ライフサイエンスコーパス: polycystic kidney disease

1 ithelial pancreatic neoplasia, and 1 case of polycystic kidney disease.

2 in either protein causing autosomal dominant polycystic kidney disease.

3 arget in the treatment of autosomal dominant polycystic kidney disease.

4 trarenal manifestation in autosomal dominant polycystic kidney disease.

5 g therapeutic strategy in autosomal dominant polycystic kidney disease.

6 ions to human PC2 (hPC2) are associated with polycystic kidney disease.

7 hannel that is mutated in autosomal dominant polycystic kidney disease.

8 2), respectively, lead to autosomal dominant polycystic kidney disease.

9 plains both renal and vascular phenotypes in polycystic kidney disease.

10 l diseases, such as diabetic nephropathy and polycystic kidney disease.

11 pathway result in deranged ciliogenesis and polycystic kidney disease.

12 humans and mice, nephronophthisis (NPHP) and polycystic kidney disease.

13 st, urine podocyte mRNAs did not increase in polycystic kidney disease.

14 a Ca(2+)-dependent channel with relevance to polycystic kidney disease.

15 obulin A nephropathy, and autosomal dominant polycystic kidney disease.

16 Persons with early autosomal dominant polycystic kidney disease.

17 2, the protein mutated in autosomal dominant polycystic kidney disease.

18 for approximately 15% of autosomal dominant polycystic kidney disease.

19 ice, a model that mimics autosomal recessive polycystic kidney disease.

20 C1) is the major cause of autosomal dominant polycystic kidney disease.

21 aintenance of tubule diameter correlate with polycystic kidney disease.

22 also suggest insight into the development of polycystic kidney disease.

23 cium signaling and causes autosomal dominant polycystic kidney disease.

24 ssociates with accelerated cyst formation in polycystic kidney disease.

25 ction has been linked to the pathogenesis of polycystic kidney disease.

26 kinesis defects in both mice and humans with polycystic kidney disease.

27 y mutated or truncated in autosomal dominant polycystic kidney disease.

28 ne proteins implicated in autosomal dominant polycystic kidney disease.

29 disorders, such as Bardet-Biedl Syndrome and Polycystic Kidney Disease.

30 mation and enlargement in autosomal dominant polycystic kidney disease.

31 1 +/- 1 years) with PLD, 117 had concomitant polycystic kidney disease.

32 in a neonatal kidney organ culture model of polycystic kidney disease.

33 ecessive disorder characterized by bilateral polycystic kidney disease.

34 >500 proteins, including several related to polycystic kidney disease.

35 c renal disorders such as autosomal dominant polycystic kidney disease.

36 ressive cyst formation in autosomal dominant polycystic kidney disease.

37 f the most common inherited human disorders, polycystic kidney disease.

38 ially novel treatment for autosomal dominant polycystic kidney disease.

39 d to preserve renal function in experimental polycystic kidney disease.

40 Dysfunction of renal primary cilia leads to polycystic kidney disease.

41 umerous disease models, including cancer and polycystic kidney disease.

42 have utility in diagnosis and monitoring of polycystic kidney disease.

43 s on renal function and favor cyst growth in polycystic kidney disease.

44 as a possible therapy for heart failure and polycystic kidney disease.

45 3 control recipients with autosomal dominant polycystic kidney disease.

46 ons in genes encoding polycystin-1 and -2 in polycystic kidney diseases.

47 on to the familial mutation, variation(s) in polycystic kidney disease 1 (PKD1) or HNF1 homeobox B (H

48 ng from inherited mutations in the genes for polycystic kidney disease 1 (PKD1) or polycystic kidney

49 The polycystic kidney disease-1 (Pkd1) gene encodes a large

50 e and a downstream domain with homology to a polycystic kidney disease-1 repeat, efficiently form amy

51 or potential (TRP) channels Trpm, NompC, and Polycystic kidney disease 2 (Pkd2) are expressed in CIII

52 The Polycystic Kidney Disease 2 (Pkd2) gene is mutated in au

53 olved in osteoblast differentiation and that polycystic kidney disease 2 (Pkd2) was a downstream targ

54 es for polycystic kidney disease 1 (PKD1) or polycystic kidney disease 2 (PKD2).

