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BJUI Mini Reviews - Non-Surgical Management of Multicystic Dysplastic Kidney Show Comments PDF Print E-mail
  
Friday, 11 April 2008
(BJUI Mini Reviews) - Objective: To better define the outcome and association of multicystic dysplastic kidney (MCDK) with hypertension, vesico-ureteric reflux (VUR), infection and cancer, as there is no consensus on the management of patients born with MCDK.

2008 BJU INTERNATIONAL | 101, 804–808 | doi:10.1111/j.1464-410X.2007.07328.x Non-surgical management of multicystic dysplastic kidney Angelo J. Cambio, Christopher P. Evans and Eric A. Kurzrock Department of Urology, University of California, Davis School of Medicine, Sacramento, CA, USA Accepted for publication 7 September 2007 RESULTS The inclusion criteria were met by 105 reports that were subsequently analysed. Of MCDK, 60% regress or involute within 3 years. About 25% of patients will have VUR into the contralateral kidney, of which 90% is grade ≤ 3. The risk of urinary tract infection appears to be associated with VUR or coexistent abnormalities rather than the MCDK. The risk of hypertension is no greater than that in the general population and nephrectomy is usually not curative. The overall risk of Wilms’ tumour developing in a MCDK is < 1 in 2000. All reported Wilms’ tumours were identified before 4 years of age and 70% presented as a palpable mass. CONCLUSIONS Published reports support the non-surgical management of MCDK. Common practice has been to remove palpable or growing MCDKs, although these represent a very small fraction of MCDKs. In theory, ultrasonographic surveillance until 4 years old might allow the earlier detection of a Wilms’ tumour, and decrease the intensity of chemotherapy and improve prognosis. Previous reports do not prove or disprove this concept, and the appropriate frequency of surveillance is not evident. KEYWORDS multicystic dysplastic kidney, Wilms’ tumour, renal cell carcinoma, vesico-ureteric reflux OBJECTIVES To better define the outcome and association of multicystic dysplastic kidney (MCDK) with hypertension, vesico-ureteric reflux (VUR), infection and cancer, as there is no consensus on the management of patients born with MCDK. The risk of cancer has dictated the surgical management of the disease in the past. METHODS The Medline database was searched for articles published between 1965 and 2006 and written in the English language, and containing the keywords ‘multicystic dysplastic kidney’. INTRODUCTION The incidence of multicystic dysplastic kidney (MCDK) is not well defined; it is reported to occur unilaterally in one in 2400, one in 4100 or one in 4300 live births, and is the most common form of cystic kidney in children [1,2]. The condition occurs more commonly in males than females (2.4:1) but females are twice as likely to have bilateral MCDK. The left The incidence of multicystic dysplastic kidney (MCDK) is not well defined; it is reported to occur unilaterally in one in 2400, one in 4100 or one in 4300 live births, and is the most common form of cystic kidney in children [1,2]. The condition occurs more commonly in males than females (2.4:1) but females are twice as likely to have bilateral MCDK. The left kidney is more often affected than the right. MCDK has two subtypes that are based on gross appearance, i.e. solid cystic dysplasia and hydronephrotic form. The former is characterized by increased stromal components and smaller cysts; the hydronephrotic form of MCDK is characterized by an identifiable renal pelvis. Differentiating MCDK from Wilms’ tumour or RCC with cystic components is a challenge and a potential source of error in reporting neoplasia associated with MCDK [3]. Recent reports support non-surgical management, with long-term follow-up [1,4], and there is no strong evidence supporting any particular follow-up regimen. Current non-surgical management protocols might include renal ultrasonography (US), growth-chart analysis, urine analysis, blood tests and blood pressure assessment, all of which are at variable