Collecting Duct Origin Research Articles

A possible critical dosing period of p-cumylphenol for development of cystic kidneys in rat neonates.

In accordance with a previous report on cystic kidneys induced in rat neonates when dosed with p-cumylphenol (PCP) for 18 days from postnatal day (PND) 4, 3 rat neonates were dosed with PCP once a day for 14 days, either from PND 14, 21, 28, 35, or 42 as W2, W3, W4, W5, and W6 groups, respectively, to investigate whether dosing periods in different PNDs influenced the development of cystic renal tubules. The lesion was striking in the W2 group and at a lesser magnitude in the W3 group, whereas either kidney was unaffected when dosing was initiated beyond PND 28. These findings, together with the results from the previous study, suggested that PND 14-28 is a critical dosing period for PCP to develop cystic kidneys in rat neonates. The lining epithelium of the cystic tubules was immunohistochemically positive for AQP2. This finding and the anatomical location indicated that the cystic tubules were of collecting duct origin. Either obstruction, fluid accumulation, or reparative hyperplasia of the lining epithelium was unlikely to be involved in the formation of cystic tubules lined with a monolayer of cuboidal or columnar epithelium with a high nuclear density. Thus, the follow-up investigation on PCP suggested a critical dosing period of PND 14-28 in rat neonates for the development of cystic dilation of renal collecting ducts. This study further supports that additive hyperplasia of the lining epithelium is a fundamental basis of this unique lesion.

Solid renal tumours of collecting duct origin in patients on chronic lithium therapy.

BackgroundLithium (Li) is an invaluable drug for the treatment of bipolar disorder. Long-term Li use is associated with renal complications including the formation of uncomplicated renal cysts caused by proliferation and expansion of collecting duct (CD) cells. We report six patients with complicated renal cysts in the context of Li nephropathy.MethodsOver a time period of 15 years, we have identified six patients with one or more solid renal tumours in our population of approximately 50 patients with chronic Li nephropathy. In this study we describe the clinical and pathological characteristics of these Li-related tumours.ResultsAll patients were on Li therapy for over 10 years and suffered from varying degrees of Li nephropathy. The tumours were all of CD origin and comprised both oncocytomas and collecting duct carcinomas. The CD carcinomas differed from the very rare “classical” CD cell carcinomas in histological appearance, multifocal presentation and non-aggressive clinical behaviourConclusionsThe increased incidence of CD derived tumours and atypical presentation of CD cell carcinomas in patients with chronic Li nephropathy suggests that Li predisposes to the development of these tumours. We hypothesize that prolonged stimulation of CD cell proliferation and expansion by Li not only causes cyst formation, but can eventually induce the formation of adenomas and carcinomas. Increased awareness of a possible relationship between chronic Li therapy and renal neoplasms, will enhance the knowledge on epidemiology, clinical behavior and optimal therapy for the Li-related renal neoplasms.

Tubulocystic carcinoma of the kidney

Examples of tubulocystic carcinoma of the kidney were introduced in an abstract presented at the Annual Meeting of the United States and Canada Academy of Pathology1 and also in the Armed Forces Institute of Pathology Atlas of Tumor Pathology, Series III, in 1994.2 However, the morphological features of this rare distinctive renal tumor were described in 1955 byMasson, who designated the lesion a “Bellinian epithelioma” because he regarded it as a neoplasm originating in the collecting ducts of Bellini. The first detailed report of the clinical and pathological details of tubulocystic carcinoma were published in 1997.3 The authors described the neoplasm as a “low-grade mucinous tubulocystic renal carcinoma of possible collecting duct origin”. The cases were initially considered to be derived from the collecting duct; however, since those reported tumors were of a low-grade malignancy, the behavior of which significantly differed from the classical highly aggressive collecting duct carcinomas, the term “low-grade collecting duct carcinoma” was coined for this peculiar renal tumor. Thereafter, with more cases showing similar clinical and pathological features, the name of the neoplasm was designated “tubulocystic carcinoma” to denote the specific morphology.4e8 To date, more than 50 cases have been reported. A review of the literature showed a male predominance (of around 7:1) with patient ages ranging from 34 years to 74 years. Tumor sizes range from 0.3 cm to 17 cm, but most are small and discovered incidentally. Tumors tend to present in a low stage (pT1a) and behave indolently. However, sarcomatoid change,9 and metastases to lymph nodes, lungs, and brain were reported.7

