ライフサイエンスコーパス: renal cyst

1 9% chance of representing a high-attenuation renal cyst.

2 rcinoma over a diagnosis of high-attenuation renal cyst.

3 creatic islet cell tumors and a premalignant renal cyst.

4 initial ultrasonographic diagnosis of simple renal cyst.

5 rized by morbidity-associated development of renal cysts.

6 tion of epithelial cells in the formation of renal cysts.

7 Most mice 6 months or older also developed renal cysts.

8 ot Hif-1alpha, suppressed the development of renal cysts.

9 er characterized by progressive expansion of renal cysts.

10 res have been implicated in the formation of renal cysts.

11 kd1 are generally normal and have few if any renal cysts.

12 10%, multiple left renal vessels, and right renal cysts.

13 eterogeneity (P <.001) than high-attenuation renal cysts.

14 e that overexpress polycystin-1 also develop renal cysts.

15 ltrasonographic (US) documentation of simple renal cysts.

16 f the peak densities of renal parenchyma and renal cysts.

17 y, result in tubular epithelial cell-derived renal cysts.

18 ary system among which 79.6% (892/1120) were renal cysts.

19 (ADPKD) is associated with the formation of renal cysts.

20 analyze activation of TMEM16A and growth of renal cysts.

21 ic hypokalemia-mediated nephrocalcinosis and renal cysts.

22 tion and may favor the development of simple renal cysts.

23 EM16A by lipid peroxidation drives growth of renal cysts.

24 opathies but share common phenotypes such as renal cysts.

25 ice were normotensive and had no evidence of renal cysts.

26 on of alpha8 integrin on epithelial cells in renal cysts.

27 and activated in cells lining PKD-associated renal cysts.

28 Renal cysts 1.0 cm or smaller showed a higher attenuatio

29 Saline-filled spheres simulating renal cysts (15 and 18 mm in diameter) were serially sus

30 old mice resulted in formation of only focal renal cysts 6 to 9 wk later but in a severe polycystic p

31 also encountered in hemorrhagic and infected renal cyst, abscess, benign neoplasms, and inflammatory

32 al consecutive measurements of total kidney, renal cyst (actual and as a percent of total volume), an

33 ll benign lesions, including pyelonephritis, renal cysts, adenomas, oncocytomas, and normal kidney, d

34 0 years and is characterized by formation of renal cysts along with the enlargement of kidneys and de

35 model features multiorgan defects including renal cysts, altered left-right laterality, and hepatobi

36 B/transcription factor 2 (HNF1B/TCF2) causes renal cyst and diabetes syndrome (OMIM #137920).

37 The 17q12 GD (diagnostic of renal cyst and diabetes syndrome) was most frequent, pre

38 gth of greater than 7.5 cm in the absence of renal cysts and a short history of renal functional dete

39 of HNF-1beta lead to a syndrome of inherited renal cysts and diabetes and are also a common cause of

40 hich harbors HNF1B, the gene responsible for renal cysts and diabetes syndrome (RCAD), in 18/15,749 p

41 betes, hence it was initially referred to as renal cysts and diabetes syndrome.

42 nal dysplasia can feature, including Fraser, renal cysts and diabetes, and Kallmann syndromes.

43 2 genes, characterized by the development of renal cysts and extrarenal complications, such as cardia

44 recapitulates NPHP-RC phenotypes, including renal cysts and hydrocephalus, which is rescued by a Wnt

45 recapitulated NPHP-RC phenotypes, including renal cysts and hydrocephalus.

46 k significantly reduces initial formation of renal cysts and kidney growth and slows the progression

47 A review of the literature regarding renal cysts and management strategies for use of cystic

48 iliopathy syndromes that are associated with renal cysts and premature renal failure are commonly the

49 ongly attenuated proliferation and growth of renal cysts and preserved renal function.

50 rome characterized by extensive formation of renal cysts and progressive renal failure.

