Developmental and Positional Anomalies of the Kidneys Flashcards
What is the clinical significance of renal anomalies?
Anomalies of renal formation and position result in interesting radiographs, but their clinical importance lies in their associated conditions.
For example, the multicystic dysplastic kidney (MCDK) often involutes, yet the initial evaluation needs to determine if the contralateral kidney is at risk for vesicoureteral reflux (VUR) or ureteropelvic junction (UPJ) obstruction.
Although no therapy is needed for unilateral renal agenesis, the link between a solitary kidney and the VACTERL (vertebral, anal, cardiac, tracheoesophageal fistula, renal, limb) and Mayer–Rokitansky (vaginal agenesis) syndromes is the main reason for further evaluation.
Hydronephrosis is often seen in abnormalities of position and rotation, but does not necessarily mean that obstruction is present.
Therefore, anomalies of renal formation and position often pose more of a diagnostic problem than a surgical one.
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How does the kidney develop?
The pronephros, which has no adult function, induces the mesonephros to differentiate into the mesonephric duct during the fourth to eighth week of fetal life.
The mesonephric duct is the basis of the Wolffian system, which develops into the seminal vesicles, vas deferens, epididymis, and efferent ductules of the testis in boys, and the epoophoron and paraophoron (vestigial remnants between the fallopian tube and ovary) in girls.
Between weeks 9 and 12, the ureteric bud branches off the mesonephric duct, contacts the metanephric blastema bud, and induces the development of the entire collecting system of ureter, renal pelvis, calyx, and collecting tubules.
The kidney develops via induction of the metanephric blastema by the ureteric bud into Bowman’s capsule, the convoluted tubules, and the loop of Henle.
The kidneys begin at the upper sacral level, with the renal pelvis facing anteriorly. The kidneys ascend either because the lumbar and sacral regions grow faster than the cervical and thoracic regions between 4 and 8 weeks, or because there is active migration.
As the kidneys ascend, the renal pelvis rotates medially by 90°, leading to the normal configuration of the renal pelvis lying medial to the parenchyma.
During this time, the blood supply shifts from inferior branches of the aorta to more cephalad branches, with the final renal artery being located at about L2. Failure of normal ascent leads to the persistence of a low-lying blood supply.
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What is the difference between renal dysplasia and hypoplasia?
As the development of the kidney depends on proper interaction between the ureteric bud and the metanephric blastema, it should not be surprising that an abnormality in the location of the ureteral orifice is associated with abnormally induced renal tissue.
Examination of the thickness of the renal parenchyma and number of glomeruli associated with normal and ectopic ureters in fetal specimens suggests that it is the initial interaction between bud and blastema, rather than subsequent obstruction or VUR, that determines whether normal renal tissue will develop. A ureter that arises in the proper trigonal location is associated with normal renal parenchyma, whereas a ureter arising from a more cranial location or caudal location is associated with progressively less normal renal parenchyma.
Renal dysplasia and hypoplasia can be considered errors in renal induction.
Although dysplasia is technically a histologic term, it refers to kidneys that contain primitive tubules either focally or diffusely. These ducts are lined by epithelium and surrounded by swirls of primitive collagen. No treatment is necessary for the dysplastic kidney, but there is an increased risk of reflux in the contralateral kidney.
Hypoplastic kidneys are small but otherwise normal with a decreased number of nephrons. Dysplasia can also occur in hypoplastic kidneys.
While secondary hypoplasia can occur due to infection or obstruction, two types of hypoplastic kidneys are clinically important: the oligomeganephronic type and the AskUpmark kidney.
In oligomeganephronia, there is a decrease in the number of nephrons with an associated hypertrophy of the ones that are present. Patients present with polyuria and failure to concentrate their urine but no hypertension. Imaging with ultrasound (US) reveals small kidneys. Medical management with protein restriction and high fluid and salt intake is initiated. Once the glomerular filtration rate drops significantly, dialysis is required.