and arbitrary intervals. The morbidity and cost of surgery have been compared to the morbidity, cost, inconvenience and bother of an extended follow-up; however, no universally accepted management protocol has emerged. After a thorough review of published reports in the English language, our goal was to present a concise statement on the risks and discuss management options. METHODS The Medline database was searched for articles published between 1965 and 2006 in the English language and containing the keywords ‘multicystic dysplastic kidney’. Case reports were excluded unless they involved cancer. The abstracts of 152 articles were analysed and of these, 105 reports were reviewed. If an article cited relevant original work in report before 1965, these were also analysed. We specifically assessed the relationship of MCDK with VUR, UTI, hypertension, cancer and the need for surgery. RESULTS DIAGNOSIS Previous reports show that historically MCDK was a rare finding that was diagnosed by a palpable abdominal mass and managed with nephrectomy [5]. The widespread use of antenatal US has led to an increasing incidence of MCDK [6,7]. Antenatal US has a sensitivity of 80–100% with a false-positive rate of ≈ 2%, the main differential diagnosis being a poorly functioning hydronephrotic kidney [8,9]. Abnormal postnatal US verifies the suspicious finding (Fig. 1). A renal isotope scan is useful NON-SURGICAL MANAGEMENT OF MULTICYSTIC DYSPLASTIC KIDNEY © 2008 THE AUTHORS JOURNAL COMPILATION © 2008 BJU INTERNATIONAL 805 when the MCDK is not easily distinguished from a hydronephrotic kidney. A renal concentration of isotope is indicative of hydronephrosis, as renal function in MCDK is exceedingly rare. If necessary, a DMSA scan is appropriate as a diuretic/excretory evaluation is unnecessary. VUR Numerous articles included voiding cysto- urethrography (VCUG) in the evaluation of MCDK. VUR was reported to occur into the contralateral kidney in 15–28% of patients [10–14]. Miller et al. [12] retrospectively investigated the fate of the refluxing contralateral kidney in 75 children with MCDK; VUR was diagnosed in 25% of patients, with grade distributed as 5% for I, 42% for II, 42% for III, 11% for IV and none of grade V. There was spontaneous resolution within 5 years in most (89%) of the patients with grade I and II VUR, and half of patients with grades III or IV VUR. Of children in this series, 19% had a documented UTI at some point during the follow-up (median 53 months). The presence of VUR did not correlate with the growth of the normal kidney in a child on antimicrobial prophylaxis. In 2005, Ismaili et al. [11] challenged the routine use of VCUG to detect contralateral VUR in patients with a MCDK. In a retrospective analysis they reported that two successive normal neonatal renal US might exclude significant contralateral anomalies, thus avoiding VCUG and its associated radiation exposure and pain. The sensitivity, specificity, positive and negative predictive value of two successive neonatal ultrasonograms to detect VUR was 75%, 95%, 80% and 93%, respectively. All patients with high-grade VUR were detected by US. Ismaili et al. recommended that VCUG not be used in those patients who have two normal contralateral postnatal renal ultrasonograms. The rate of UTI, with or without antibiotics, was not reported, and is a major limitation of the study. INVOLUTION The fate of the affected kidney is variable; affected kidneys involute or decrease in size in 60–89% of cases, some stay the same (2–37%) and few increase in size (0–18%) [13,15,16]. The timeline to involution is variable; the mean time was reported as 20 months in one study [13] and 122 months in another [16]. Statistically derived estimates show that 20% and 50% of MCDKs will become undetectable by US (involution) at 3 and 5 years of follow-up, respectively [17]. HYPERTENSION Hypertension associated with MCDK has been anecdotally reported; the true incidence is unknown, but thought to be extremely low. In a systematic review of 29 studies, including 1115 patients, Narchi [18] recently reported the incidence of hypertension associated with MCDK as 5.4 per 1000 patients. Surprisingly, this is lower than the incidence of hypertension in the general paediatric population. However, Narchi caution that their comparison of series was hampered by disparities in patient age, follow-up and criteria for defining hypertension. In another large study, Wacksman and Phipps [19] found no cases of hypertension in a series of 441 cases reported to the Multicystic Kidney Registry. Hypertension in a patient with MCDK might be an indication for nephrectomy, but in about two-thirds of cases the hypertension will persist after nephrectomy [20]. WILMS’ TUMOUR (WT) There were reports on the association of WT with MCDK, primarily based on case studies and small series (Table 1 [21–28]). Evidence supporting these case reports is often incomplete and not supported by outside pathological review [3]. Despite the nature of this evidence, the purported increased risk of cancer continues to dictate the management of MCDK for many urologists. Many patients have had and continue to have nephrectomies [29]. In response to this issue, Beckwith [3] calculated the risk of WT in MCDK, based on work by Gordon et al. [2], in which 10 unilateral cases of MCDK were detected in 43 175 live births, thereby estimating an incidence of 1 in 4300 live births. The National Wilms’ Tumor Study Pathology Center provided data on 7500 WTs collected over 26 years; only five of the 7500 WTs occurred in a MCDK. The risk of WT in the general population is 1 in 8000–10 000. Taking into account the risk of MCDK during the same 26-year period, the calculated risk of WT in association with MCDK is 1 in 2000. With a 90% cure rate for WT, Beckwith concluded that nephrectomy and routine monitoring are not justified [3]. Surprisingly, through a completely different approach, Noe et al. [30] had previously calculated that 2000 nephrectomies would be necessary to prevent one WT. Nephrogenic rests are a precursor to WT and the incidence is ≈ 1% in the general population, or ≈ 100 times the incidence of WT. The incidence of nephrogenic rests in those with WT is higher, at 12–40% [31], and in those with MCDK is reported to be to 3–5% [31]. Assuming 1% of cases of nephrogenic rests degenerate to WT [31] and there is a 5% increased risk of nephrogenic rests with MCDK, 2000 nephrectomies would be needed to prevent one WT [30]. The calculation by Noe et al. supports the estimate generated by Beckwith [3]. In the Preliminary Report of the Multicystic Kidney Registry, Wacksman and Phipps [19] report only two cases of WT in the 25 years before their 1993 publication. A 10-month- old and 4-year-old both presented with a palpable mass. Of the 260 cases of MCDK in the registry that were managed without surgery, there were no cases of WT. The Multicystic Kidney Registry stopped enrolling patients in the late 1990s, but only one patient in ≈ 900 cases registered developed a malignancy, and this malignancy did not develop in a true MCDK (J Wacksman, personal communication 2006). Wacksman and Phipps [19] estimate that 8000 MCDKs would have to be removed to prevent one tumour. In a systematic review of 26 studies including 1041 patients, Narchi [32] reported that there were no WTs in patients with MCDK. While the results from this systematic review are promising, the author noted that the study was limited by heterogeneity of the populations, an 18-year span of studies and availability/accuracy of antenatal US, the varied duration of follow-up and varied FIG. 1. An ultrasonogram of a MCDK. CAMBIO ET AL. © 2008 THE AUTHORS 806 JOURNAL COMPILATION © 2008 BJU INTERNATIONAL frequency of US surveillance. Nevertheless, there is no large review or meta-analysis reporting an association of MCDK with WT. In our review of 10 reported cases of WT associated with a purported MCDK (Table 1), seven presented with a palpable abdominal mass. No patient with documented WT presented after 4 years of age; only four had a known history of MCDK, and none presented with metastatic