51 associated with both hereditary and sporadic renal cysts and renal cell carcinoma, which are commonly

52 These patients often presented with renal cysts and renal function decline that preceded the

53 g5 is causally involved in hydrocephalus and renal cysts and reveal that targeted membrane delivery o

54 when accurate differentiation between small renal cysts and solid masses is critical, particularly f

55 apeutic targets to slow the formation of new renal cysts and the growth of existing cysts.

56 Considering the diverse genes that cause renal cysts and the multiorgan involvement of these dise

57 Patients with TSC often develop renal cysts and those with inherited co-deletions of the

58 Hif2a completely prevented the formation of renal cysts and tumors in Vhl/Trp53 mutant mice.

59 Renal cysts and tumors were diagnosed on the basis of de

60 onately early in patients with pretransplant renal cysts and was associated with a worse prognosis an

61 f 528 patients, 330 (62.5%) had at least one renal cyst, and 315 (59.7%) had cysts of 10 mm or less.

62 graphy is capable of measuring total kidney, renal cyst, and renal parenchymal volumes reproducibly;

63 f volumetric determinations of total kidney, renal cyst, and renal parenchymal volumes, using fast el

64 ased glycogen and lipid deposition, multiple renal cysts, and early onset of clear cell renal cell ca

65 sed an absence of distal convoluted tubules, renal cysts, and fibrosis with beta-catenin/mTOR hyperac

66 of 18-29-year-old subjects had at least two renal cysts, and five of 493 subjects aged 30-59 years h

67 that normally accompanies the development of renal cysts, and this correlated with an improvement in

68 kidneys caused by progressive development of renal cysts, and thus assessment of total kidney volume

69 Renal cysts are also a frequent manifestation.

70 Renal cysts are linked to defective silencing of Bicc1 t

71 t many more symptoms occur, and diabetes and renal cysts are not always present.

72 In all cases, renal cysts arise from renal tubular cells that lose the

73 e mutations in PRKCSH are thought to develop renal cysts as a result of somatic loss of the second al

74 masses and in the gallbladder or low-density renal cysts as controls.

75 e laterality defects of the visceral organs, renal cysts as part of nephronophthisis and congenital h

76 as kidney length and the presence of simple renal cysts assessed by ultrasound examination.

77 mutant mice were all alive and had far fewer renal cysts at this age.

78 can be differentiated from high-attenuation renal cysts at unenhanced computed tomography (CT) based

79 It is unknown how these mutations result in renal cysts, but dysregulation of calcium (Ca(2+)) signa

80 Thus, it is suggested that renal cyst-causing genes may be part of a shared functio

81 25 years ago, now referred to as the Bosniak renal cyst classification, remains pertinent to the diag

82 Glis3(zf/zf) mice form normal primary cilia, renal cysts contain relatively fewer cells with a primar

83 We conclude that regional hypoxia in renal cysts contributes to cyst growth, primarily due to

84 Although benign, ADPKD renal cysts created by the sustained proliferation of ep

85 Renal cyst development and expansion in autosomal domina

86 rast, no beneficial effects were observed on renal cyst development because of the treatment.

87 ive new insights into the pathophysiology of renal cyst development in patients.

88 ry cilium provides a potential mechanism for renal cyst development in VHL disease and may help in th

89 e previously shown that in the case of PKD1, renal cyst development is likely to require somatic inac

90 lts implicate AQP1 as a novel determinant in renal cyst development that may involve inhibition of Wn

91 tion of VHL in PEPCK-Cre mutants resulted in renal cyst development that was associated with increase

92 notypes associated with human NPH, including renal cyst development, tubular basement membrane thicke

93 ry cilium as a critical mechanism underlying renal cyst development.

94 disruption of the Ca(2+) signaling leads to renal cyst development.

95 Significant interactions were noted between renal cyst diameter, background renal attenuation, and C

96 rity proteins and renal diseases, especially renal cyst diseases.

97 ngs implicate AQP3 as a novel determinant of renal cyst enlargement and hence a potential drug target

98 he ion transport processes required to drive renal cyst enlargement has remained elusive.