The Ask–Upmark kidney was initially felt to be a developmental problem but is now believed to represent reflux nephropathy. The key finding is a small kidney with segmental hypoplasia, probably secondary to ascending pyelonephritis. VUR and hypertension are usually present. Most patients are older than 10 years of age with a 2:1 female:male ratio. If the disease is unilateral, nephrectomy may cure the hypertension. Bilateral disease is managed medically.
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What are associated findings in patients with unilateral renal agenesis?
Absence of a kidney may be due to abnormal induction of the metanephric blastema or involution of a multicystic dysplastic kidney.
The presence or absence of the ureter is helpful in suggesting the cause of the renal agenesis. Absence of a hemitrigone implies that the ureteral bud failed to form properly. A normal trigone, with some evidence of a ureter leading to a nubbin, suggests involution of a multicystic dysplastic kidney.
Unilateral renal agenesis occurs in 1 per 1000 live births, with a 2:1 male predominance.
Unilateral renal agenesis can result in compensatory hypertrophy of the contralateral kidney. The left kidney is more likely to be affected in unilateral renal agenesis.
As unilateral renal agenesis is asymptomatic and eventual renal function is normal, the diagnosis is usually made on prenatal US, or it is incidentally found during imaging for other abdominal symptoms. Sometimes it can be suspected on plain abdominal films if the colon is medially deviated at the splenic or hepatic flexures.
These patients should consider obtaining a medical alert bracelet so that in case of traumatic injury, the solitary kidney is not inadvertently removed.
In a newborn with the prenatal diagnosis of unilateral renal agenesis, physical examination at the time of birth should be focused on detecting the anomalies present in the VACTERL association (Box 53.1).
A voiding cystourethrogram (VCUG) should also be obtained because approximately 30% of VACTERL patients with unilateral renal agenesis will have VUR in the contralateral kidney.
Males with unilateral renal agenesis are at risk for abnormal Wolffian structures. The vas and seminal vesicle may be absent (or the seminal vesicle may be present as a cyst), but the ipsilateral testis will be normal.
As the seminal vesicle develops as a separate bud from the Wolffian duct at 12 weeks, it can be present in cases of unilateral renal agenesis due to regression of a multicystic dysplastic kidney. Seminal vesicle cysts that are causing symptomatic obstruction are usually removed via a transvesical approach.
Conversely, if a vas is found to be abnormal or absent during a hernia repair or orchiopexy, the kidneys should be evaluated postoperatively with US.
Females with unilateral renal agenesis should have their genital anatomy evaluated, as up to 30% will have an abnormality of the Müllerian duct due to the Mayer–Rokitansky syndrome (Müllerian, or uterine, or upper vaginal duplications with or without obstruction, or vaginal agenesis).
The abnormal induction of the mesonephric duct is believed to cause partial or complete nonunion of the paired Müllerian ducts.
Conversely, 40% of patients with abnormalities of the Müllerian organs will have unilateral renal agenesis or ectopia. In patients with duplicated vaginas but with one of the vaginas being absent or atrophic, the side that is absent/atrophic is also the side without a kidney.
If the diagnosis of Mayer–Rokitansky is not made prenatally, the patients can present either as infants with hydrocolpos, or as adolescents with lower abdominal pain after the onset of menses due to an obstructed vagina or uterus (with or without duplication).
Magnetic resonance imaging (MRI) is useful in delineating the pelvic anatomy in these cases.
In vaginal agenesis, the vagina is present only as a shallow pouch. There is a wide variety of abnormalities of the vagina, uterus, and fallopian tubes, but the ovaries are embryologically normal.
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How do infants with bilateral renal agenesis present?
Bilateral renal agenesis occurs once in 4800 live births and has a 3:1 male predominance.
Infants affected with bilateral renal agenesis present with oligohydramnios, pulmonary hypoplasia, and Potter’s facies (low-set ears, broad flat nose, a prominent skin fold beginning over the eye and running to the cheek).