disease. Survival data were available for eight of the 10 cases. The follow- up ranged from 7 months to 12 years and no recurrences or deaths were reported. There were no reports of WT associated with an involuted kidney. RCC We found six reports of RCC associated with MCDK in patients aged 15–44 years; all cases were of advanced stage with large tumours. The accuracy of the pathological diagnosis of MCDK with these large tumours is debatable. None were subject to outside pathological review, as with WT. None of the patients had a pre-existing history of MCDK. As such, it is possible that some of these were cystic RCCs. DISCUSSION Before antenatal US was routinely used most identified MCDKs were large and palpable. This abnormal finding on physical examination led to the preferred treatment of nephrectomy. In the era of antenatal US the prevalence of MCDK has increased and the size of affected kidneys has decreased [5]. High rates of spontaneous partial or complete involution [1,13,15–17] and low rates of hypertension [18] and neoplasia [32] have shifted the management to a non-surgical approach. There is little controversy about the diagnostic evaluation of MCDK. The argument for VCUG in patients with MCDK parallels the controversy and rhetoric about infants with pre- and postnatal mild hydronephrosis; VUR is found in 15–40% of these infants [33]. Evidence suggests that the finding of low- grade VUR might not be clinically important [33]. Unlike infants with prenatal hydronephrosis, children with MCKD have half the renal reserve. The recognition of reflux and prevention of pyelonephritis in children with a solitary functioning kidney is important. Cystography is still practised routinely, as reported in the vast majority of published series. Some authors include urine culture and blood pressure assessment as components of the follow-up for MCDK. Urine culture in children carries an inherent rate of false-positive results. The preliminary report of the Multicystic Registry reported only 12 cases of UTI in the 260 cases that were managed without surgery [19]. Similar to the management of VUR, routine urine culture in asymptomatic children is hampered by a significant false-positive rate, which negates its value. Paediatricians recommend blood pressure monitoring in all children during clinical encounters after the age of 3 years. Children aged < 3 years should have their blood pressure measured under special circumstances, such as MCDK [34]. Complete involution, meaning that the MCDK has become imperceptible to US, is a satisfying outcome. However, the malignant potential of even small amounts of residual tissue is uncertain. In our review we were unable to find one case of WT associated with an involuted MCDK. All cases of WT presented before 4 years old and at least seven of the 10 were palpable. These are new findings from our review. No deaths from WT were reported. Two investigators, with different methods, have calculated the risk of developing a WT to be 1 in 2000 for children with MCDK (the risk in the general paediatric population is 1 in 8–10 000). An estimated 36 000 new cases of RCC were diagnosed in the USA in 2005. Considering the higher incidence of RCC in men and the higher incidence of MCDK in newborn boys, there should be ≈ 10 random associations of RCC with MCDK per year. As there are only six reported in the English language, MCDK TABLE 1 Case reports of Wilms’ tumour associated with MCDK Reference Age*, months/sex Presentation Outcome [21] 18/M Prenatal US showing renal cysts; L flank mass on physical exam; confirmed by postnatal US; 14 months persistent cystic disease with no evidence of tumour; 4 months later parent noticed increasing abdominal girth; 16 × 10 × 13 cm solid tumour with calcifications; L total nephrectomy; favourable histology WT with invasion into perirenal fat Chemo for 6 months NED 13 month f/u [22] 11/M Prenatal diagnosis MCDK, lost to f/u, 11 months presented with abdominal mass Positive response to chemo f/u NR [23] 5/F Prenatal diagnosis of MCDK, abdominal swelling NED 6 