99 Renal cyst enlargement in ADPKD in adults is associated

100 Our data suggest that the slowed renal cyst enlargement in AQP3 deficiency involves impai

101 Renal cyst enlargement is increased by adenosine cAMP, w

102 Recent studies suggest that renal cyst epithelial cells actively secrete Cl across t

103 These results demonstrate that some renal cyst epithelial cells exhibit clonal chromosomal a

104 ly 1 in 500 people, in which accumulation of renal cysts eventually destroys kidney function.

105 enal tubule development during the time when renal cysts first appear in PKD kidneys and that PKD-def

106 synergy of an Smac-mimetic and TNF-alpha in renal cyst fluid, that attenuates cyst development, prov

107 nhibitor SKI-606 resulted in amelioration of renal cyst formation and biliary ductal abnormalities in

108 , a common genetic disorder characterized by renal cyst formation and extrarenal complications such a

109 The former includes induction of renal cyst formation and interstitial fibrosis while the

110 pel-Lindau associated mechanisms involved in renal cyst formation and renewed appreciation for the in

111 flox/flox);Cdh16-Cre mutant mice resulted in renal cyst formation and severe stromal fibrosis, while

112 e earliest cellular defects occurring during renal cyst formation because its kidney (the pronephros)

113 Renal cyst formation begins at embryonic day 15.5 (E15.5

114 We hypothesize that primary cilia prevent renal cyst formation by suppressing pathologic tubular c

115 fore, this study sought to determine whether renal cyst formation could be prevented by genetic compl

116 ression is both necessary and sufficient for renal cyst formation in ADPKD, suggesting that PKD2 occu

117 roliferation in human ADPKD cells and blocks renal cyst formation in an adult and a neonatal PKD mous

118 een proposed to explain the focal nature for renal cyst formation in autosomal dominant polycystic ki

119 ding Crb3 and Wwtr1/Taz, have been linked to renal cyst formation in mice before.

120 Cilia dysfunction contributes to renal cyst formation in multiple human syndromes includi

121 kouts of Pkd1 and Sirt1 demonstrated delayed renal cyst formation in postnatal mouse kidneys compared

122 Extensive renal cyst formation in these mice is accompanied by bro

123 n, R2b resident macrophage accumulation, and renal cyst formation in two mouse models of cystic disea

124 ermine whether CFTR activity is required for renal cyst formation in vivo.

125 expression of the human PC1 tail results in renal cyst formation in zebrafish embryos.

126 leading from primary ciliary dysfunction to renal cyst formation is unknown.

127 g of the importance of the primary cilium in renal cyst formation may guide potential therapy for cys

128 Currently, the mechanism for renal cyst formation remains unclear.

129 enal injury can also markedly accelerate the renal cyst formation that occurs after disruption of cil

130 This syndrome, in addition to renal cyst formation, includes the presence of an invari

131 1 and PKD2 genes, and it is characterized by renal cyst formation, inflammation and fibrosis.

132 c kidney disease (ADPKD) is characterized by renal cyst formation, inflammation, and fibrosis.

133 ific knockout of polycystin-1 caused massive renal cyst formation, kidney enlargement, and severe kid

134 increased renal hypertrophy and accelerated renal cyst formation, leading to renal dysfunction.

135 Because the primary cilium suppresses renal cyst formation, loss of the cilium may be an initi

136 n of PKD1 or PKD2 in mouse models results in renal cyst formation, suggesting that the quantity of PC

137 s the contribution of the PDE1A subfamily to renal cyst formation, we examined the expression and fun

138 t is directly part of the disease pathway of renal cyst formation, we used a genetic approach to intr

139 g cilia proteins have an established role in renal cyst formation.

140 cription factor implicated in cAMP-dependent renal cyst formation.

141 tructural and functional hypertrophy without renal cyst formation.

142 ilia genes, in response to tissue damage and renal cyst formation.