The great majority die soon after birth from their pulmonary hypoplasia.
The renal arteries and ureters are usually absent, and the bladder is underdeveloped.
The vas is usually present, but female genital structures are usually abnormal.
The adrenals are usually present but appear round, instead of flattened, due to the lack of compression by the kidneys.
Prenatal evaluation and diagnosis are helpful in determining that heroic efforts with extracorporeal membrane oxygenation or hemodialysis are not indicated after delivery if there is no improvement in the thoracic to abdominal circumference during pregnancy.
In one case, serial amnioinfusion during pregnancy was successful at reversing pulmonary hypoplasia, and the child did not require intubation after delivery. She underwent peritoneal dialysis and eventual renal transplantation.
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What is a supernumerary kidney?
This is a rare condition in which a completely separate kidney is found in addition to two normally positioned kidneys.
The additional kidney has its own blood supply and parenchyma and usually is found caudal to the normal kidney.
It is usually smaller than the normally positioned kidney.
This additional kidney represents abnormal induction of metanephric blastema by an abnormally directed ureteric bud, either as a separate ureteral bud from the mesonephric duct, or as part of a “Y” duplication.
If the supernumerary kidney is located cranial to the normal kidney, the ureter is usually completely separate and may enter the bladder ectopically. Presumably this is a result of a completely separate ureteral bud inducing the metanephric blastema and migrating very low on the mesonephric duct, separate from the normally positioned kidney.
If the ureter ends ectopically, it may present as incontinence in a girl, or as infection in a poorly functioning renal unit. The diagnosis can be difficult.
Stone disease and hydronephrosis can be found in up to 50% of patients.
Treatment should be reserved for these problems as the presence of a supernumerary kidney itself is not concerning.
Like other ectopic kidneys, these kidneys are more susceptible to trauma, so a medical alert bracelet may be helpful.
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What are the possible locations for ectopic kidneys?
Failure of rotation, while not strictly ectopia, usually results in a kidney in which the renal pelvis is anteriorly directed.
In the unusual situation in which hyper-rotation occurs, the renal pelvis can actually point posteriorly. The renal vessels are normally positioned.
The renal pelvis and calyces will often appear abnormal on an intravenous urogram due to their unusual orientation. With oblique views, the anatomy can be established and does not usually require repair, even in poorly functioning units.
One method to localize even poorly functioning ectopic renal tissue is with a nuclear medicine study.
There are two technical factors to be considered in interpreting renal scans in ectopic kidneys.
First, the radionuclide in the bladder can overlay a pelvic kidney so a urinary catheter may need to be inserted for the study.
Second, the pelvic kidney is located further anterior than orthotopic kidneys, and the function may be artificially lowered by the distance of the kidney from the camera. Placing the patient prone may result in a more accurate assessment.
Magnetic resonance urography (MRU) is helpful for localizing ectopic renal units not seen on US.
Simple ectopia results in a kidney that is located anywhere from the pelvis to the diaphragm. The incidence is 1 per 1000 live births with a 3:2 male predominance.
The contralateral kidney often also has a rotational abnormality or ectopia.
The development of the ipsilateral adrenal gland is unaffected.
A “thoracic kidney” is actually subdiaphragmatic, although it may lie in the chest through a focal eventration of the diaphragm. It is not associated with a true congenital diaphragmatic hernia.
An ectopic “abdominal kidney” is above the iliac crest, the “lumbar kidney” is anterior to the iliac vessels at the sacral promontory, and the “pelvic kidney” is below the aortic bifurcation and opposite the sacrum.
All of these ectopic kidneys are more susceptible to trauma because they are not as well protected by the lower rib cage and are anterior in position. It may be advisable for these patients to avoid contact sports in which there is a risk of abdominal trauma.
Most ectopic kidneys are asymptomatic and are detected either on prenatal US or incidentally on other imaging studies. Ectopic kidneys are at higher risk for UPJ obstruction, VUR, and stone formation.