55 ith polycystin-2 (the protein product of the polycystic kidney disease 2 gene), and, when disrupted,

56 Here, we show that disruption of the polycystic kidney disease 2-like 1 (Pkd2l1 or Pkdl), enc

57 ociated with higher 16:1n-7, whereas PKD2L1 (polycystic kidney disease 2-like 1; P=5.7x10(-15)) and a

58 ate-dependent kinase, and the cation channel polycystic kidney disease 2.

59 and other secretory diarrheas [7] as well as polycystic kidney disease [8-10].

60 linical manifestations seen in patients with polycystic kidney disease, a cilia-associated pathology

61 liver disease can complicate adult dominant polycystic kidney disease, a genetic disease caused by d

62 rited co-deletions of the autosomal dominant polycystic kidney disease (ADPKD) 1 gene (PKD1) develop

63 and comparing with IgAN, autosomal dominant polycystic kidney disease (ADPKD) and diabetic nephropat

64 ps early in patients with autosomal dominant polycystic kidney disease (ADPKD) and is associated with

65 Hypertension is common in autosomal dominant polycystic kidney disease (ADPKD) and is associated with

66 Autosomal-dominant polycystic kidney disease (ADPKD) and von Hippel-Lindau

67 anisms of cystogenesis in autosomal dominant polycystic kidney disease (ADPKD) are not fully understo

68 Prenatal forms of autosomal dominant polycystic kidney disease (ADPKD) are rare but can be re

69 -Biedl syndrome (BBS) and autosomal dominant polycystic kidney disease (ADPKD) are two genetically di

70 l epigenetic regulator of autosomal dominant polycystic kidney disease (ADPKD) but also as a novel cl

71 a cohort of patients with autosomal dominant polycystic kidney disease (ADPKD) compared with a contro

72 Autosomal dominant polycystic kidney disease (ADPKD) constitutes the most i

73 elegans and mammals, the autosomal dominant polycystic kidney disease (ADPKD) gene products polycyst

74 ponse is blocked when the autosomal-dominant polycystic kidney disease (ADPKD) gene products, polycys

75 ation and modification in autosomal dominant polycystic kidney disease (ADPKD) have helped to explain

76 elopment and expansion in autosomal dominant polycystic kidney disease (ADPKD) involves both fluid se

77 Autosomal dominant polycystic kidney disease (ADPKD) is a common cause of E

78 Autosomal dominant polycystic kidney disease (ADPKD) is a common cause of r

79 Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited

80 Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited

81 Autosomal-dominant polycystic kidney disease (ADPKD) is a common life-threa

82 Autosomal-dominant polycystic kidney disease (ADPKD) is a common, progressi

83 Autosomal dominant polycystic kidney disease (ADPKD) is a commonly inherite

84 Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder

85 Autosomal dominant polycystic kidney disease (ADPKD) is a leading cause of

86 Autosomal dominant polycystic kidney disease (ADPKD) is a progressive genet

87 Autosomal dominant polycystic kidney disease (ADPKD) is an important cause

88 Autosomal dominant polycystic kidney disease (ADPKD) is associated with pro

89 Autosomal dominant polycystic kidney disease (ADPKD) is caused by inactivat

90 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

91 Autosomal-dominant polycystic kidney disease (ADPKD) is caused by mutations

92 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

93 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

94 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

95 Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations

96 Autosomal dominant polycystic kidney disease (ADPKD) is characterized by ag

97 Autosomal dominant polycystic kidney disease (ADPKD) is characterized by in

98 Autosomal dominant polycystic kidney disease (ADPKD) is characterized by re

99 Autosomal dominant polycystic kidney disease (ADPKD) is driven by mutations

100 Autosomal dominant polycystic kidney disease (ADPKD) is heterogeneous with

101 The course of autosomal dominant polycystic kidney disease (ADPKD) is often associated wi

102 Autosomal dominant polycystic kidney disease (ADPKD) is one of the most com

103 Autosomal dominant polycystic kidney disease (ADPKD) is the most common gen

104 Autosomal-dominant polycystic kidney disease (ADPKD) is the most common her

105 Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inh

106 Autosomal dominant polycystic kidney disease (ADPKD) is the most common lif

107 Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent g

108 olume and hypertension in autosomal dominant polycystic kidney disease (ADPKD) occurs in childhood.