year f/u 3/F L flank mass on US Chemo; NED 8 year f/u [24] 17/M MCDK discovered on MRI when evaluating anorectal malformation NR [25] 5/NR Nephrectomy for abnormal sonogram NED, 1 year f/u [26] 48/F Palpable abdominal mass NR [27] 10/M Palpable abdominal mass NED, 11 year f/u [28] 9/F Palpable abdominal mass NED, 5 year f/u 1/M Palpable abdominal mass NED, 5 month f/u f/u, follow-up; L, left, NED, no evidence of disease; NR, not reported; chemo, chemotherapy. *Age at diagnosis of growing abdominal mass that prompted surgical intervention. NON-SURGICAL MANAGEMENT OF MULTICYSTIC DYSPLASTIC KIDNEY © 2008 THE AUTHORS JOURNAL COMPILATION © 2008 BJU INTERNATIONAL 807 might carry an equal or lesser risk of developing RCC than a normal kidney. In urological reports, proponents of surgery argue that non-surgical management requires a long-term follow-up with frequent, costly US, leaving patients at risk of infection, hypertension and cancer, especially in those cases lost to follow-up. A few studies showed that early nephrectomy is more cost-effective than non-surgical follow-up. These types of analyses are arbitrary, as the necessary frequency of US surveillance is unknown and costs are highly variable among health systems. This surgical bias is absent in the nephrological literature. There are various and similar surveillance regimens used for MCDK. Generally, these include renal US every 3–6 months for the first year, every 6 months in the second year and then annually thereafter. The main indication for frequent surveillance is to detect WT. The prognosis after treating WT depends on the stage and histology at surgery. Children with lower stage disease (I, II) have an excellent 4-year recurrence-free survival ( ≈ 95%) compared to higher-stage disease (III, IV; ≈ 85%) for both the National WT Study Group and the Société Internationale d’Oncologie Pédiatrique protocols. More important than stage is tumour histology; children with stage I and unfavourable histology (anaplasia) have a significantly lower overall survival (83%) than children with stage I and favourable histology (98%). Although time and growth will inevitably increase the stage, there is no evidence that time does or does not affect histology. There are disorders that have a well documented association with WT, i.e. Beckwith–Wiedmann syndrome (BWS) and idiopathic hemihypertrophy (IHH). As WTs grow so rapidly, experience with screening children with BWS/IHH has shown that US is needed every 3–4 months to effectively lower the tumour stage [35,36]. Notably, in the screened population, 20% of children had false-positive results and thus had surgery for benign lesions. Frequent surveillance is not recommended after 6 years of age in the BWS/IHH population. The incidence of WT in these patients ( ≈ 5%) is 100 times higher than the theoretical incidence (0.05%) of WT in patients with MCDK. How does the risk of WT compare with other childhood malignancies? The incidence of WT, brain cancer and leukaemia per million children per year is 8, 33 and 44, respectively; the last two cancers are significantly more deadly. Unfortunately, there is no economic, noninvasive manner to screen all children for these grave cancers. As the incidence of MCDK is only 1 in 4000, there is a small at-risk population who can be screened. Fortunately, US is relatively inexpensive and not invasive. Beyond cancer screening, surveillance of these kidneys is advantageous as some will grow. What has not been answered is the appropriate frequency of surveillance. If the goal is to down-stage a WT, a 4-month frequency until age 4 years would be necessary. In conclusion, the incidence of MCDK is ≈ 1 in 4000 live births, of which 60% will regress or involute within 3 years. Up to a third of patients will have VUR into the contralateral kidney, of which 90% is grade I–III. The risk of UTI appears to be associated with VUR or coexistent urological abnormalities rather than the MCDK. The risk of hypertension is no greater than that in the general population and nephrectomy is usually not curative. The