The anatomy can include an extrarenal pelvis and infundibulum, and a high insertion of the ureter into the pelvis. This anatomic arrangement can mimic a UPJ obstruction, so careful evaluation is necessary to avoid unnecessary surgery.
More than half will have a dilated renal pelvis. Of these, half are due to obstruction, 25% are due to reflux, and 25% are merely dilated without UPJ obstruction.
For repair of UPJ obstruction with a high insertion of the ureter, a side-to-side ureteropyelostomy or ureterocalycostomy to a dilated lower pole calyx is sometimes required to obtain dependent drainage.
While endoscopic techniques for treatment of UPJ obstruction have been used in children, a laparoscopic approach has been shown to be safe and effective, given the presence of anomalous vessels.
The advent of computed tomography (CT) angiography and MRU has made the assessment of anomalous vessels in ectopic or horseshoe kidneys easier and less invasive.
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How do patients with horseshoe kidney usually present?
A horseshoe kidney is found in 1 per 400 live births and has a 2:1 male predominance.
The kidney is usually lower than normal, since the lower poles fuse in the midline and drape anteriorly over the spine.
The isthmus can be fibrotic or contain parenchyma.
Because the orientation of the renal pelvis is anterior, this anomaly is believed to develop between 4 and 6 weeks of gestation.
It is proposed that as the kidneys “hurdle” the iliac vessels during ascent, they come into contact at the lower pole and fuse. Other variations of upper pole and mid-pole contact are possible, but much less common than the usual lower pole fusion.
The kidney is usually low due to its inability to ascend past the inferior mesenteric artery.
Each renal moiety retains its ureter, which is draped over the isthmus. The arterial supply varies from the normal single vessel to each moiety to vessels arising from any conceivable nearby blood supply.
Horseshoe kidneys are more commonly found in patients with sacral agenesis, high cloacas, and Turner syndrome (45,XO gonadal dysgenesis).
They are associated with a higher risk of renal cell carcinoma and Wilms tumor.
In one report from the National Wilms Tumor Study Group, the presence of a Wilms tumor in a horseshoe kidney was not suspected preoperatively in 13 of 41 patients despite imaging studies.
One-third of patients with a horseshoe kidney have no symptoms. The patients with symptoms often complain of vague abdominal or back pain. Ten percent have ureteral duplication, 50% have VUR, and 33% have UPJ obstruction.
Repair of UPJ obstruction in a horseshoe kidney requires placement of the anastomosis to avoid a secondary kinking at the UPJ. Division of the isthmus is not required.
Treatment of kidney stones in horseshoe kidneys can be accomplished by extracorporeal shock wave lithotripsy, ureteroscopy, or percutaneous nephrolithotomy. Percutaneous approaches are sometimes difficult, as the kidneys do not reside next to the body wall, making access to the collecting system difficult. However, percutaneous nephrolithotomy and ureteroscopy result in a higher stone-free rate than shock wave lithotripsy.
Although there is no increase in the rate of metabolic abnormalities in patients with horseshoe kidneys and kidney stones, patients with a horseshoe kidney and kidney stones are more likely to have hypocitraturia than other patients with kidney stones.
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What is cross-fused renal ectopia?
This anomaly is more common than crossed, non-fused renal ectopia and is more common in boys.
The lower pole of one kidney crosses the midline to fuse with an orthotopically placed contralateral kidney. Usually the left kidney crosses the midline.
Presumably during ascent, the left kidney encounters a roadblock, rotates, and fuses with the lower pole of the right kidney.
The ureters insert in the normal position in the bladder.
This has been described as an S- or L-shaped kidney.
Diagnosis can be made using intravenous pyelogram (IVP), CT, or MRU.
Solitary crossed ectopia (unilateral renal agenesis, contralateral kidney crossed to opposite side) is a rare finding.
Multicystic dysplasia, obstruction, and VUR can be found in the ectopic kidney.