109 Patients with autosomal dominant polycystic kidney disease (ADPKD) often need to undergo

110 Autosomal dominant polycystic kidney disease (ADPKD) often results in ESRD

111 gression in patients with autosomal dominant polycystic kidney disease (ADPKD) remains untested.

112 Autosomal dominant polycystic kidney disease (ADPKD) results from mutations

113 etic nephropathy (DN) and autosomal-dominant polycystic kidney disease (ADPKD) served as "external" n

114 Novel therapies in autosomal dominant polycystic kidney disease (ADPKD) signal the need for ma

115 Patients with autosomal dominant polycystic kidney disease (ADPKD) typically carry a muta

116 The course of autosomal dominant polycystic kidney disease (ADPKD) varies among individua

117 er disease may complicate autosomal dominant polycystic kidney disease (ADPKD), a disease caused by m

118 lycystin-1 (PC1) leads to autosomal dominant polycystic kidney disease (ADPKD), a disorder characteri

119 hich, when mutated, cause autosomal dominant polycystic kidney disease (ADPKD), a highly prevalent hu

120 olycystin-1 (PC1) lead to autosomal-dominant polycystic kidney disease (ADPKD), a leading cause of re

121 ed Pkd1 protein result in autosomal dominant polycystic kidney disease (ADPKD), a serious inherited s

122 D2, whose mutations cause autosomal dominant polycystic kidney disease (ADPKD), belongs to the superf

123 Autosomal dominant polycystic kidney disease (ADPKD), characterized by the

124 In autosomal dominant polycystic kidney disease (ADPKD), cysts accumulate and

125 compared with those with autosomal dominant polycystic kidney disease (ADPKD), in which the native k

126 idely among patients with autosomal dominant polycystic kidney disease (ADPKD), necessitating optimal

127 Autosomal dominant polycystic kidney disease (ADPKD), one of the most commo

128 (Pkd2) gene is mutated in autosomal dominant polycystic kidney disease (ADPKD), one of the most commo

129 cally identified cases of autosomal dominant polycystic kidney disease (ADPKD), one of the most commo

130 Autosomal dominant polycystic kidney disease (ADPKD), the most common form

131 ssion to renal failure in autosomal dominant polycystic kidney disease (ADPKD).

132 n genetic kidney disorder autosomal dominant polycystic kidney disease (ADPKD).

133 uses ciliopathies such as autosomal dominant polycystic kidney disease (ADPKD).

134 ain cause of mortality in autosomal-dominant polycystic kidney disease (ADPKD).

135 t for almost all cases of autosomal dominant polycystic kidney disease (ADPKD).

136 the genes responsible for autosomal dominant polycystic kidney disease (ADPKD).

137 ses, including cancer and autosomal dominant polycystic kidney disease (ADPKD).

138 polycystin-1 (PC1), cause autosomal-dominant polycystic kidney disease (ADPKD).

139 ng pathway is aberrant in autosomal-dominant polycystic kidney disease (ADPKD).

140 rthologous mouse model of autosomal dominant polycystic kidney disease (ADPKD).

141 nes, PKD1 and PKD2, cause autosomal dominant polycystic kidney disease (ADPKD).

142 escribed manifestation of autosomal dominant polycystic kidney disease (ADPKD).

143 the most common cause of autosomal dominant polycystic kidney disease (ADPKD).

144 ibute to >85% of cases of autosomal dominant polycystic kidney disease (ADPKD).

145 ed to the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD).

146 concern in patients with autosomal dominant polycystic kidney disease (ADPKD).

147 t for nearly all cases of autosomal dominant polycystic kidney disease (ADPKD).

148 olycystin-2 (PC2) lead to autosomal dominant polycystic kidney disease (ADPKD).

149 rgement of renal cysts in autosomal dominant polycystic kidney disease (ADPKD).

150 nsion and cystogenesis in autosomal dominant polycystic kidney disease (ADPKD).

151 PKD2 gene, which leads to autosomal dominant polycystic kidney disease (ADPKD).

152 lving patients with early autosomal dominant polycystic kidney disease (ADPKD; estimated creatinine c

153 s of inherited disorders, autosomal dominant polycystic kidney diseases (ADPKD), a significant cause

154 a role in the pathogenesis of hypertension, polycystic kidney disease, AKI, and CKD.

