ライフサイエンスコーパス: ADPKD

1 ADPKD genetic diagnosis is complicated by PKD1 pseudogen

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

5 ved differences in compound response amongst ADPKD and NHK cell preparation, we identified 18 compoun

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

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

8 od, and the mechanistic relationship between ADPKD and ciliopathic PKD is not known.

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

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

11 Subjects were stratified by ADPKD diagnosis at age <=18 (childhood diagnosis [CD]) o

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

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

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

15 rgeted enrichment methodologies in detecting ADPKD mutations in the PKD1 and PKD2 genes in patients w

16 utosomal dominant polycystic kidney disease (ADPKD) affects an estimated 1 in 1,000 people and slowly

17 utosomal dominant polycystic kidney disease (ADPKD) affects one in 400 to one in 1000 individuals; 10

18 utosomal Dominant Polycystic Kidney Disease (ADPKD) and affect many cellular pathways.

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

20 utosomal dominant polycystic kidney disease (ADPKD) and ultimately renal failure.

21 utosomal dominant polycystic kidney disease (ADPKD) are genetically distinct, with ADPKD usually caus

22 utosomal dominant polycystic kidney disease (ADPKD) are not well understood.

23 utosomal dominant polycystic kidney disease (ADPKD) but the reference standard method of MRI planimet

24 utosomal dominant polycystic kidney disease (ADPKD) by promoting cyst formation that, ultimately, cul

25 utosomal dominant polycystic kidney disease (ADPKD) can enable earlier management and improve outcome

26 utosomal dominant polycystic kidney disease (ADPKD) cause progressive increases in total kidney volum

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

28 utosomal dominant polycystic kidney disease (ADPKD) constitutes the fourth cause of end-stage renal d

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

30 utosomal dominant polycystic kidney disease (ADPKD) experience progressive decline in renal function,

31 utosomal dominant polycystic kidney disease (ADPKD) from paediatric and adult nephrology, human genet

32 utosomal-dominant polycystic kidney disease (ADPKD) induces a secretory phenotype, resulting in multi

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

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

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

36 utosomal dominant polycystic kidney disease (ADPKD) is an inherited monogenic renal disease character

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

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

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

40 utosomal dominant polycystic kidney disease (ADPKD) is caused by mutations in PKD1 and PKD2 encoding

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

42 utosomal dominant polycystic kidney disease (ADPKD) is characterized by bilateral renal cysts that le

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

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

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

46 utosomal dominant polycystic kidney disease (ADPKD) is one of the most common inherited monogenic dis

47 utosomal dominant polycystic kidney disease (ADPKD) is the leading genetic cause of renal failure.

48 utosomal dominant polycystic kidney disease (ADPKD) is the most common genetic disorder causing renal

49 utosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease and

50 utosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary renal disease, char

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

52 utosomal dominant polycystic kidney disease (ADPKD) is the most common monogenic cause of end-stage r

53 utosomal dominant polycystic kidney disease (ADPKD) is the most common renal genetic disorder, howeve

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

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

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

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

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

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

60 utosomal dominant polycystic kidney disease (ADPKD) uses height-adjusted total kidney volume (htTKV)

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

62 utosomal dominant polycystic kidney disease (ADPKD), a condition characterized by numerous fluid-fill

63 utosomal dominant polycystic kidney disease (ADPKD), a debilitating condition for which there is no c

64 utosomal dominant polycystic kidney disease (ADPKD), caused by mutations in either PKD1 or PKD2 genes

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

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

67 utosomal dominant polycystic kidney disease (ADPKD), encode the multipass transmembrane proteins poly

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

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

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

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

72 utosomal dominant polycystic kidney disease (ADPKD), the most common monogenic kidney disease.

73 utosomal dominant polycystic kidney disease (ADPKD), which is caused by mutations in the PKD1 or PKD2

74 utosomal dominant polycystic kidney disease (ADPKD).

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; estimated creatinine clearance, >/=60 ml per minu

86 utosomal dominant polycystic kidney disease [ADPKD]).

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

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

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

90 s a potential novel therapeutic approach for ADPKD.

91 r further evaluation in drug development for ADPKD.

92 age of the N-terminus of PC-1, a hotspot for ADPKD mutations, produces a soluble ligand in vivo.

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

94 ism represents a potential new mechanism for ADPKD progression.

95 Unfortunately, treatment options for ADPKD are limited.

96 or developing new therapeutic strategies for ADPKD.

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

98 family as the primary therapeutic target for ADPKD.

99 ancer drugs in a quest to repurpose them for ADPKD.

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

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

102 NA-17 (miR-17), as a potential treatment for ADPKD.

103 lopment as a disease-modifying treatment for ADPKD.

104 targets that may be useful as treatments for ADPKD.