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What is the treatment for autosomal recessive polycystic kidney disease (ARPKD)?
Autosomal recessive polycystic kidney disease (ARPKD) was formerly called infantile polycystic kidney disease, which is inaccurate since it can present in older patients.
While it occurs in 1 per 40,000 live births, many patients die soon after birth. The kidneys are bilaterally enlarged, with very small cysts radially oriented throughout parenchyma.
The cysts represent dilated collecting tubules.
Periportal hepatic fibrosis also occurs in varying degrees and can lead to portal hypertension.
The hepatic involvement appears to be inversely proportional to the renal involvement.
The disease has been classified into four forms.
The severe perinatal form (>90% renal involvement) leads to death by 6 weeks from pulmonary hypoplasia.
The neonatal form (60% renal involvement) is usually lethal by 1 year.
The infantile form (25% renal involvement) results in hepatosplenomegaly, with survival up to 15 years.
The juvenile form (<10% renal involvement) has severe periportal fibrosis. Some patients survive up to 15 years, but the development of portal hypertension is usually lethal without liver transplantation.
As this is an autosomal recessive disease, family screening should be undertaken to determine which siblings are carriers. While ARPKD is caused by mutations in the PKDH1 gene, no correlation between specific mutations and phenotype have been shown to date.
A prenatal US showing bilaterally enlarged echogenic kidneys suggests ARPKD.
The IVP or CT shows a classic striated “sunburst” pattern.
Unfortunately, the prognosis is poor for the perinatal or neonatal forms of ARPKD. The patients who survive the neonatal period seem to do well with some degree of renal insufficiency.
Eventually, dialysis is usually required, and bilateral nephrectomy may be needed to achieve adequate space in the abdomen in some patients who require peritoneal dialysis.
In older patients, the kidneys become smaller as renal failure develops.
The overall treatment for ARPKD is supportive, with renal transplantation being the ultimate therapy.
Fortunately, patients who receive a renal transplant are unlikely to require a liver transplant.
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How is autosomal dominant polycystic kidney disease different from ARPKD?
While autosomal dominant polycystic kidney disease (ADPKD) tends to present clinically in the third to fifth decade, it has been diagnosed in the US era in asymptomatic children as well.
The cysts in ADPKD are different in configuration, being few and scattered, in distinction from those seen in ARPKD.
This condition occurs in 1 per 500 patients.
Patients usually present with flank pain, hematuria, hypertension, and possibly renal failure, if there are extensive bilateral cysts.
Neonates can present with renal enlargement, although children from affected families who are screened usually only have a few cysts.
Failure to see cysts on screening US in a child at risk for ADPKD does not exclude the disease because the cysts can develop later in life.
ADPKD is caused by mutations in PKD1 and PKD2, with renal failure occurring earlier in patients with PKD1 than PKD2 mutations (54 vs 74 years).
The cysts are located throughout the cortex and medulla, although the fetal form seems to affect the glomeruli predominantly.
For families with an unknown genotype, the criteria for an ADPKD diagnosis by US for patients between ages 15 and 39 years requires three or more unilateral or bilateral cysts.
Therefore, the most useful examination in a child with cystic renal disease of unknown cause is a renal US of the parents to differentiate between ADPKD (parents will have cysts) versus ARPKD (parents will not have cysts).
Hepatic involvement in ADPKD is limited to biliary cysts.
Associated findings include cysts in the spleen, pancreas, and lungs; mitral valve prolapse; colon diverticuli; and berry aneurysms of the circle of Willis.
Hypertension is commonly found in these children and may be part of the presentation.
Renal failure in childhood is very rare.
Periodic evaluation of blood pressure and proteinuria during childhood is recommended.
Unlike ARPKD, there is no increased risk of renal cell carcinoma.
Renal transplant candidates can obtain organs from family members who have been screened for the disease.
Pregnancy poses higher risks for preeclampsia, hypertension, renal insufficiency, and urinary tract infection for the mother with ADPKD, but there is no significant increased risk to the fetus.