Tight junction composition is altered in the epithelium of polycystic kidneys

Kidney cysts in autosomal dominant polycystic kidney disease (ADPKD) undergo progressive enlargement together with luminal fluid secretion. This involves active, uphill transcellular Cl(-) transport which drives passive Na(+) and water secretion. Implicit in this mechanism is the assumption that the paracellular permeability of the cyst epithelium to Cl(-) must be very low. Claudins are tight junction (TJ) transmembrane proteins that determine the ion selectivity of paracellular barriers. The aim of this study was to determine the expression and localization of claudins within renal cysts in a mouse hypomorphic model of ADPKD and in human patients. We found that the majority of cysts were of collecting duct origin. Claudins normally expressed in collecting duct (3, 4, 7, 8, and 10) were found in small cysts. However, only claudin-7 persisted at substantive levels in the dedifferentiated epithelium of large, presumably late-stage cysts, where it was localized both at the TJ and basolaterally. The constitutively expressed TJ proteins, ZO-1 and occludin, were also abundantly expressed and correctly localized, suggesting that the basic infrastructure of the TJ is preserved. A previous study suggested that claudin-7 may function as a paracellular Cl(-) barrier. We postulate that the role of claudin-7 in ADPKD is to seal the paracellular route in Cl(-)-secreting cyst epithelium, preventing backleak of Cl(-), and that it thereby plays a permissive role in fluid secretion and cyst growth.

Polycystic kidney disease: genes, proteins, animal models, disease mechanisms and therapeutic opportunities

An increased understanding of the genetic, molecular and cellular mechanisms responsible for the development of polycystic kidney disease has laid out the foundation for the development of rational therapies. Many animal models where these therapies can be tested are currently available. This review summarizes the rationale for these treatments, the results of preclinical trials and the prospects for clinical trials, some already in early phases of implementation.

Early Embryonic Renal Tubules of Wild-Type and Polycystic Kidney Disease Kidneys Respond to cAMP Stimulation with Cystic Fibrosis Transmembrane Conductance Regulator/Na+,K+,2Cl− Co-Transporter–Dependent Cystic Dilation

Metanephric organ culture has been used to determine whether embryonic kidney tubules can be stimulated by cAMP to form cysts. Under basal culture conditions, wild-type kidneys from embryonic day 13.5 to 15.5 mice grow in size and continue ureteric bud branching and tubule formation over a 4- to 5-d period. Treatment of these kidneys with 8-Br-cAMP or the cAMP agonist forskolin induced the formation of dilated tubules within 1 h, which enlarged over several days and resulted in dramatically expanded cyst-like structures of proximal tubule and collecting duct origin. Tubule dilation was reversible upon withdrawal of 8-Br-cAMP and was inhibited by the cAMP-dependent protein kinase inhibitor H89 and the cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor CFTR(inh)172. For further testing of the role of CFTR, metanephric cultures were prepared from mice with a targeted mutation of the Cftr gene. In contrast to kidneys from wild-type mice, those from Cftr -/- mice showed no evidence of tubular dilation in response to 8-Br-cAMP, indicating that CFTR Cl(-) channels are functional in embryonic kidneys and are required for cAMP-driven tubule expansion. A requirement for transepithelial Cl(-) transport was demonstrated by inhibiting the basolateral Na(+),K(+),2Cl(-) co-transporter with bumetanide, which effectively blocked all cAMP-stimulated tubular dilation. For determination of whether cystic dilation occurs to a greater extent in PKD kidneys in response to cAMP, Pkd1(m1Bei) -/- embryonic kidneys were treated with 8-Br-cAMP and were found to form rapidly CFTR- and Na(+),K(+),2Cl(-) co-transporter-dependent cysts that were three- to six-fold larger than those of wild-type kidneys. These results suggest that cAMP can stimulate fluid secretion early in renal tubule development during the time when renal cysts first appear in PKD kidneys and that PKD-deficient renal tubules are predisposed to abnormally increased cyst expansion in response to elevated levels of cAMP.