155 The polycystic kidney disease allele in this model, Bicc1, i

156 stin-1 (PC1) give rise to autosomal dominant polycystic kidney disease, an important and common cause

157 his case involves a 54-year-old patient with polycystic kidney disease and a history of hyperacute al

158 ce of renal epithelial cells is perturbed in polycystic kidney disease and apical expression of recep

159 allele significantly ameliorated the severe polycystic kidney disease and consequent runting caused

160 sing for the treatment of autosomal dominant polycystic kidney disease and have been approved in Japa

161 d Safety in Management of Autosomal Dominant Polycystic Kidney Disease and Its Outcomes) trial, tolva

162 vels of this eicosanoid are also elevated in polycystic kidney disease and may contribute to cyst for

163 It has a critical role in polycystic kidney disease and nephronophthisis.

164 weights and cyst growth in animal models of polycystic kidney disease and PLD, and might be develope

165 In polycystic kidney disease and polycystic liver disease (

166 The first case is a 67-year-old man with polycystic kidney disease and recipient of a zero-antige

167 el are predicted to slow cyst enlargement in polycystic kidney disease and reduce intestinal fluid lo

168 athology resembling human autosomal dominant polycystic kidney disease and represent a useful model t

169 mbryonic development to adult progression of polycystic kidney disease and some cancers.

170 s, diabetes, chronic interstitial nephritis, polycystic kidney disease, and 1-3 years of prior dialys

171 iseases such as ischemia/reperfusion injury, polycystic kidney disease, and congenital solitary kidne

172 th refractory symptoms of autosomal dominant polycystic kidney disease (APKD) in need of a renal tran

173 Polycystic kidney diseases are characterized by numerous

174 Polycystic kidney diseases are the most common genetic d

175 C and PKD), identified in linkage studies of polycystic kidney disease, are candidate channels divide

176 e autosomal dominant and autosomal recessive polycystic kidney diseases, are incurable pathological c

177 Autosomal recessive polycystic kidney disease (ARPKD) is a significant hered

178 Autosomal recessive polycystic kidney disease (ARPKD) is an important childh

179 rmation and expansion in autosomal recessive polycystic kidney disease (ARPKD) is poorly understood,

180 rats, an animal model of autosomal-recessive polycystic kidney disease (ARPKD), decreased intracellul

181 Autosomal recessive polycystic kidney disease (ARPKD), the most common cilio

182 BACKGROUND & AIMS: Autosomal recessive polycystic kidney disease (ARPKD), the most common cilio

183 Autosomal recessive polycystic kidney disease (ARPKD), usually considered to

184 Caroli disease (CD), and autosomal recessive polycystic kidney disease (ARPKD).

185 codes fibrocystin, cause autosomal recessive polycystic kidney disease (ARPKD).

186 ed in cancer cells, ciliopathies such as the polycystic kidney disease, as well as in the genetic dis

187 Furthermore, autosomal dominant polycystic kidney disease-associated TRPP2 mutant T448K

188 laying an important role in the formation of polycystic kidney disease, but not for Rab8 another cili

189 s the juvenile cystic kidneys (jck) model of polycystic kidney disease, but the functions of Nek8 are

190 dentical to those seen in autosomal dominant polycystic kidney disease, but without clinically releva

191 G protein-coupled receptors (GPCRs) and the polycystic kidney disease-causing polycystin 1/2 complex

192 In PCLD associated with polycystic kidney disease, cell proliferation is one of

193 utosomal recessive disorder characterized by polycystic kidney disease, central nervous system defect

194 mice, an animal model of autosomal dominant polycystic kidney disease, developed hepatic cysts.

195 acterized internal domain is a member of the polycystic kidney disease domain family but also how the

196 erties of PC2 are lost in autosomal dominant polycystic kidney disease, emphasizing the importance of

197 APK activation, all of which are features of polycystic kidney disease, especially nephronophthisis.

198 potential polycystic (TRPP) channel PKD1L2 (polycystic kidney disease gene 1-like 2) underlies this

199 riched miRNA family, and upregulation of the polycystic kidney disease gene Pkd1.

200 ozygous mutations in the autosomal recessive polycystic kidney disease gene PKHD1, indicating that ad

201 f fibrocystin, the human autosomal recessive polycystic kidney disease gene product.