105 7 compounds to identify novel treatments for ADPKD.

106 sues, has been suggested as a factor fueling ADPKD progression.

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

108 isease gene in the genetically heterogeneous ADPKD spectrum.

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

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

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

112 Similarly, conditioned media from human ADPKD cystic epithelial cells increased myofibroblast ac

113 lts, cyst-lining epithelial cells from human ADPKD kidneys had a twofold increase in mitochondria and

114 AP by an ERK1/2-dependent mechanism in human ADPKD cystic epithelial cells.

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

116 itioned media from primary cultures of human ADPKD cystic epithelial cells on myofibroblast activatio

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

118 could lead to new therapeutic approaches in ADPKD.

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

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

121 d theophylline, which are contraindicated in ADPKD patients.

122 ell proliferation typical of kidney cysts in ADPKD.

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

124 s linking polycystins to cyst development in ADPKD are still unclear.

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

126 on in cysts derived from collecting ducts in ADPKD.

127 rate oxidative stress to be present early in ADPKD.

128 ls plays a crucial role in cyst expansion in ADPKD.

129 olycystin-1-the predominant causal factor in ADPKD-itself contributes to ADPKD hypertension independe

130 amined its role in V2R-dependent fibrosis in ADPKD as well as that of yes-associated protein (YAP).

131 interstitial myofibroblasts and fibrosis in ADPKD kidneys.

132 tic microenvironment, leading to fibrosis in ADPKD.

133 potential therapeutic target for fibrosis in ADPKD.

134 l abnormalities facilitate cyst formation in ADPKD.

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

136 3 is not a critical driver of cyst growth in ADPKD but rather plays a major role in the crosstalk bet

137 standing the role of PC-1/PC-2 heteromers in ADPKD and suggest new therapeutic strategies that would

138 y analysis and were previously implicated in ADPKD pathogenesis.

139 nes and restrict immune cell infiltration in ADPKD.

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

141 Here, we investigate the role of JAK2 in ADPKD using a murine model of ADPKD (Pkd1(nl/nl)).

142 e pathophysiological role of mitochondria in ADPKD remains uncharacterized.

143 s showed that WES detected PKD1 mutations in ADPKD patients with 50% sensitivity, as the reading dept

144 tin- and cilia-dependent cyst progression in ADPKD remain incompletely understood.

145 crucial for studying disease progression in ADPKD.

146 n early driver of cyst cell proliferation in ADPKD due to Pkd1 inactivation.

147 complement as disease-associated proteins in ADPKD.

148 up-regulation of vasopressin V2 receptors in ADPKD.

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

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

151 lated with cyst size and disease severity in ADPKD patients.

152 e found alterations in Hedgehog signaling in ADPKD-related models and tissues, the relationship betwe

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

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

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

156 -protein signalling and the immune system in ADPKD.

157 ows promise as a novel therapeutic target in ADPKD.

158 rgement and hence a potential drug target in ADPKD.

159 tion as biomarkers or targets for therapy in ADPKD.

160 the inter- and intrafamilial variability in ADPKD.

161 ation highlights major limitations of WES in ADPKD genetic diagnosis.

162 al and human cell models of ADPKD, including ADPKD patient-derived primary cell cultures, we demonstr

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

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

165 lity that inhibiting HDAC6 might help manage ADPKD.

166 demonstrate that ADPKD mouse and rat models, ADPKD patient renal biopsies and PKD1-/- cells exhibited

167 tic kidney disease 1 (PKD1) account for most ADPKD cases.

168 referentially affected the viability of most ADPKD cells with minimal effects on NHK cells.

169 dly reduced cystic growth of human and mouse ADPKD-derived cells in cystogenesis assays.

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

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

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

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

174 strong understanding of the genetic basis of ADPKD, we do not know how most variants impact channel f

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

176 In a cohort of ADPKD patients, lower levels of urinary excretion of cit

177 nct and important extrarenal complication of ADPKD.

178 d management can alter the disease course of ADPKD.

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

180 e affordable and its use in the detection of ADPKD mutations for diagnostic and research purposes mor

181 dard (Sanger sequencing) in the detection of ADPKD mutations?

182 genetically unresolved clinical diagnosis of ADPKD or polycystic liver disease to identify a candidat

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

184 personalization of therapeutic management of ADPKD.

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

186 ole of JAK2 in ADPKD using a murine model of ADPKD (Pkd1(nl/nl)).

187 However, in an adult model of ADPKD utilizing inducible conditional Pkd1 deletion, con

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

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

190 improved survival of an orthologous model of ADPKD.

191 was similarly dysregulated in Pkd1 models of ADPKD, and conditional inactivation of Cdk1 with Pkd1 ma

192 Using both animal and human cell models of ADPKD, including ADPKD patient-derived primary cell cult

193 both early- and adult-onset mouse models of ADPKD, we used conditional inactivation of Pkd1 combined

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

195 y studies in advanced pre-clinical models of ADPKD.