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What is the most common renal cystic mass in the newborn?
The MCDK is believed to be caused by severe early ureteral obstruction or a failure in ureteric bud-metanephric blastema induction.
The main differential diagnosis is severe hydronephrosis due to UPJ obstruction. Radiographically, this occurs when the peripheral cysts surround a dominant central cyst mimicking the renal pelvis (“hydronephrotic” form of MCDK).
The classic US appearance shows cysts randomly distributed throughout the kidney without a dominant medial cyst or evidence of communication between cysts. The parenchyma, if present, has abnormal echogenicity and is seen between the cysts, instead of being arranged on their periphery.
A renal scan will show no function in an MCDK. The affected area may be the upper pole of a duplicated collecting system or one half of a horseshoe kidney.
The MCDK is the most common renal cystic mass in the newborn. Most are detected on prenatal US. Bilateral forms are not compatible with life.
The need for a VCUG to look for VUR in the contralateral kidney, which is found 30% of the time, has been questioned. In one study, the likelihood of detecting VUR was only 7% if the contralateral kidney was normal, with a renal pelvis diameter <7 mm, and no calyceal or ureteral dilation. If there is significant hydronephrosis (caliectasis) in the contralateral kidney (this occurs 10% of the time), then a diuretic renal scan may be helpful.
Contralateral UPJ obstruction or VUR is more likely with a smaller MCDK or a lower ureteral atresia ipsilateral to the MCDK.
There are reports of malignancy arising from a MCDK, although it is unclear whether the affected kidneys were truly MCDK.
Hypertension has also been reported in association with MCDK, although resection is not always curative, and the rate does not appear to be any higher than the general population.
MCDK usually involute, but they can occasionally grow. Follow-up is repeat imaging with US every 6 months for the first 2 years of life.
In another study, longterm follow-up of MCDK showed that complete involution occurred in 47% at 5 years and 59% at 10 years, which suggests that US follow-up be performed at 5 and 10 years of life, if a nonoperative approach is taken.
Between 18 and 24 months of life, the MCDK can be removed via laparoscopy or a small flank incision as an outpatient procedure.
Occasionally, the MCDK can involute prenatally, leaving a ureter with a small nubbin of tissue in the renal fossa. These were previously called “aplastic kidneys” but are now felt to represent the remnants of a MCDK.
Patients who require closer follow-up are those with abnormalities of the solitary contralateral kidney, such as hydronephrosis, urinary tract infection, and atrophic kidney.
In a recent report, the median age to develop stage 2 chronic kidney disease was 10 years in those with contralateral abnormalities versus 18 years in those with compensatory hypertrophy.
As renal length does not correlate with renal function, follow-up is important.
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What is the treatment for cystic nephroma?
Formerly called a “multilocular cyst,” this is a well demarcated tumor of cysts with an overall round configuration, lined with epithelium and septae that contain tubules.
It is considered to be the benign end of a spectrum progressing from cystic Wilms tumor, cystic partially differentiated nephroblastoma, to cystic nephroma.
It usually is found in boys under age 4 (male:female ratio 2:1) or women over 30 (female:male ratio 8:1).
It is rarely bilateral and is cured by partial nephrectomy, shelling out the tumor by following the plane of the pseudocapsule.
There is a risk of sarcomatous degeneration in adults if it has not been removed.
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How do you distinguish cystic nephroma from cystic partially differentiated nephroblastoma?
This lesion was formerly called a multilocular cystic nephroma. It is radiologically identical to the cystic nephroma and can be diagnosed only histologically.
The majority of patients are boys younger than 2 years old or women in their third to fourth decade.
A classic (but not diagnostic) radiologic finding is herniation of a parenchymal mass into the renal pelvis.
The tumor is usually well circumscribed. Hemorrhage and calcification are usually absent.
Histologically, it differs from the cystic nephroma in that blastema is found in the septations.