202 te expression of a functional complex of the polycystic kidney disease gene products, polycystin-1 an

203 lting from mutations in Pkhd1, the recessive polycystic kidney disease gene.

204 Knockout of the polycystic kidney disease genes PKD1 or PKD2 induces cys

205 uires lov-1 and pkd-2 (homologs of the human polycystic kidney disease genes, PKD1 and PKD2), which a

206 Deletion of Lgr4 in mouse led to aniridia, polycystic kidney disease, genitourinary anomalies, and

207 on is under study in the Halt Progression of Polycystic Kidney Disease (HALT PKD) trial.

208 Autosomal dominant polycystic kidney disease has been linked to mutations i

209 Ectopic cAMP signaling is pathologic in polycystic kidney disease; however, its spatiotemporal a

210 or down-regulation of PKD1 or PKD2 leads to polycystic kidney disease in animal models, but their in

211 Polycystic kidney disease is a common genetic disorder i

212 Autosomal dominant polycystic kidney disease is a genetic disorder associat

213 Autosomal dominant polycystic kidney disease is caused by mutations in the

214 Autosomal dominant polycystic kidney disease is caused by mutations in the

215 Recent evidence suggests that polycystic kidney disease is characterized by defects in

216 The third-hit hypothesis of polycystic kidney disease is discussed.

217 Autosomal dominant polycystic kidney disease is the most common inherited k

218 nction between the N-terminal region and the polycystic kidney disease-like domain is highly crucial

219 a suspected diagnosis of autosomal dominant polycystic kidney disease, medullary cystic kidney disea

220 Using human ADPKD tissues and polycystic kidney disease mouse models, we show that the

221 The most severe form of autosomal dominant polycystic kidney disease occurs in patients with mutati

222 beings, and patients with autosomal-dominant polycystic kidney disease or ARPKD.

223 fective for patients with autosomal dominant polycystic kidney disease or polycystic liver disease; e

224 m that may play a role in autosomal dominant polycystic kidney disease pathogenesis.

225 ls (NL, 42 vs. 17; US, 40 vs. 13 points) and polycystic kidney disease patients without PLD (22 point

226 es of PLD patients with general controls and polycystic kidney disease patients without PLD.

227 Cysts and aneurysms from polycystic kidney disease patients, Pkd mouse, and zebra

228 of PCK rats and ARPKD or autosomal-dominant polycystic kidney disease patients.

229 ectomies exist for patients with symptomatic polycystic kidney disease (PCKD).

230 in a disruption of renal ciliogenesis and a polycystic kidney disease phenotype in zebrafish and mic

231 unction by re-expressing survivin can rescue polycystic kidney disease phenotypes.

232 ious studies report a cross-talk between the polycystic kidney disease (PKD) and tuberous sclerosis c

233 insulinemic hypoglycemia (HI) and congenital polycystic kidney disease (PKD) are rare, genetically he

234 Polycystic kidney disease (PKD) can arise from either de

235 denosine monophosphate (cAMP) drives genetic polycystic kidney disease (PKD) cystogenesis.

236 s to drive the aggregation of the downstream polycystic kidney disease (PKD) domain into a melanosoma

237 ncluding the leucine-rich repeats, the first polycystic kidney disease (PKD) domain, and the C-type l

238 multimodular structure including 16 Ig-like polycystic kidney disease (PKD) domains.

239 Polycystic kidney disease (PKD) exhibits an inflammatory

240 Polycystic kidney disease (PKD) family proteins associat

241 at is defective in expression of the sensory polycystic kidney disease (PKD) gene battery and male ma

242 nd their disruption has been associated with polycystic kidney disease (PKD) genes, the majority of w

243 Polycystic kidney disease (PKD) in mice can arise from d

244 Polycystic kidney disease (PKD) is a common human geneti

245 Polycystic kidney disease (PKD) is a genetic disorder th

246 Polycystic kidney disease (PKD) is a leading cause of ES

247 Autosomal-dominant (AD) polycystic kidney disease (PKD) is a leading cause of re

248 Polycystic kidney disease (PKD) is a life-threatening di

249 Polycystic kidney disease (PKD) is one of the most commo

250 and interstitial fibrosis, similar to known polycystic kidney disease (PKD) models.

