ライフサイエンスコーパス: ADPKD

1 ADPKD-associated PC1 mutants failed to regulate Jade-1,

2 .61-0.70), DN (HR, 0.50; 95% CI, 0.47-0.52), ADPKD (HR, 0.85; 95% CI, 0.82-0.88).

3 of 174 (14.4%, P=0.001) patients with adult ADPKD.

4 up avenues for combination therapies against ADPKD and cancer.

5 s in these mice indicate that FR ameliorates ADPKD through a mechanism involving suppression of the m

6 tigation of Gb4Cer isoforms in kidneys of an ADPKD rat model revealed increased levels of sphingoid b

7 r, physical interactions between the BBS and ADPKD proteins may underline the overlapping renal pheno

8 l cells derived from both Pkd1-null mice and ADPKD patients.

9 upregulated in all rodent models of PKD and ADPKD patients with unknown mechanism.

10 ian target of rapamycin (mTOR) signaling and ADPKD cell proliferation in vitro Homozygous deletion of

11 Although benign, ADPKD renal cysts created by the sustained proliferation

12 We investigated the overlap between ADPKD and MFS by breeding mice with targeted mutations i

13 and 2.57 (2.35 to 2.82), respectively], but ADPKD associated with a lower HR for allograft failure e

14 ransplant, RRs attenuated substantially, but ADPKD remained associated with biliary tract disease (RR

15 timulated cAMP levels and Cl(-) secretion by ADPKD cells than inhibition of PDE1, and inhibition of P

16 Overall, we show that GANAB mutations cause ADPKD and ADPLD and that the cystogenesis is most likely

17 Mutations to PKD1 or PKD2 cause ADPKD; both loci have high levels of allelic heterogenei

18 PC1, PKD1) or polycystin-2 (PC2, PKD2) cause ADPKD, and PKD1 mutations are associated with more sever

19 ion in pkd1a mutants, suggesting a conserved ADPKD model.

20 ly are no approved therapies to slow or cure ADPKD.

21 utosomal dominant polycystic kidney disease (ADPKD) and diabetic nephropathy associated with higher H

22 utosomal dominant polycystic kidney disease (ADPKD) and is associated with disease progression.

23 utosomal dominant polycystic kidney disease (ADPKD) and is associated with increased total kidney vol

24 utosomal-dominant polycystic kidney disease (ADPKD) and von Hippel-Lindau (VHL) disease lead to large

25 utosomal dominant polycystic kidney disease (ADPKD) are not fully understood.

26 utosomal dominant polycystic kidney disease (ADPKD) are rare but can be recurrent in some families, s

27 utosomal dominant polycystic kidney disease (ADPKD) are two genetically distinct ciliopathies but sha

28 utosomal dominant polycystic kidney disease (ADPKD) but also as a novel client protein of Hsp90.

29 utosomal dominant polycystic kidney disease (ADPKD) compared with a control group without ADPKD that

30 utosomal dominant polycystic kidney disease (ADPKD) constitutes the most inherited kidney disease.

31 utosomal dominant polycystic kidney disease (ADPKD) gene products polycystin-1 and polycystin-2 local

32 utosomal dominant polycystic kidney disease (ADPKD) have helped to explain some extreme disease manif

33 utosomal dominant polycystic kidney disease (ADPKD) is a common cause of ESRD.

34 utosomal dominant polycystic kidney disease (ADPKD) is a common cause of renal failure that is due to

35 utosomal dominant polycystic kidney disease (ADPKD) is a common inherited nephropathy responsible for

36 utosomal-dominant polycystic kidney disease (ADPKD) is a common life-threatening genetic disease that

37 utosomal-dominant polycystic kidney disease (ADPKD) is a common, progressive, adult-onset disease tha

38 utosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder characterized by the accumu

39 utosomal dominant polycystic kidney disease (ADPKD) is a leading cause of ESRD.

40 utosomal dominant polycystic kidney disease (ADPKD) is a progressive genetic syndrome with an inciden

41 utosomal dominant polycystic kidney disease (ADPKD) is an important cause of ESRD for which there exi

42 utosomal dominant polycystic kidney disease (ADPKD) is associated with progressive enlargement of mul

43 utosomal dominant polycystic kidney disease (ADPKD) is caused by inactivating mutations in PKD1 (85%)

44 utosomal-dominant polycystic kidney disease (ADPKD) is caused by mutations in either PKD1 or PKD2 and

45 utosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in either PKD1 or PKD2.