Calcium phosphate–induced renal epithelial injury and stone formation: Involvement of reactive oxygen species

Crystal formation and retention are critical events for the formation of kidney stones. Oxalate and calcium oxalate (CaOx) crystals are injurious to renal epithelium, and membranes of injured cells promote crystal adherence and retention. Calcium phosphate (CaP) is the most common crystal in both urine and stones, most likely to form in the early segments of the nephron and can nucleate CaOx in a metastable solution. We hypothesized that CaP can also injure the renal epithelial cells. We exposed proximal tubular origin line derived from pig proximal tubules (LLC-PK1), and collecting duct origin Madin-Darby canine kidney (MDCK) cell lines to various concentrations of Brushite (Br) crystals and investigated staining with Trypan Blue and the release of lactate dehydrogenase (LDH) into the medium as an indicator of injury. In order to determine the involvement of reactive oxygen species, we also measured LDH release in the presence of superoxide dismutase (SOD) and production of hydrogen peroxide (H2O2) and 8-isoprostane (8-IP) in the presence of the catalase. Exposure to Br crystals was associated with LDH release by both cell types, induced the production of H2O2 and 8-IP. Presence of SOD and catalase reduced LDH release as well as staining with trypan blue. Catalase was also associated with reduced production of H2O2 and 8-IP. Brushite crystals are injurious to cells of both the proximal tubules as well as collecting ducts. Injury is mediated by reactive oxygen species. We propose that CaP crystals can independently interact with renal epithelium, promote sites for crystal attachment, and then either grow into mature CaP stones or create sites for CaOx crystal nucleation, retention, and stone development.

Low-Grade Tubular-Mucinous Renal Neoplasms: Morphologic, Immunohistochemical, and Genetic Features

The current classification system of renal tumors is based on morphologic criteria, as supported by genetic findings. We present a group of previously unclassified tumors with similar morphologic and genetic features, suggesting a new entity within renal neoplasms. Seven renal tumors from five patients (ages 31–67 years) were analyzed. All cases were stained with periodic acid–Schiff, Hale's colloidal iron (HCI), and Alcian blue (AB) at pH 2.5/1.0 with and without hyaluronidase (HA) digestion. Immunohistochemical (IHC) stains were performed for CK8, CK18, CK19, vimentin, villin, Tamm-Horsfall protein (THP), renal cell carcinoma marker (RCC), epithelial membrane antigen (EMA), ulex europaeus agglutinin (UEA-1), soy bean agglutinin (SBA), peanut agglutinin (PNA), and MIB-1. Comparative genomic hybridization (CGH) and loss of heterozygosity (LOH) studies were performed on all cases. All tumors showed circumscribed growth, a tubular growth pattern with focal solid areas, no significant nuclear atypia and absence of necrosis, desmoplasia, or inflammation. Abundant extracellular mucin was present. Immunohistochemistry stains support collecting duct origin (EMA+, PNA+, SBA±, CK 8/18/19+, vimentin±, UEA-1−, RCC−, villin−, THP−). The proliferative rate was low (<1%). CGH showed multiple consistent chromosomal losses (−1,-4, −6, −8, −9, −13, −14, −15, −22). Clinical outcome was favorable, with recurrences but no known distant metastases or death of disease. These findings are distinct from all previously classified renal neoplasms. Our data suggest the presence of a unique tumor entity within tumors of probable collecting duct origin: tubular-mucinous renal tumors of low malignant potential.

Renal pathology of polycystic kidney disease and concurrent hereditary nephritis in Bull Terriers.

To describe the renal lesions in Bull Terrier polycystic kidney disease (BTPKD), to confirm that the renal cysts in BTPKD arise from the nephron or collecting tubule, and to identify lesions consistent with concurrent BTPKD and Bull Terrier hereditary nephritis (BTHN). Renal tissue from five Bull Terriers with BTPKD and eight control dogs was examined by light and transmission electron microscopy. Clinical data were collected from all dogs, and family history of BTPKD and BTHN for all Bull Terriers. In BTPKD the renal cysts were lined by epithelial cells of nephron or collecting duct origin that were usually squamous or cuboidal, with few organelles. They had normal junctional complexes, and basal laminae of varying thicknesses. Glomeruli with small, atrophic tufts and dilated Bowman's capsules, tubular loss and dilation, and interstitial inflammation and fibrosis were common. Whereas the lesions seen in BTHN by light microscope were nonspecific, the presence of characteristic ultrastructural glomerular basement membrane (GMB) lesions and a family history of this disease indicated concurrent BTHN was likely in three of five cases of BTPKD. This paper provides evidence that renal cysts in BTPKD are of nephron or collecting duct origin. In addition, GBM lesions are described that strongly suggest that BTPKD and BTHN may occur simultaneously.