overall risk of WT developing in a MCDK is < 1 in 2000. All reported WTs were identified before 4 years of age and seven of 10 presented as a palpable mass. There is no reported case of WT in association with an involuted MCDK. As such, the risk of WT developing in an MCDK which is regressing or involuted is substantially < 1 in 2000, and is probably less than the risk of neoplasia in a normal size kidney. There is no evidence to support an increased risk of RCC with MCDK. Previous reports support the non-surgical management of MCDK. Although not supported by firm published evidence, the common practice has been to remove palpable or growing MCDKs; however, such cases are rare. The increased risk of WT supports surveillance with US up to 4 years old, but there is no evidence to guide the appropriate frequency of renal imaging. ACKNOWLEDGEMENTS We appreciate the input and review of this manuscript before submission by J. Bruce Beckwith, MD. Angelo Cambio, MD, was supported by the Aventis Clinical Research Fellowship in Urologic Oncology. CONFLICT OF INTEREST None declared. REFERENCES 1 Kuwertz-Broeking E, Brinkmann OA, Von Lengerke HJ et al. Unilateral multicystic dysplastic kidney: experience in children. BJU Int 2004; 93 : 388–92 2 Gordon AC, Thomas DF, Arthur RJ, Irving HC. Multicystic dysplastic kidney: is nephrectomy still appropriate? J Urol 1988; 140 : 1231–4 3 Beckwith JB. Wilms tumor and multicystic dysplastic kidney disease. Editorial Comment. J Urol 1997; 158 : 2259–60 4 Rickwood AM, Anderson PA, Williams MP. Multicystic renal dysplasia detected by prenatal ultrasonography. Natural history and results of conservative management. Br J Urol 1992; 69 : 538–40 5 Bloom DA, Brosman S. The multicystic kidney. J Urol 1978; 120 : 211–5 6 Eckoldt F, Woderich R, Smith RD, Heling KS. Antenatal diagnostic aspects of unilateral multicystic kidney dysplasia – sensitivity, specificity, predictive values, differential diagnoses, associated malformations and consequences. Fetal Diagn Ther 2004; 19 : 163–9 7 Mandell J, Paltiel HJ, Peters CA, Benacerraf BR. Prenatal findings associated with a unilateral nonfunctioning or absent kidney. J Urol 1994; 152 : 176–8 8 Bhide A, Sairam S, Farrugia MK, Boddy SA, Thilaganathan B. The sensitivity of antenatal ultrasound for predicting renal tract surgery in early childhood. Ultrasound Obstet Gynecol 2005; 25 : 489–92 9 Eckoldt F, Woderich R, Wolke S, Heling KS, Stover B, Tennstedt C. Follow-up of unilateral multicystic kidney dysplasia after prenatal diagnosis. J Matern Fetal Neonatal Med 2003; 14 : 177–86 10 Flack CE, Bellinger MF. The multicystic dysplastic kidney and contralateral vesicoureteral reflux: protection of the solitary kidney. J Urol 1993; 150 : 1873–4 11 Ismaili K, Avni FE, Alexander M, Schulman C, Collier F, Hall M. Routine voiding cystourethrography is of no value in neonates with unilateral multicystic dysplastic kidney. J Pediatr 2005; 146 : 759–63 12 Miller DC, Rumohr JA, Dunn RL, Bloom CAMBIO ET AL. DA, Park JM. What is the fate of the refluxing contralateral kidney in children with multicystic dysplastic kidney? J Urol 2004; 172 : 1630–4 13 Rottenberg GT, Gordon I, De Bruyn R. The natural history of the multicystic dysplastic kidney in children. Br J Radiol 1997; 70 : 347–50 14 Selzman AA, Elder JS. Contralateral vesicoureteral reflux in children with a multicystic kidney. J Urol 1995; 153 : 1252–4 15 Heymans C, Breysem L, Proesmans W. Multicystic kidney dysplasia: a prospective study on the natural history of the affected and the contralateral kidney. Eur J Pediatr 1998; 157 : 673–5 16 Rabelo EA, Oliveira EA, Diniz JS et al. Natural history of multicystic kidney conservatively managed: a prospective study. Pediatr Nephrol 2004; 19 : 1102–7 17 Rabelo EA, Oliveira EA, Silva GS, Pezzuti IL, Tatsuo ES. Predictive factors of ultrasonographic involution of prenatally detected multicystic dysplastic kidney. BJU Int 2005; 95 : 868–71 18 Narchi H. Risk of hypertension with multicystic kidney disease: a systematic review. Arch Dis Child 2005; 90 : 921–4 19 Wacksman