251 There are no proven, effective therapies for polycystic kidney disease (PKD) or polycystic liver dise

252 olysis Site (GPS) of cell-adhesion GPCRs and polycystic kidney disease (PKD) proteins constitutes a h

253 ptor potential channel polycystin (TRPP) and polycystic kidney disease (PKD) proteins, play key roles

254 eracts predominantly with the second Ig-like polycystic kidney disease (PKD) repeat domain (PKD2) pre

255 Polycystic kidney disease (PKD) represents a family of g

256 be an underlying cause of autosomal dominant polycystic kidney disease (PKD), and ciliary-EV interact

257 ) allele) results in proteinuria, hematuria, polycystic kidney disease (PKD), and death 3 to 4 weeks

258 In polycystic kidney disease (PKD), genetic mutations in po

259 ney disease (ADPKD), the most common form of polycystic kidney disease (PKD), is a disorder with char

260 In polycystic kidney disease (PKD), renal parenchyma is des

261 Polycystic kidney disease (PKD), the most common genetic

262 tro and in vivo models of autosomal dominant polycystic kidney disease (PKD).

263 is an important mediator of cystogenesis in polycystic kidney disease (PKD).

264 indicates the importance of elevated cAMP in polycystic kidney disease (PKD).

265 ding the kidney, liver and pancreas features polycystic kidney disease (PKD).

266 involved in pathological conditions, such as polycystic kidney disease (PKD).

267 s phenotype is reminiscent of human forms of polycystic kidney disease (PKD).

268 target of rapamycin (mTOR) pathway occurs in polycystic kidney disease (PKD).

269 P signaling contribute to the development of polycystic kidney disease (PKD).

270 shows beneficial effects in animal models of polycystic kidney disease (PKD); however, two clinical t

271 Polycystic kidney diseases (PKD) are a group of inherite

272 Polycystic kidney diseases (PKD) are genetic disorders c

273 g is a key feature in the pathophysiology of polycystic kidney diseases (PKD).

274 e (Pu-Py) mirror repeat tract from the human polycystic kidney disease (PKD1) intron 21 forms non-B D

275 ost frequently mutated in autosomal dominant polycystic kidney disease (PKD1).

276 Polycystic kidney diseases (PKDs) are genetic disorders

277 Polycystic kidney diseases (PKDs) comprise a subgroup of

278 Genetic forms of polycystic kidney diseases (PKDs), including nephronopht

279 h autosomal dominant and autosomal recessive polycystic kidney disease (polycystin-1, polycystin-2, a

280 In contrast to many models of polycystic kidney disease, precystic Ift140-deleted coll

281 f a 21-year-old man with autosomal recessive polycystic kidney disease, presenting with subarachnoid

282 may predict and/or effect autosomal dominant polycystic kidney disease progression.

283 Furthermore, the polycystic kidney disease protein IFT88 binds IFT52281-3

284 ensitive complex with the autosomal dominant polycystic kidney disease protein polycystin 2.

285 GPS is also shared by polycystic kidney disease proteins and it precedes the f

286 , and ciliary dysfunction is associated with polycystic kidney disease, retinal degeneration, polydac

287 who participated in the Halt Progression of Polycystic Kidney Disease Study A were categorized on th

288 For patients with autosomal dominant polycystic kidney disease that progressed more slowly, t

289 tin 2 are responsible for autosomal dominant polycystic kidney disease, the most common heritable hum

290 ) mice, a mouse model of autosomal recessive polycystic kidney disease; this gene encodes cystin, a 1

291 rize for Advancement in the Understanding of Polycystic Kidney Disease to participate in a forward-th

292 h G proteins are regulated in the context of polycystic kidney disease to promote abnormal epithelial

293 al mass, may accelerate progression of adult polycystic kidney disease toward end-stage renal disease

294 enal disease secondary to autosomal dominant polycystic kidney disease was referred to a quaternary c

295 om GPCRs and fibrocystin (also implicated in polycystic kidney disease), we demonstrate these motifs

296 To gain insights into autosomal dominant polycystic kidney disease, we performed yeast two-hybrid

297 , recipient employment, and the diagnosis of polycystic kidney disease were significantly associated

298 Here we focus on autosomal dominant polycystic kidney disease, which is attributable to muta

299 ferral before dialysis were the diagnosis of polycystic kidney disease, white recipient race, referra

300 to identify patients with autosomal dominant polycystic kidney disease who are most likely to benefit