Low-grade Collecting Duct Carcinoma Of The Kidney: A Potential Mimic Of Conventional Clear Cell Carcinoma

Collecting duct carcinoma of the kidney is a well-known, but relatively uncommon tumor characterized by a high cytologic grade, desmoplastic stroma and a poor clinical outcome. Since 1979, however, there have been several reports of low-grade renal carcinoma of putative collecting duct origin. These low-grade tumors were extensively papillary, tubulopapillary or tubulocystic, with a low nuclear grade (usually Furhman grade 1 or 2). Most have conferred a benign follow-up course, even when treated only by partial nephrectomy. The previous reports of such tumors have been variably characterized immunohistochemically and ultrastructurally. We report the cases of a low-grade renal carcinoma of collecting duct origin, arising in the right renal lower pole of a 47-year-old-male with a history of gout and nephrolithiasis. Microscopically, the tumor showed a tubular and tubulocystic pattern and was composed almost exclusively of clear cells, closely mimicking conventional (clear cell) renal cell carcinoma. Tumor cells stained positively for PAS, showed droplet-like staining with Hale\'s colloidal iron, were variably alcian blue positive and were mucicarmine negative. They were reactive with immunohistochemical antibodies to peanut agglutinin (PNA), Ulex europaeus-1 agglutinin (UEA-1), pan-cytokeratin, CAM 5.2, cytokeratin 7, epithelial membrane antigen (EMA) and vimentin. Electron microscopy showed microvillous-lined tubules, desmosomes, and tonofilaments, with a paucity of mitochondria. The patient was treated by partial nephrectomy and has been without evidence of disease for a follow-up period of 10 months.

Low-grade collecting duct carcinoma of the kidney: report of 13 cases of low-grade mucinous tubulocystic renal carcinoma of possible collecting duct origin

To assess the nature of a series of unusual low-grade mucin-producing tubulocystic renal cancers diagnosed at the Mayo Clinic since 1985. We reviewed the clinical, radiologic, and pathologic features of 13 unusual low-grade renal carcinomas with features most suggestive of collecting duct origin. In 8 cases, the tumor was discovered incidentally. Presenting symptoms in the other 5 patients were similar to those of typical renal carcinoma. Imaging studies and angiography disclosed solid, cystic, or complex masses that were relatively avascular. Pathologic assessment revealed good circumscription, minimal hemorrhage and/or necrosis, minimal tendency to extend beyond the kidney, tubulocystic architecture, a fibrotic interface with adjacent normal renal parenchyma, low nuclear grade, and minimal mitotic activity. Mucin production was noted in all evaluable cases. All tumors expressed keratins AE1/AE3 and/or Cam 5.2. The tumors showed immunoreactivity to antibodies directed against keratin 34 beta E12 (8 of 13 cases), and Ulex Europeus antigen 1 (6 of 10 cases). Follow-up ranged from 12 to 114 months (mean 62). No metastases occurred in 12 patients. One patient died of metastatic carcinoma morphologically identical to the primary renal neoplasm 46 months after his tumor had been misinterpreted as a benign condition. We believe the tumors described in this article may be of collecting duct origin, representing the low-grade end of a spectrum of cancers arising in collecting duct epithelium.