46 utosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 or PKD2 which enco

47 utosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in two large genes, PKD1 a

48 utosomal dominant polycystic kidney disease (ADPKD) is caused by mutations to PKD1 or PKD2, triggerin

49 utosomal dominant polycystic kidney disease (ADPKD) is characterized by innumerous fluid-filled cysts

50 utosomal dominant polycystic kidney disease (ADPKD) is characterized by renal cyst formation, inflamm

51 utosomal dominant polycystic kidney disease (ADPKD) is driven by mutations in PKD1 and PKD2 genes.

52 utosomal dominant polycystic kidney disease (ADPKD) is heterogeneous with regard to genic and allelic

53 utosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic disorders cause

54 utosomal dominant polycystic kidney disease (ADPKD) is the most common genetic cause of renal failure

55 utosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inherited disorder of the kidn

56 utosomal dominant polycystic kidney disease (ADPKD) is the most common life-threatening hereditary di

57 utosomal dominant polycystic kidney disease (ADPKD) is the most frequent genetic cause of renal failu

58 utosomal dominant polycystic kidney disease (ADPKD) often need to undergo native nephrectomy and are

59 utosomal dominant polycystic kidney disease (ADPKD) often results in ESRD but with a highly variable

60 utosomal dominant polycystic kidney disease (ADPKD) remains untested.

61 utosomal-dominant polycystic kidney disease (ADPKD) served as "external" non-GN comparators.

62 utosomal dominant polycystic kidney disease (ADPKD) signal the need for markers of disease progressio

63 utosomal dominant polycystic kidney disease (ADPKD) typically carry a mutation in either the PKD1 or

64 utosomal dominant polycystic kidney disease (ADPKD) varies among individuals, with some reaching ESRD

65 utosomal dominant polycystic kidney disease (ADPKD), a disorder characterized by the formation of mul

66 utosomal dominant polycystic kidney disease (ADPKD), a serious inherited syndrome affecting approxima

67 utosomal dominant polycystic kidney disease (ADPKD), characterized by the formation of numerous kidne

68 utosomal dominant polycystic kidney disease (ADPKD), cysts accumulate and progressively impair renal

69 utosomal dominant polycystic kidney disease (ADPKD), in which the native kidney disease cannot recur.

70 utosomal dominant polycystic kidney disease (ADPKD), necessitating optimal patient selection for enro

71 utosomal dominant polycystic kidney disease (ADPKD), one of the most common human genetic diseases.

72 utosomal dominant polycystic kidney disease (ADPKD), one of the most common human monogenic disorders

73 utosomal dominant polycystic kidney disease (ADPKD), one of the most common monogenetic disorders, is

74 utosomal dominant polycystic kidney disease (ADPKD), the most common form of polycystic kidney diseas

75 utosomal dominant polycystic kidney disease (ADPKD).

76 utosomal dominant polycystic kidney disease (ADPKD).

77 utosomal dominant polycystic kidney disease (ADPKD).

78 utosomal dominant polycystic kidney disease (ADPKD).

79 utosomal dominant polycystic kidney disease (ADPKD).

80 utosomal dominant polycystic kidney disease (ADPKD).

81 utosomal dominant polycystic kidney disease (ADPKD).

82 utosomal-dominant polycystic kidney disease (ADPKD).

83 utosomal dominant polycystic kidney disease (ADPKD).

84 utosomal dominant polycystic kidney disease (ADPKD).

85 utosomal dominant polycystic kidney disease (ADPKD).

86 utosomal-dominant polycystic kidney disease (ADPKD).

87 utosomal-dominant polycystic kidney disease (ADPKD).

88 utosomal dominant polycystic kidney disease (ADPKD).

89 utosomal dominant polycystic kidney disease (ADPKD).

90 utosomal dominant polycystic kidney disease (ADPKD).

91 utosomal dominant polycystic kidney disease (ADPKD).

92 utosomal dominant polycystic kidney disease (ADPKD; estimated creatinine clearance, >/=60 ml per minu

93 tosomal dominant polycystic kidney diseases (ADPKD), a significant cause of ESRD, and autosomal domin

94 In early ADPKD, the combination of lisinopril and telmisartan did

95 ated with the familial PKD mutation in early ADPKD, these four genes were screened in 42 patients wit

96 enes were screened in 42 patients with early ADPKD in 41 families.