Patients usually present with an asymptomatic flank mass, and occasionally hematuria.
Operative treatment consists of partial nephrectomy as for cystic nephroma, as the tumors rarely recur and are not multifocal.
No chemotherapy is required for stage I (limited to capsule, fully resected) tumors.
Although experience is limited, stage II (outside renal capsule but fully resected) are usually treated with vincristine, dactinomycin, and doxorubicin. Fouryear survival for both stages is 100%.
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How do simple renal cysts present on ultrasound?
The simple renal cyst seen on US has the following characteristics: distinct wall, no internal echoes, and posterior enhancement.
If these criteria are not present, a CT or MRI is obtained to confirm that the fluid does not enhance.
In a recent review, using a modified Bosniak classification in which suspicious cysts had >1 mm wall thickness with Doppler flow or multiple septations with Doppler flow, only 4% of pediatric renal cysts were classified as suspicious. Of these 10 cysts, only one was a multicystic cystic nephroma.
The differential diagnosis of benign conditions causing a complex cyst is a calyceal diverticulum or hydrocalyx, both of which communicate with the collecting system. The fluid should enhance on either IVP or CT. US is able to detect milk of calcium layering within a diverticulum. Calyceal diverticuli require treatment when they harbor stones or infection.
In the IVP era, 40% of calyceal diverticuli were felt to be symptomatic. In the US era, with its greater number of incidental findings, it is not clear how often calyceal diverticuli require treatment.
Minimally invasive approaches such as percutaneous, laparoscopic, and ureteroscopic ablation appear to be equally successful.
Simple cysts reside in the cortex and are lined by simple columnar epithelium. They can grow, resorb, or remain the same size. They are usually asymptomatic and are found incidentally. Once they are found, they are usually followed with US at 3- to 6-month intervals to determine if the cyst is growing.
The underlying concern is whether or not this cyst is the first sign of ADPKD. A family history of renal cystic disease, renal failure, or death in the neonatal period from unknown causes should be sought.
Biopsy to rule out tumor, followed by drainage or unroofing, should be undertaken only if the cyst characteristics are other than those listed for a simple cyst, or if the cyst becomes symptomatic due to obstruction of an infundibulum or UPJ.
Minimally invasive approaches such as percutaneous puncture with instillation of sclerosing agents (absolute alcohol, bismuth, povidone-iodine66 ) or laparoscopic decortication may shift the threshold for treatment of large asymptomatic simple cysts.
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Polycystic kidney shows the following features except:
A. Many cysts in both kidneys
B. No continuity between glomeruli and calyces
C. Congenital variety is autosomal recessive
D. Adult variety is autosomal dominant
E. No renal dysplasia
B
There is continuity between glomeruli and calyces. No continuity between glomeruli and calyces is seen in multicystic kidney.
Syed/MCQ
Regarding anomalies related to abnormal ascent of the kidney (ectopic kidney), which of the following statements is true?
A. Thoracic ectopic kidney is the most common.
B. Pelvic ectopic kidney is a rare variety.
C. Iliac variety is fixed below the crest of the ileum.
D. Lumbar variety is below the level of L2 and L3.
E. Lumbar and iliac ectopic kidney are the same thing
E
Pelvic ectopic kidney is most common ectopic variety.
Thoracic is rare.
Lumbar and iliac ectopic kidney is same thing, fixed above the crest of ilium but below the level of L2 and L3.
Syed/MCQ
Horseshoe kidney shows the following features except:
A. It is the most common fusion defect.
B. In 95 per cent of cases, the upper poles of the kidney are joined.
C. The bridge of tissues between two kidneys can be either normal, dysplastic or fibrous tissue.
D. It is postulated that inferior mesenteric artery obstructs the isthmus and prevents ascent.
E. Correction of ureteropelvic junction obstruction is the most frequent indication for surgical intervention.
B
In 95 percent of cases, the lower poles of the two kidneys are joined.
Syed/MCQ