143 hile activation of mTOR has been observed in renal cysts from ADPKD patients, Pkd1(-/-) MEFs did not

144 tudy may help differentiate high-attenuation renal cysts from renal cell carcinomas at unenhanced CT

145 in-1 (PC1) mutations result in proliferative renal cyst growth and progression to renal failure in au

146 These results implicate CFTR in renal cyst growth and suggest that CFTR inhibitors may h

147 st the involvement of HIF1alpha in promoting renal cyst growth and suggest that the formation of simp

148 SMYD2 deficiency delayed renal cyst growth in postnatal kidneys from Pkd1 mutant

149 orter 1, and report that HIF-1alpha promotes renal cyst growth in two in vitro cyst models-principal-

150 Renal cyst growth is, at least in part, driven by the pr

151 sage resulted in a significant inhibition of renal cyst growth while maintaining more normal renal st

152 in ADPKD and PKD mouse models and may drive renal cyst growth, but the mechanisms leading to persist

153 ethyltransferase activity, as a regulator of renal cyst growth.

154 erized by kidney failure caused by bilateral renal cyst growth.

155 ed YAP-mediated transcriptional activity and renal cyst growth.

156 ngly suppressed STAT3 activation and reduced renal cyst growth.

157 ions in PKD1 and PKD2 in a minority of human renal cysts has led to the proposal that such mutations

158 iver anomalies have been carefully detailed, renal cysts have yet to be fully characterized in inv/in

159 targeting replicated limb malformations and renal cysts identical to the models of established disea

160 d1 mutants invariably develop pancreatic and renal cysts if they survive to day 15.5 post coitum and

161 range, 23-90 years) and 56 high-attenuation renal cysts in 51 patients (30 men and 21 women; average

162 sts and have used it to show that individual renal cysts in ADPKD are monoclonal.

163 le, protein-rich, hemorrhagic, and enhancing renal cysts in an in vitro phantom through simultaneous

164 on, promoting the progressive enlargement of renal cysts in autosomal dominant polycystic kidney dise

165 mTOR inhibition ameliorated renal cysts in both the embryonic and adult zebrafish mo

166 aging depicted an increased number of simple renal cysts in healthy individuals because of its increa

167 xpression may contribute to the formation of renal cysts in humans with MODY5.

168 ion markers were co-expressed with p-Creb in renal cysts in Itf88 knockout mice subjected to ischemia

169 d been shown that glucocorticoids can induce renal cysts in the neonatal rodent, only when given at a

170 ull mutant for galectin-3 had more extensive renal cysts in vivo.

171 as inversely correlated with the severity of renal cysts in young adult zebrafish, suggesting a prima

172 increases, and the number and size of simple renal cysts increase with age.

173 Attenuation values in the renal cysts increased artifactually on contrast-enhanced

174 deletion mutant in transgenic mice produces renal cysts, increased cell proliferation, and dilatatio

175 ice resulted in the transformation of benign renal cysts into a hyperplastic lesion, suggesting that

176 mal-dominant PLD (ADPLD) with no or very few renal cysts is a separate disorder caused by PRKCSH, SEC

177 If only simple renal cysts larger than 1 cm are considered, US criteria

178 None of the renal cysts larger than 1.0 cm demonstrated an increase

179 We found that renal cyst-lining cells highly express the folate recept

180 bulin receptor (pIgR) is highly expressed by renal cyst-lining cells.

181 The most common lesions were renal cysts, liver hemangiomas, liver cysts, thyroid nod

182 we demonstrate that targeting antibodies to renal cyst lumens is possible with the use of dimeric Ig

183 dies that are not expected to gain access to renal cyst lumens.

184 th cilia dysfunction, including retinopathy, renal cysts, male infertility, and a deficit in olfactio

185 Renal cysts may negatively impact outcomes with SWL.

186 Pseudoenhancement of renal cysts may occur if helical CT is performed during

187 creas, aorta, kidney, 0- and 50-HU cylindric renal cysts, muscle, and fat.