97 oving the prospects for available, effective ADPKD treatments.

98 Renal imaging may not exclude ADPKD particularly in younger donors and molecular genet

99 g HSP90 inhibitors as therapeutic agents for ADPKD.

100 extracellular domain of PKD2, a hotspot for ADPKD pathogenic mutations, contributes to channel assem

101 SBN in patients undergoing LDKT for ADPKD does not have a significant negative impact on pat

102 ism represents a potential new mechanism for ADPKD progression.

103 Of potential LRKD, one tested positive for ADPKD and one with a diagnostic ultrasound tested negati

104 or developing new therapeutic strategies for ADPKD.

105 to develop unique therapeutic strategies for ADPKD.

106 miR-17 family is a promising drug target for ADPKD, and miR-17-mediated inhibition of mitochondrial m

107 ploration of MIF as a therapeutic target for ADPKD.

108 l LRKD were referred for genetic testing for ADPKD between April 2010 and October 2012.

109 e evaluating the role of genetic testing for ADPKD in LRKD assessment.

110 tional development of novel therapeutics for ADPKD.

111 autophagy activation as a novel therapy for ADPKD, and presented zebrafish as an efficient vertebrat

112 At present, the treatment for ADPKD is largely supportive.

113 targets that may be useful as treatments for ADPKD.

114 Whole-exome sequencing of six GUR ADPKD-affected families identified one with a missense m

115 445 patients, 18 to 50 years of age, who had ADPKD with a total kidney volume of 750 ml or more and a

116 However, ADPKD iPS cells as well as somatic epithelial cells and

117 Human ADPKD cysts frequently express cadherin-8 (cad8), and ex

118 s induced in kidney cysts of mouse and human ADPKD.

119 Consistent with these findings, human ADPKD cyst-derived cells with heterozygous and homozygou

120 ate Nedd9 expression is deregulated in human ADPKD and a mouse ADPKD model.

121 In human ADPKD studies, sirolimus, a mammalian target of rapamyci

122 nd PDE4 expression levels are lower in human ADPKD tissue and cells compared with those of normal hum

123 To mimic human ADPKD in mice more precisely, we reduced the percentage

124 oach is a suitable model for mimicking human ADPKD and can be used for preclinical testing.

125 d2WS25/- mice, an orthologous model of human ADPKD caused by a mutation in the Pkd2 gene, had an earl

126 dneys and accumulated in cyst fluid of human ADPKD kidneys.

127 ere PKD that was remarkably similar to human ADPKD.

128 Using human ADPKD tissues and polycystic kidney disease mouse models

129 rative signaling pathways often activated in ADPKD.

130 induced by cyst fluid IL-6 and TNF-alpha in ADPKD kidneys.

131 y function as a novel epigenetic approach in ADPKD.

132 could lead to new therapeutic approaches in ADPKD.

133 issues from Pkd1-knockout mice as well as in ADPKD patients.

134 inforces the central role of AC6 and cAMP in ADPKD pathogenesis and highlights the likely benefit of

135 hown to be activated in cyst-lining cells in ADPKD and PKD mouse models and may drive renal cyst grow

136 ned the mitochondria of cyst-lining cells in ADPKD model mice (Ksp-Cre PKD1 (flox/flox)) and rats (Ha

137 arly events leading to renal cystogenesis in ADPKD and suggest that the integrin signaling pathway ma

138 ha (PGC-1alpha) expression were decreased in ADPKD model animal kidneys, with PGC-1alpha expression i

139 slowing the progression of cystic disease in ADPKD are inconclusive, and we hypothesized that current

140 rate oxidative stress to be present early in ADPKD.

141 l abnormalities facilitate cyst formation in ADPKD.

142 ly more abundant (by two-fold or greater) in ADPKD-uEVs than in healthy- and CKD-uEVs.

143 as an important regulator of cyst growth in ADPKD.

144 The unraveled link between Brd4 and Hsp90 in ADPKD may also be a general mechanism for the upregulati

145 cial anomalies have never been identified in ADPKD patients, we carried out three-dimensional photogr

146 nst many of the growth factors implicated in ADPKD are already available, they are IgG isotype antibo

147 y analysis and were previously implicated in ADPKD pathogenesis.