Bradykinin-induced translocation of cytoplasmic phospholipase A2in MDCK cells

The nonapeptide bradykinin (BK) plays an important role in the production of eicosanoids within the collecting duct of the nephron. We have shown previously that BK can initiate a complex signaling cascade that causes the release of arachidonic acid (AA) from MDCK-D1 cells, a canine cell line of distal tubule and collecting duct origin. This release is dependent upon early activation of specific upstream enzymes, including phosphatidylcholine-specific phospholipase C (PC-PLC) and phospholipase D (PLD). Ultimately, the release of this precursor of eicosanoids is effected by recruitment of the cytoplasmic 85-kDa form of phospholipase A2 (cPLA2). This enzyme is thought to translocate from the cytosol to cellular membranes following stimulation by agonists that cause elevations of intracellular calcium ([Ca2+]i). The present study was undertaken to examine the dependence of AA release upon Ca2+ influx in BK-stimulated MDCK cells. For this purpose, cells were incubated with 1 microM BK for 1 min and lysed in Ca(2+)-free Tris buffer. The high-speed 100000 x g pellet was extracted with 10 mM octyl glucoside and the cPLA2 protein level was determined. Previous results from our laboratory indicated that BK induced a 1.81-fold increase in cPLA2 activity associated with cellular membranes, while in the present study, Western blotting with a specific cPLA2 antibody demonstrated a similar elevation in protein detected with these same membranes. A selective inhibitor of receptor-mediated Ca2+ entry, SK&F 96365, was used to resolve the role of extracellular Ca2+ in BK's ability to evoke AA release. Pretreatment of cells with SK&F 96365 resulted in an inhibition of greater than 60% of the BK response. Taken together, these results strongly suggest that BK-mediated AA release in MDCK-D1 cells is at least partly contingent upon translocation of cPLA2 to membranes initiated by an influx of extracellular Ca2+.

Expression of E‐ and N‐cadherin in renal cell carcinomas, in renal cell carcinoma cell lines in vitro and in their xenografts

E- and N-cadherins are proteins involved in intercellular adhesion and are localized, e.g., in the adherens junctions of epithelial cells. Kidney tubules express these molecules in a distinctive pattern, the expression of N-cadherin being restricted to proximal tubules and that of E-cadherin to distal tubules and collecting ducts. Renal cell carcinomas (RCCs) and oncocytomas are considered to originate from these tubular epithelia. To find out whether cadherins could serve as markers for a cellular origin of these tumors, we studied the expression of E- and N-cadherins in RCCs and oncocytomas, in cell lines derived from RCCs as well as in tumors grown in nude mice. Most RCCs co-expressed E- and N-cadherins, as did 2 of the 4 cell lines studied. The expression pattern did not correlate with the histological grade of the tumors, and even the least differentiated tumors, as well as metastases, showed expression of cadherins. Renal oncocytomas expressed E-cadherin but not N-cadherin, which is in line with previous studies that have proposed a collecting duct origin for these tumors. Papillary renal neoplasms, a separate entity usually not classified as RCC, expressed neither of the cadherins studied despite the abundant expression of beta-catenin. Our results suggest that most RCCs co-express the characteristic adhesion molecules of both proximal and distal tubules, which makes it questionable whether the origin of these tumors can be reliably located to any distinct part of the renal tubule. Our results also suggest that in RCCs the increased histological grade is not directly associated with changes in the expression of either of the cadherins, indicating other mechanisms underlying the deficient capacity to form polarized tubular structures.

Atypical renal adenocarcinoma with features suggesting collecting duct origin and mimicking a mucinous adenocarcinoma

We report a case of an atypical renal adenocarcinoma of the renal medulla associated with a marked desmoplastic response and interstitial mucin production. Collecting duct epithelium of the renal medulla throughout the kidney showed cytologic atypia. These features have been described by others as suggestive of a collecting duct histogenesis. This case represents the fifteenth reported case known to us of a renal adenocarcinoma of collecting duct origin. Prior reports, however, have not described the extensive mucin production that may be associated.

Renal cellular biology of growth hormone and insulin-like growth factor I.

Growth hormone (GH) and insulin-like growth factor I (IGF-I) exert a variety of actions in renal tissue. To shed light upon the renal GH-IGF I axis we have characterized the cell biology of GH and IGF I in two parts of the nephron that are targets for these peptides, proximal tubule and collecting duct. Receptors for both GH and IGF I are present in the basolateral membrane of the renal proximal tubular cell. GH activates phospholipase C and IGF I stimulates phosphorylation of its receptor at this site. Both peptides directly enhance gluconeogenesis in proximal tubule. GH stimulates IGF I gene expression in collecting duct. IGF I of collecting duct origin could act as a paracrine growth factor in other portions of the nephron. IGF I may be causative of renal hypertrophy that occurs in the settings of hypersomatotropism, unilateral nephrectomy (compensatory hypertrophy) and diabetes mellitus.