188 tween the copeptin level and the presence of renal cysts (odds ratio, 1.6; 95% CI, 1.1 to 2.4; P=0.02

189 ted with abrogation of the primary cilium in renal cysts of patients with VHL disease and in VHL-defe

190 ed absence of polycystin-2 expression in the renal cysts of Pkd2+/- mice.

191 ted with progressive enlargement of multiple renal cysts, often leading to renal failure that cannot

192 ns that causes the formation of fluid-filled renal cysts, often leading to renal failure.

193 cause of the detection of stage I ("simple") renal cysts on computed tomography.

194 de important insights into the mechanisms of renal cyst pathogenesis and lead to better approaches fo

195 Because the development of renal cysts precedes tumor formation, and because the dy

196 To prospectively determine the dependence of renal cyst pseudoenhancement on multidetector computed t

197 ages at an optimal energy level can overcome renal cyst pseudoenhancement.

198 The progressive growth and expansion of the renal cysts replace existing renal tissue within the ren

199 a mutation in the inv gene (inv/inv) develop renal cysts resembling autosomal-recessive polycystic ki

200 The inv mutant mouse has renal cysts resembling infantile NPHP2 and will provide

201 ciliopathies, presenting symptoms including renal cysts, retinal degeneration, and situs inversus [7

202 ontrol of a kidney-specific promoter develop renal cysts, similarly to humans with MODY5.

203 All of the renal cysts stained for epithelial membrane antigen, whi

204 ase presented here, 131I activity within the renal cyst supports the concept that iodide is subject t

205 Men (mean, 2.0; 95% CI: 1.5, 2.5) had more renal cysts than women (mean, 1.2; 95% CI: 0.9, 1.5) (P

206 Mutants develop embryonic renal cysts that appear indistinguishable from mice comp

207 failure, caused by appearance and growth of renal cysts that can lead to renal failure in middle age

208 ases are characterized by numerous bilateral renal cysts that continuously enlarge and, through compr

209 isease (ADPKD) is characterized by bilateral renal cysts that lead to a decline in kidney function.

210 zed by the development of multiple bilateral renal cysts that replace normal kidney tissue.

211 st that the formation of simple and atypical renal cysts that resemble ccRCC precursor lesions is gre

212 gressive expansion of bilateral fluid-filled renal cysts that ultimately lead to renal failure.

213 carcinomas and 37 high-attenuation (>20 HU) renal cysts that were at least 1 cm in diameter were ret

214 rized by the formation of multiple bilateral renal cysts, the progressive accumulation of extracellul

215 calization in a previously unsuspected large renal cyst; the lesion was not visualized on routine pre

216 e cilia were short and malformed, whereas in renal cysts they appeared normal.

217 quired for the progression of VHL-associated renal cysts to clear cell renal cell carcinoma.

218 om the Pkd1 knockout mice showed no apparent renal cysts, tubule dilation, or increased cell prolifer

219 logical and histological diagnosis of benign renal cysts versus cystic RCC, adenoma versus RCC, and o

220 cant correlation between rate of increase in renal cyst volume and the rate of decline in GFR.

221 At entry, total kidney and renal cyst volumes correlated positively with age, while

222 l volumes reproducibly; (2) total kidney and renal cyst volumes increase, while parenchymal volumes d

223 ring the 8 yr of follow-up, total kidney and renal cyst volumes increased, while renal parenchymal vo

224 The rate of increase in total kidney and renal cyst volumes varied markedly from patient to patie

225 olycystic kidney disease, the progression of renal cysts was examined in cpk mutants carrying one or

226 tage of enhancement at MR imaging for the 50 renal cysts was less than 5%; for the 50 renal tumors, i

227 le, protein-rich, hemorrhagic, and enhancing renal cysts was scanned with an experimental grating-bas

228 itivity for renal tumors and specificity for renal cysts were established by using percentage of enha

229 presence of growth factors in the lumens of renal cysts, which are enclosed spaces lacking connectio