148 d in clinical trials with mTOR inhibitors in ADPKD.

149 in 79, and AVP increased this interaction in ADPKD but not NHK cells.

150 amide (Gb4Cer) have not been investigated in ADPKD yet, and mass spectrometry analysis of Gb4Cer from

151 bly, TNF-alpha accumulates to high levels in ADPKD cyst fluid.

152 e pathophysiological role of mitochondria in ADPKD remains uncharacterized.

153 toplasmic tail, PC1-p30, is overexpressed in ADPKD.

154 rstanding of aberrant downstream pathways in ADPKD, such as proliferation/secretion-related signaling

155 more, ectopic expression of wild-type PC1 in ADPKD iPS-derived hepatoblasts rescued ciliary PC2 prote

156 nd 2 inhibition has therapeutic potential in ADPKD.

157 crucial for studying disease progression in ADPKD.

158 complement as disease-associated proteins in ADPKD.

159 cells highly express the folate receptor in ADPKD and mouse models.

160 The genotype-phenotype relationship in ADPKD is not completely understood.

161 ses, but the role of these noncoding RNAs in ADPKD pathogenesis is still poorly defined.

162 sion and protein function may play a role in ADPKD pathogenesis.

163 the use of 2DG as a therapeutic strategy in ADPKD.

164 gh this remains lower than graft survival in ADPKD, and confirms that the reluctance to use living do

165 esion loss due to cadherin type switching in ADPKD suffices to drive cystogenesis.

166 tion as biomarkers or targets for therapy in ADPKD.

167 mat can be exploited for targeted therapy in ADPKD.

168 ent living related kidney transplantation in ADPKD.

169 the inter- and intrafamilial variability in ADPKD.

170 er complications, and a range of other known ADPKD manifestations were adjusted for potential confoun

171 patients occurred in 39 families with known ADPKD and were associated with PKD1 mutation in 36 famil

172 for future genetic characterization of large ADPKD populations.

173 lity that inhibiting HDAC6 might help manage ADPKD.

174 e, STA-2842, induces the degradation of many ADPKD-relevant HSP90 client proteins in Pkd1(-/-) primar

175 on is deregulated in human ADPKD and a mouse ADPKD model.

176 ition delayed cyst growth in multiple murine ADPKD models.

177 The ADPKD versus non-ADPKD RRs for biliary tract disease were larger for men

178 patients with ADPKD versus patients with non-ADPKD CKD).

179 Compared with non-ADPKD hospital controls, those with ADPKD had higher rat

180 After screening, 7%-10% of ADPKD-affected and approximately 50% of ADPLD-affected f

181 cases, respectively) are the known causes of ADPKD.

182 ut may relate to biologic characteristics of ADPKD or to cancer risk behaviors associated with ADPKD.

183 nalysis revealed specific characteristics of ADPKD patient faces, some of which correlated with those

184 An easily applied classification of ADPKD based on HtTKV and age should optimize patient sel

185 nct and important extrarenal complication of ADPKD.

186 ation on computed tomography (CT) dataset of ADPKD patients exhibiting mild to moderate or severe ren

187 diverticulum and the first demonstration of ADPKD.

188 a1 in vitro and on the cystic development of ADPKD in vivo.

189 jor challenge is to exclude the diagnosis of ADPKD in potential donors.

190 ation analysis, which can aid diagnostics of ADPKD.

191 aneurysms, are a well recognized feature of ADPKD, and a subgroup of families exhibits traits remini

192 tabolism has been identified as a feature of ADPKD, and inhibition of glycolysis using glucose analog

193 ular causes, incidence of pain, frequency of ADPKD-related symptoms, quality of life, and adverse stu

194 personalization of therapeutic management of ADPKD.

195 ul in detecting extrarenal manifestations of ADPKD, most significant of which include intracranial an

196 n PCK rats and Pkd2(WS25/-) mice (a model of ADPKD).

197 hd1-Cre mice, a rapidly progressive model of ADPKD, decreased renal Akt/mTOR activity, cell prolifera

198 oss of Gpsm1 in the Pkd1(V/V) mouse model of ADPKD, which displays a hypomorphic phenotype of polycys

199 onal Pkd1 systemic-knockout mice, a model of ADPKD.

200 improved survival of an orthologous model of ADPKD.

201 ducible Pkd1fl/fl;Cre/Esr1(+) mouse model of ADPKD.

