parenchyma thinning. And then there is one more ONIONS classification which is quite similar to the SFU grading system. There are high chances of subjective error and in these classification systems a lot of confusion is created and therefore there is variability in the post-tetal management. So in 2014 there came consensus on the classification of the prenatal and post-natal urinary tract dilatation called the UTD classification system. The UTD affects nearly 1 to 5% of all pregnancies and a lot of confusing terminologies like hydronephrosis, pilectasis, pelvic calyctasis and et cetera are used. So the consensus opinion is that instead of using confusing terminologies a common terminology is proposed and that is the urinary tract dilation. According to this classification the parenchyma thinning are divided into the low and the high risk group. And important thing is that the UTD classification system is endorsed by the Society of Fatal Fetal Medicine, the AIUM, ACR and also the SFU. So what are the ultrasound parameters used in this UTD classification system? The anterior posterior renal pelvic diameter is one of the important factors. Also we evaluate the central and the peripheral calyctal dilatation. Then the parenchyma thickness is evaluated which is the subjective assessment. Then the parenchyma appearance we need to evaluate where we see the ecogenicity, the cortico-modular differentiation and the presence or absence of any cortical cyst. Then ureters are also evaluated and we see for the dilatation of the ureter. The transiently dilated ureters are visualized then they are considered to be normal. Then we evaluate here the bladder where we evaluate the bladder wall thickness the presence or absence of ureterosy and we see even for the posterior urethral wall. The RPD cut-offs used are the same that means if it is less than four millimeters it is normal. The RPD cut-offs are the same that means four and seven millimeters but the weeks of the gestations are changed here. That means between 16 to up to 28 weeks if the RPD if it is less than four millimeters then it is normal and it should be less than seven millimeters after 28 weeks to call it as normal. And then the cholesterol dilatation the parent camel thickness all these appearances should be normal. So according to the UTD classification system there are two groups UTD A1 which is a low risk group and UTD A2 and 3 which are the high risk group. So when the RPD is between four to 6.9 millimeters between 16 to 27 weeks and when it is between seven to 9.9 millimeters after 28 weeks with central or no cholesterol dilation then it is UTD A1 or a low risk group. And when the RPD is more than seven millimeters between 16 to 27 weeks and after 28 weeks when the RPD is more than 10 millimeters and there is associated any one of this finding like peripheral cholesterol dilatation or abnormal parent camel thickness or abnormal appearance of the parent camel or abnormal urator. Any of this when it is present then it is UTD A2 dash 3 means it is a increased risk group or a high risk group. And the follow up protocol is also suggested by the UTD classification system where in the low risk group one additional follow up is required after or at 32 weeks of gestation and here we can very well reassure the parents that the chances of the disease in progression will be less. And in the high risk group we need to follow up every four to six weeks and postnatally the ultrasound should be done after 48 hours of the delivery. And we have to have a detailed discussion with the parents regarding the progression of the disease and whenever required we need to take the help of the geneticist or the specialist consultation who will do the postnatal management is also important in the high risk group. There is diverse etiology for the UTD. In majority of the cases it is transient. Majority of the mild hydronephrosis are transient or physiological and this could be because of the insufficient maturation of the pelvic retic or the vesicle retic junction or due to uretic folds or due to overproduction of the urine. Next common is the pelvic retic junction obstruction and then with the decreasing rate of incidence it is VU reflux and then the uretrovasicle junction obstruction deplex collecting system, multi-cystic dysplastic kidney and the LUTO. The studies regarding the prognosis of the hydronephrosis were done before the UTD classifying system and they were done depending based on the RPDs. When the RP dilatation is mild that is less than seven millimeters only 10 to 15% progress to the postnatal disease. Whereas when the RP dilatation is severe that is more than 10 millimeters then nearly 90% of the patient will require postnatal therapy. The other prognostic factors will include if it's a bilateral or bilateral involvement, parenchymal ecogenicity, presence or absence of cortical cysts, oligo-hydrimonious and associated malformation and markers of aneuploidy. So let's see how to report the case of UTD. So first you have to mention about the renal pelvic diameters. Then you have to see for the callusial status to see if the major calluses and the minor calluses are dilated. Then look at the parenchymal thickness and the parenchymal ecogenicity. Here the parenchymal thickness is slightly reduced while the parenchymal ecogenicity is highly ecogenic parenchymal. Look for the urators. Here in this case you can see a dilated urator. Then you have to mention about the bladder. The bladder size here is apparently normal. It is not too much dilated bladder. And then we also need to report about the bladder outlet and the plicar status. And if in any case you see that there is only dilated renal pelvis, other things are normal. Then your report should include the RPD diameters. And then you have to write that the renal parenchyma, the calluses, the urator, bladder, everything is normal. This will be the complete reporting according to the UTD classification system. Now the second set is the abnormalities in the number and allocation of the kidneys which will include unilateral urgenesis, bilateral renal urgenesis, ectopic kidney and the fusion anomalies. The sonographic finding in the renal urgenesis is that we will see an empty renal fossa. We will see a lined on or a sleeping adrenal sign which is a elongated adrenal in the renal fossa. Because the other kidney is seen and is normal, the AFI can be normal. But we should also look in this case for the anomalies of the visualizer, the present kidney. Because renal urgenesis is associated with factor anomalies, we need to evaluate the vertebral spinal, the cardiac, the GI system very thoroughly. Bilateral renal urgenesis is again a