J, Phipps L. Report of the Multicystic Kidney Registry: preliminary findings. J Urol 1993; 150 : 1870–2 20 Husmann DA. Renal dysplasia: the risks and consequences of leaving dysplastic tissue in situ. Urology 1998; 52 : 533–6 21 de Oliveira-Filho AG, Carvalho MH, Sbragia-Neto L, Miranda ML, Bustorff- Silva JM, de Oliveira ER. Wilms tumor in a prenatally diagnosed multicystic kidney. J Urol 1997; 158 : 1926–7 22 Minevich E, Wacksman J, Phipps L, Lewis AG, Sheldon CA. The Importance of accurate diagnosis and early close followup in patients with suspected multicystic dysplastic kidney. J Urol 1997; 158 : 1301–4 23 Homsy YL, Anderson JH, Oudjhane K, Russo P. Wilms tumor and multicystic dysplastic kidney disease. J Urol 1997; 158 : 2256–9 24 Oddone M, Marino C, Sergi C et al. Wilms’ tumor arising in a multicystic kidney. Pediatr Radiol 1994; 24 : 236–8 25 Dimmick JE, Johnson HW, Coleman GU, Carter M. Wilms tumorlet, nodular renal blastema and multicystic renal dysplasia. J Urol 1989; 142: 484–5 26 Hartman GE, Smolik LM, Shochat SJ. The dilemma of the multicystic dysplastic kidney. Am J Dis Child 1986; 140: 925– 8 27 Raffensperger J, Abousleiman A. Abdominal masses in children under on year of age. Surgery 1968; 63: 514–21 28 Uson AC, Del Rosario C, Melicow MM. Wilms tumor in association with cystic renal disease: report of two cases. J Urol 1960; 83: 262–6 29 Elder JS, Hladky D, Selzman AA. Outpatient nephrectomy for nonfunctioning kidneys. J Urol 1995; 154: 712–4 30 Noe HN, Marshall JH, Edwards OP. Nodular renal blastema in the multicystic kidney. J Urol 1989; 142: 486–8 31 Beckwith JB. The John Lattimer lecture. Wilms tumor and other renal tumors of childhood: an update. J Urol 1986; 136: 320–4 32 Narchi H. Risk of Wilms’ tumour with multicystic kidney disease: a systematic review. Arch Dis Child 2005; 90: 147–9 33 Yerkes EB, Adams MC, Pope J, Ct Brock JW 3rd. Does every patient with prenatal hydronephrosis need voiding cystourethrography? J Urol 1999; 162: 1218–20 34 Anonymous National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adults. The fourth report on the diagnosis, evaluation, and treatment of high blood pressure in children and adolescents. Pediatrics 2004; 114: 555–76 35 Choyke PL, Siegel MJ, Craft AW, Green DM, DeBaun MR. Screening for Wilms tumor in children with Beckwith– Wiedemann syndrome or idiopathic hemihypertrophy. Med Pediatr Oncol 1999; 32: 196–200 36 Hoyme HE, Seaver LH, Jones KL, Procopio F, Crooks W, Feingold M. Isolated hemihyperplasia (hemihypertrophy): report of a prospective multicenter study of the incidence of neoplasia and review. Am J Med Genet 1998; 79: 274–8 Correspondence: Eric A. Kurzrock, Department of Urology, 4860 Y St., Suite 3500, Sacramento, CA 95817, USA. e-mail: <script language='JavaScript' type='text/javascript'> <!-- var prefix = 'ma' + 'il' + 'to'; var path = 'hr' + 'ef' + '='; var addy61575 = 'eric.kurzrock' + '@'; addy61575 = addy61575 + 'ucdmc' + '.' + 'ucdavis' + '.' + 'edu'; document.write( '<a ' + path + '\'' + prefix + ':' + addy61575 + '\'>' ); document.write( addy61575 ); document.write( '<\/a>' ); //-->\n </script><script language='JavaScript' type='text/javascript'> <!-- document.write( '<span style=\'display: none;\'>' ); //--> </script>This email address is being protected from spam bots, you need Javascript enabled to view it <script language='JavaScript' type='text/javascript'> <!-- document.write( '</' ); document.write( 'span>' ); //--> </script> Abbreviations: MCDK, multicystic dysplastic kidney; US, ultrasonography; VCUG, voiding cysto-urethrography; WT, Wilms’ tumour; BWS, Beckwith–Wiedmann syndrome; IHH, idiopathic hemihypertrophy.

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Non surgical management of MCDK
Written by This email address is being protected from spam bots, you need Javascript enabled to view it on 2008-10-30 10:24:55
Vivid explanations. Are we sure that this will help the practioners be more aware of the cost effectiveness of the screening programme for MCDK kids?

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