Mechanisms of Endothelin-1 mRNA and Peptides Induction by TGF-β and TPA in MDCK Cells

Mechanisms of prepro-ET-1 mRNA expression and mature endothelin-1 (ET-1) peptide secretion in MDCK cells (dog collecting duct origin) were investigated. MDCK cells constitutively expressed prepro-ET-1 mRNA (approximately 2.3 kb). TGF-beta time-dependently increased prepro-ET-1 mRNA levels between 30 min and 6 h. Induction of the mRNA 6 h following TGF-beta addition was dose-dependent with a half-maximal concentration of 10 pM. The half-life of prepro-ET-1 mRNA was 15 min in controls when the cells were treated with 10 micrograms/ml of actinomycin D, whereas it was extended to 30-45 min by TGF-beta treatment. Prepro-ET-1 mRNA was rapidly (15-30 min) induced by 0.5 microM TPA, one of the phorbol esters, but downregulated below baseline after 1 h. Our data show that MDCK cells constitutively secrete ET-1 and increase its production in response to TGF-beta. An axis of TGF-beta-ET-1-collecting duct may play an important role in regulation of electrolyte transport and cell growth of the renal tubules.

Growth hormone stimulates IGF I gene expression in isolated rat renal collecting duct

To determine whether growth hormone (GH) directly stimulates insulin-like growth factor I (IGF I) gene expression in renal collecting duct, plasma membranes prepared from collecting ducts isolated from rat kidney, and collecting ducts themselves were incubated in presence and absence of GH. GH enhanced phospholipase C activity in collecting duct plasma membranes establishing the potential for GH-signal transduction. Inclusion of GH in suspensions of collecting ducts increased production of immunoreactive IGF I in a time-dependent and concentration-dependent manner. Production was stimulated significantly by addition of 10(-10), 10(-8), or 10(-6) M GH to suspensions for 2 h. IGF I produced in isolated collecting ducts was released into the suspending media. Levels of IGF I mRNA in collecting ducts were increased 2.8-fold after incubation with 10(-6) M GH in vitro. IGF I of collecting duct origin was indistinguishable from recombinant human IGF I in terms of its size and receptor-binding characteristics. Our findings demonstrate a direct action of GH to enhance collecting duct IGF I gene expression in vitro. Such enhancement is likely to reflect the mechanism by which GH stimulates renal IGF I production in intact kidney.

Collecting duct origin of rat renal clear cell tumors

The renal tubular segment from which clear cell tumors originate was investigated in the kidneys of rats treated with N-nitrosomorpholine. This tumor type, which in the rat closely resembles that in man, is made up of clear and granular acidophilic cells and arises from tubules lined by clear cells. The tubular origin of the tumors was established in serial sections by demonstrating connections between both clear cell tumors and tubules lined by clear cells, and renal tubules of normal appearance. In 45 clear cell lesions (17 tumors and 28 tubules) one or more such connections were identified which belonged to the collecting system. In accordance with their localisation in the kidney, the clear cell lesions were connected predominantly to tubules of the cortical collecting system and occasionally to outer medullary collecting ducts. As previously reported, oncocytic tubules and microoncocytomas were observed to originate from the same portions of the collecting system. Rarely, microadenomas and tubules consisting of both oncocytes and clear or granular acidophilic cells were also observed in the kidneys studied.

Renal cystic disease of infancy: results of histochemical studies. A report of the Southwest Pediatric Nephrology Study Group.

Histochemical techniques utilizing Tetragonolobus lotus (proximal tubules), Arachis hypogaea (distal nephron, i.e., distal convoluted tubules and collecting ducts), and antibodies against Tamm-Horsfall protein (thick ascending limbs of Henle) were used to determine the site of origin of renal cysts in five children with autosomal recessive polycystic kidney disease (ARPKD) and three patients with glomerulocystic disease (GCD) presenting in the 1st year of life. The findings support a distal nephron origin for the cysts in the children who had ARPKD, whereas the majority of cysts in the children with GCD were confirmed as having a glomerular origin. Tamm-Horsfall protein was identified in the cysts of both ARPKD and GCD; this finding suggests free communication between some of the cysts with the thick ascending limb of Henle. An unexpected finding was the frequent presence of cysts surrounded by muscle fibers. We suggest that these cysts are of collecting duct origin.

Collecting Duct Origin of Multilocular Renal Cyst by Peroxidase-Labelled Lectin Studies

Collecting Duct Origin of Multilocular Renal Cyst by Peroxidase-Labelled Lectin Studies