202 cyst formation in an organ culture model of ADPKD.

203 the course of the disease in mouse models of ADPKD.

204 s, including two long-lived, mouse models of ADPKD.

205 ing mutations in PC2 and the pathogenesis of ADPKD is not well understood.

206 b4Cer may play a role in the pathogenesis of ADPKD.

207 SIRT1) is involved in the pathophysiology of ADPKD.

208 -regulated kinase (ERK) and proliferation of ADPKD cells than inhibition of PDE4, and inhibition of P

209 y and regulates AVP-induced proliferation of ADPKD cells.

210 amilial variation in the progression rate of ADPKD suggests involvement of additional factors other t

211 s MIF is a central and upstream regulator of ADPKD pathogenesis and provides a rationale for further

212 Severity of ADPKD varies throughout the population, for reasons thou

213 nly uEVs of patients with advanced stages of ADPKD had increased levels of villin-1, periplakin, and

214 tify miR-17 as a target for the treatment of ADPKD.

215 e factors will increase our understanding of ADPKD and could ultimately help in the development of a

216 he glucose analog 2-deoxy-d-glucose (2DG) on ADPKD progression in orthologous and slowly progressive

217 suggested a modifying effect of autophagy on ADPKD, established autophagy activation as a novel thera

218 ted an important modifier action of Nedd9 on ADPKD pathogenesis involving failure to activate Aurora-

219 icant cause of symptomatic, very early onset ADPKD.

220 for DN to 0.92 for membranous nephropathy or ADPKD) than by lower rates of deceased donor kidney tran

221 terozygous mutations in PKD1 of the parental ADPKD fibroblasts but no pathogenic mutations in PKD2.

222 respectively, cause autosomal dominant PKD (ADPKD), whereas mutations in PKHD1, which encodes fibroc

223 s, and patients with autosomal dominant PKD (ADPKD); and (2) hepatorenal cystogenesis in vivo in PCK

224 By introducing single-point ADPKD pathogenic mutations into the GOF TRPP2, we showed

225 ses proliferation and cyst growth of primary ADPKD cysts cultures derived from multiple human donors.

226 rity of pathogenic mutations in Pkd2-related ADPKD.

227 ffected individuals were identified in seven ADPKD- and two ADPLD-affected families.

228 to the gDNA direct sequencing method for six ADPKD samples, a total of 89 variants were detected incl

229 ated with rate of progression in early-stage ADPKD.

230 iates with faster progression in early-stage ADPKD.

231 ty of tolvaptan in patients with later-stage ADPKD are unknown.

232 a 1-year period in patients with later-stage ADPKD.

233 se PRKCSH encodes GIIbeta, GANAB is a strong ADPKD and ADPLD candidate gene.

234 t whose expression is sufficient to suppress ADPKD-related phenotypes in vitro and in vivo.

235 007 patients, which raised a hypothesis that ADPKD is associated with biliary tract disease.

236 The ADPKD proteins encoded by these genes, polycystin-1 (PC1

237 The ADPKD proteins, termed as polycystin-1 (PC1) and polycys

238 The ADPKD versus non-ADPKD RRs for biliary tract disease wer

239 onmental factors significantly affecting the ADPKD phenotype.

240 teracts with all subunits of the BBSome, the ADPKD protein polycystin-1 (PC1) interacts with BBS1, BB

241 and surface and ciliary localization of the ADPKD proteins (PC1 and PC2), and reduced mature PC1 was

242 Studies of the ADPKD proteins, polycystin-1 and -2, and the development

243 In addition, activation of the ADPKD-associated signaling effectors Src, Erk, and the m

244 enic and PKD1 allelic effects and sex to the ADPKD phenotype.

245 m (iPS) cell lines from fibroblasts of three ADPKD and two ARPKD patients.

246 ysregulation of cAMP signaling is central to ADPKD, but the molecular mechanism is unresolved.

247 of death-adjusted graft failure compared to ADPKD ranged from 1.17 (95% confidence interval [95% CI]

248 that confer altered Ca(2+) signaling lead to ADPKD cysts.

249 n PKD1 and PKD2 genes are causally linked to ADPKD, but how these mutations drive cell behaviors that

250 We have further applied WGA to ADPKD mutation analysis of low DNA-yield specimens, succ

251 be a novel and effective agent for treating ADPKD.