lethal condition and associated cardiac, cerebral and skeletal anomalies and is quite common. On ultrasound, we see early anhydromanias which is seen from 16 weeks onwards. The bladder is not seen, the renal fossa are empty, there are bilateral sleeping adrenal sign and on color Doppler, we see the absent renal arteries. Emerilologically, kidneys are formed in the pelvis and they ascend to the normal position. Failure to ascend leads to the ectopic kidney. Pelvic location is quite common where we can see the kidneys very close to the bladder. Orchid kidney and cross fused ectopic kidneys are the type of fusion anomalies which can be detected antinatally. Now coming to the echogenic kidneys, when kidneys are more echogenic than liver and spleen after 17 weeks, then they are called as the echogenic kidneys. The common non hereditary causes are obstructive dysplasia and multi-cystic kidney disease. The rare causes are like nephroblastomatosis, renal ven thrombosis, ischemia, aneuploidies and the infections. The common hereditary causes include the heterosomal recessive and the dominant type of the polycystic kidney disease. And then, echogenic kidneys are a part of certain syndromes. Now how to evaluate a case of hyperequipped kidneys? First and foremost, we should see for the volume or the size of the kidney. The kidneys can be small as in cases of obstructive renal dysplasia or they can be increased in the volume because of macrosis or microsis. Macrosis are commonly seen with multi-cystic kidneys. Microcystic pattern is seen with polycystic kidney and can be associated with other anomalous and syndrome. Hyperequic kidneys with a normal volume is a real troublesome issue because it can be a variant of normal. We must thoroughly scan the fetus before labeling it as a normal variant. In report, we should mention about the normalcy of the bladder and the lycra. And then also we should ask for any family history of the renal disease or any previous child having renal disease. And then we should suggest a follow-up when suspected cases of normal variation of the hyperequic kidneys. Now, the autosomal recessive polycystic kidney disease or the ARPKD, it is caused because of the monogenic mutation in the PKHD1 gene. There is fusiform cystic dilation of the collecting duct to begin with the medulla becomes ecogenic and then the tubular strands reach up to the cortex and then the whole of the cortex becomes ecogenic and the cortico-medulla junction is lost and whole of the kidney looks ecogenic. But an ultrasound, we can have normal kidneys up to 20 weeks of gestation. Later, the size of the kidney can increase. And it can increase up to plus one, two, plus five of the standard deviation. As I told, the kidneys are hyperequic with loss of CM differentiation. Because the nephrons are now non-functioning, the urine is not produced and the bladder is not visualized. And because urine is not produced, there is severe oligohydraminous and it is a lethal condition mainly because of the pulmonary hypoplasia caused because of oligohydraminous. While the atosomal dominant polycystic kidney disease is characterized by multiple cysts that arise mainly from all the areas of the nephron and very few from the collecting ducts. These are tiny cysts and as we know that the nephrons are in the cortex, these tiny cysts in the nephron will first cause increase in the cortical ecogenicity. And therefore the hyperequic cortex and the hyperequic medulla is the commonst sonographic finding in ADPKD. In few cases, we can get cortical cysts also while ecogenic medulla with loss of CM differentiation, the typical lack of that of ARPKD is very less common. And when it is seen, the differentiation between the ARPKD and the ADPKD becomes very difficult. As this tiny cyst will not compromise the urine production in this early stage, we can see the renal pelvis and the bladder. And therefore the AF act is normal. And now the multi cystic kidney dysplasia. For the formation of the nephrons, there should be stimulus from the uretric bud. The uretric bud is not formed, then the metanephric vesicles will convert into multiple cysts of various sizes. And this is nothing but the multi cystic kidney dysplasia. This is usually a unilateral condition. And an ultrasound, we get increased volume of the kidney. There are multiple non-communicating cyst of variable sizes. And because of the cyst, the outline is irregular. And because of the cyst also, there is absence in the central sinus structures that is no parankarma only connective tissue is seen. In 25 to 40% of cases, the contralateral kidney can be also abnormal. And the abnormal abnormality is the reflux because the origin is basically from the uretric bud. The pathology originates in the abnormal uretric bud. And therefore the reflux is quite common in the contralateral kidney. Bilateral MCKD is quite rare. And because in this condition, as it will not be produced, there will be severe oligohydrium in us and it will be a lethal condition. Obstructive cystic dysplasia is caused because of a very early and a severe obstruction of the eugenic tract. It can be unilateral or bilateral. Bilateral involvement is common with the lower eugenic tract obstruction. We may be able to find the cause of obstruction. Actually the cortex is hyper-equic. And at times we can see the pericarticle cysts. Penal function is impaired in the obstructive cystic dysplastic kidney. For the 13-mix, you can see a hydronephalotic kidney which is enlarged and having an eugenic cortex. The other kidney is showing just a pelvic-oluscial fullness. The affected kidney at 19-mix is now showing the pericarticle cyst while the other kidney is showing a mildly dilated renal pelvis. And then this is a case of mechal grubber syndrome where the hyper-equic kidney is associated with occipital NK fallacy and polydactyly, which is seen in both upper and lower extremities. The incidence of renal tumor is extremely rare. Usually they are diagnosed in the third trimester. It's usually a unilateral renal involvement. The kidneys partly or totally replaced by mass show increased vascularity and may or may not have the capsule. Wilms tumor have association with beckwith fitment and other syndromes and then we have to look for the features of other syndromes on the ultrasound. Conclusion of part one is that GOT evaluation begins from the first trimester. Cacut are evolving anomalies. Description of the renal pelvis, calluses, parenchymal characteristics, ubrators and bladder is must in a case of urinary tract dilation. Ultrason findings can prognosticate the renal outcome. Follow the algorithms which will help us to reach the diagnosis. Thank you very much.