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

197 and disease progression in animal models of ADPKD.

198 se models of developmental or adult-onset of ADPKD.

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

200 ortant contributor to the pathophysiology of ADPKD.

201 the candidate pathway in the progression of ADPKD.

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

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

204 For asymptomatic minors at risk of ADPKD, ongoing surveillance (repeated screening for trea

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

206 At the early stages of ADPKD typical markers of severity and progression of the

207 in an at-risk child is highly suggestive of ADPKD, but a negative scan cannot rule out ADPKD in chil

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

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

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

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

212 icant cause of symptomatic, very early onset ADPKD.

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

214 miR-19 or miR-25 families in an orthologous ADPKD model.

215 f ADPKD, but a negative scan cannot rule out ADPKD in childhood.

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

217 valuation of compounds in a panel of primary ADPKD and normal human kidney (NHK) epithelial cells.

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

219 rity of pathogenic mutations in Pkd2-related ADPKD.

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

221 Because it is known that several ADPKD therapies with promising outcomes in animal models

222 oliferation is an effective means of slowing ADPKD progression caused by inactivation of Pkd1.

223 srupting cilia structure significantly slows ADPKD progression following inactivation of polycystins.

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

225 iates with faster progression in early-stage ADPKD.

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

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

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

229 We demonstrate that ADPKD mouse and rat models, ADPKD patient renal biopsies

230 007 patients, which raised a hypothesis that ADPKD is associated with biliary tract disease.

231 sms, and cardiac valvular disease, show that ADPKD is a systemic disorder.

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

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

234 onmental factors significantly affecting the ADPKD phenotype.

235 pression, maturation, or localization of the ADPKD polycystin proteins, with no interaction detected

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

237 polycystic kidney and liver diseases on the ADPKD spectrum are also caused by mutations in at least

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

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

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

241 n-1 deficiency does not itself contribute to ADPKD hypertension and that it may, in fact, exert a rel

242 ggesting that ectopic JAK2 may contribute to ADPKD.

243 causal factor in ADPKD-itself contributes to ADPKD hypertension independent of cystogenesis.

244 y is aberrantly activated and contributes to ADPKD pathogenesis via enhancing epithelial proliferatio

245 atients with polycystic liver disease due to ADPKD, lanreotide for 120 weeks reduced the growth of li

246 enic contribution of these miRNA families to ADPKD progression is unknown.

247 tanding key signalling pathways that lead to ADPKD.

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

249 be a novel and effective agent for treating ADPKD.

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

251 n important part of the mechanism underlying ADPKD pathogenesis.

252 sights into the cellular pathways underlying ADPKD have revealed striking similarities to cancer.

253 and attenuates cyst growth in human in vitro ADPKD models and multiple PKD mouse models after subcuta

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

255 Of 558 adults with ADPKD in the HALT-A study, we identified 25 patients of

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

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

258 ssification of PKD2 variants associated with ADPKD, where polycystin-2 channel dysregulation in the p

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

260 Children with ADPKD should be strongly encouraged to achieve the low d

261 sease (ADPKD) are genetically distinct, with ADPKD usually caused by the genes PKD1 or PKD2 (encoding

262 By contrast, in kidneys of mice with ADPKD, JAK2 is higher in cyst-lining cells when compared

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

264 r 2016 to June 2017, adult participants with ADPKD underwent one MRI and two CT examinations.

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

266 eotide vs standard care in 305 patients with ADPKD (the DIPAK-1 study).

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

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

269 at MR angiography screening of patients with ADPKD every 5 years and annual follow-up in patients wit

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

271 f declining kidney function in patients with ADPKD is unknown.

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

273 aluable for clinical trials in patients with ADPKD or in older children with tuberous sclerosis compl

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

275 HASTE coronal sequences) from patients with ADPKD to train the network and the remaining 20% for val

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

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

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

279 e assessed suPAR levels in 649 patients with ADPKD who underwent scheduled follow-up for at least 3 y

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

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

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

283 es that are mutated in >99% of patients with ADPKD), may in part affect cellular metabolism through d

284 function and incident ESRD in patients with ADPKD, and may aid early identification of patients at h

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

286 r and kidney volume (hTLKV) in patients with ADPKD.

287 pathogenesis of a subgroup of patients with ADPKD.

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

289 tyrosine kinase inhibitor, in patients with ADPKD.

290 ve and therapeutic options for patients with ADPKD.

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

292 om three independent groups of patients with ADPKD.

293 potential utility for treating patients with ADPKD.

294 he disease varies widely among patients with ADPKD.

295 ured intracranial aneurysms 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