252 Polycystin-1 (PC1) and -2 (PC2), the two ADPKD gene products, are large transmembrane proteins th

253 gical features of in utero-onset and typical ADPKD, respectively, correlating the level of functional

254 ts in 115 (63%) of 183 patients with typical ADPKD.

255 mutations drive cell behaviors that underlie ADPKD pathogenesis is unknown.

256 n important part of the mechanism underlying ADPKD pathogenesis.

257 ts a new molecular paradigm in understanding ADPKD pathogenesis.

258 iallelic disease including at least one weak ADPKD allele is a significant cause of symptomatic, very

259 ed 486 patients, 18 to 64 years of age, with ADPKD (estimated glomerular filtration rate [GFR], 25 to

260 Eight genes have been associated with ADPKD (PKD1 and PKD2), ADPLD (PRKCSH, SEC63, LRP5, ALG8,

261 A central defect associated with ADPKD pathology is elevated levels of 3', 5'-cyclic AMP

262 isk of biliary tract disease associated with ADPKD was larger than that for serious liver disease, ce

263 or to cancer risk behaviors associated with ADPKD.

264 ins encoded by two genes are associated with ADPKD: PC1 (pkd1), primarily a signaling molecule, and P

265 he Mayo Clinic Translational PKD Center with ADPKD (n=590) with computed tomography/magnetic resonanc

266 assigned 558 hypertensive participants with ADPKD (15 to 49 years of age, with an estimated glomerul

267 Overall, 441 nondiabetic participants with ADPKD and an eGFR>60 ml/min per 1.73 m(2) who participat

268 Patients with ADPKD (n = 110) with mutations identified in PKD1 or PKD

269 Patients with ADPKD and a pancreatic cyst were 5.9 times more likely t

270 ely predicts renal outcomes in patients with ADPKD and may enable the personalization of therapeutic

271 A cohort of patients with ADPKD and potential LRKD were referred for genetic testi

272 Whereas uEVs of young patients with ADPKD and preserved kidney function already had higher l

273 blood-pressure control in most patients with ADPKD and stage 3 chronic kidney disease.

274 Here, we studied 741 patients with ADPKD from 519 pedigrees in the Genkyst cohort and confi

275 , cysts in kidney samples from patients with ADPKD had increased levels of miR-21.

276 ibute to cardiac remodeling in patients with ADPKD in the absence of renal dysfunction.

277 l to predict renal outcomes in patients with ADPKD on the basis of genetic and clinical data.

278 view board-approved study, all patients with ADPKD provided informed consent; for control subjects, i

279 mutated polycystins predispose patients with ADPKD to cardiac pathologies before development of renal

280 uEVs from healthy controls and patients with ADPKD using a labeled approach and then used a label-fre

281 jects (healthy controls versus patients with ADPKD versus patients with non-ADPKD CKD).

282 Results Patients with ADPKD were significantly more likely than control subjec

283 ide effects was assessed, 1370 patients with ADPKD who were either 18 to 55 years of age with an esti

284 c cysts were more prevalent in patients with ADPKD with mutations in PKD2 than in PKD1 (21 of 34 pati

285 c cysts were more prevalent in patients with ADPKD with PKD2 mutation than in control subjects or pat

286 Patients with ADPKD, eGFR>/=60 ml/min per 1.73 m(2), and total kidney

287 om three independent groups of patients with ADPKD.

288 ence of pancreatic cysts among patients with ADPKD.

289 fit of combination therapy for patients with ADPKD.

290 mg/d reduced kidney growth in patients with ADPKD.

291 athogenesis of hypertension in patients with ADPKD.

292 o characterize a cohort of 230 patients with ADPKD.

293 tyrosine kinase inhibitor, in patients with ADPKD.

294 ve and therapeutic options for patients with ADPKD.

295 s), which include exosomes, in patients with ADPKD.

296 ithin which we identified 23,454 people with ADPKD and 6,412,754 hospital controls.

297 xtensively studied for its relationship with ADPKD and its importance in PC2 regulation, there are mi

298 with non-ADPKD hospital controls, those with ADPKD had higher rates of admission for biliary tract di

299 ADPKD) compared with a control group without ADPKD that was matched for age, sex, and renal function.

300 in PKD1 or PKD2 and control subjects without ADPKD or known pancreatic disease (n = 110) who were mat