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1 ogical symptoms, cardiovascular defects, and polycystic kidneys.
2 nd polycystic kidney (PCK) rats, control and polycystic kidney 2 (Pkd2(ws25/-)) mice, healthy individ
3 duced levels of Cdc25A) were cross-bred with polycystic kidney and hepatic disease 1 (Pkhd1(del2/del2
4 ted from the unaffected parent, or biallelic polycystic kidney and hepatic disease 1 (PKHD1) mutation
5 e 1 region that includes a novel mutation in polycystic kidney and hepatic disease 1 (Pkhd1).
6 ischemic injured and uninjured Pkd1 knockout polycystic kidneys and in human ADPKD kidneys.
7  mutant alleles of IFT complex B genes cause polycystic kidneys, but the influence of IFT complex A p
8        talpid(3) mutant embryos also develop polycystic kidneys, consistent with widespread failure o
9  and comparing with IgAN, autosomal dominant polycystic kidney disease (ADPKD) and diabetic nephropat
10 ps early in patients with autosomal dominant polycystic kidney disease (ADPKD) and is associated with
11 Hypertension is common in autosomal dominant polycystic kidney disease (ADPKD) and is associated with
12                           Autosomal-dominant polycystic kidney disease (ADPKD) and von Hippel-Lindau
13 anisms of cystogenesis in autosomal dominant polycystic kidney disease (ADPKD) are not fully understo
14         Prenatal forms of autosomal dominant polycystic kidney disease (ADPKD) are rare but can be re
15 -Biedl syndrome (BBS) and autosomal dominant polycystic kidney disease (ADPKD) are two genetically di
16 l epigenetic regulator of autosomal dominant polycystic kidney disease (ADPKD) but also as a novel cl
17 a cohort of patients with autosomal dominant polycystic kidney disease (ADPKD) compared with a contro
18                           Autosomal dominant polycystic kidney disease (ADPKD) constitutes the most i
19  elegans and mammals, the autosomal dominant polycystic kidney disease (ADPKD) gene products polycyst
20 ponse is blocked when the autosomal-dominant polycystic kidney disease (ADPKD) gene products, polycys
21 ation and modification in autosomal dominant polycystic kidney disease (ADPKD) have helped to explain
22 elopment and expansion in autosomal dominant polycystic kidney disease (ADPKD) involves both fluid se
23                           Autosomal dominant polycystic kidney disease (ADPKD) is a common cause of E
24                           Autosomal dominant polycystic kidney disease (ADPKD) is a common cause of r
25                           Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited
26                           Autosomal dominant polycystic kidney disease (ADPKD) is a common inherited
27                           Autosomal-dominant polycystic kidney disease (ADPKD) is a common life-threa
28                           Autosomal-dominant polycystic kidney disease (ADPKD) is a common, progressi
29                           Autosomal dominant polycystic kidney disease (ADPKD) is a commonly inherite
30                           Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder
31                           Autosomal dominant polycystic kidney disease (ADPKD) is a leading cause of
32                           Autosomal dominant polycystic kidney disease (ADPKD) is a progressive genet
33                           Autosomal dominant polycystic kidney disease (ADPKD) is an important cause
34                           Autosomal dominant polycystic kidney disease (ADPKD) is associated with pro
35                           Autosomal dominant polycystic kidney disease (ADPKD) is caused by inactivat
36                           Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations
37                           Autosomal-dominant polycystic kidney disease (ADPKD) is caused by mutations
38                           Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations
39                           Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations
40                           Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations
41                           Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations
42                           Autosomal dominant polycystic kidney disease (ADPKD) is characterized by in
43                           Autosomal dominant polycystic kidney disease (ADPKD) is characterized by re
44                           Autosomal dominant polycystic kidney disease (ADPKD) is driven by mutations
45                           Autosomal dominant polycystic kidney disease (ADPKD) is heterogeneous with
46             The course of autosomal dominant polycystic kidney disease (ADPKD) is often associated wi
47                           Autosomal dominant polycystic kidney disease (ADPKD) is one of the most com
48                           Autosomal dominant polycystic kidney disease (ADPKD) is the most common gen
49                           Autosomal-dominant polycystic kidney disease (ADPKD) is the most common her
50                           Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inh
51                           Autosomal dominant polycystic kidney disease (ADPKD) is the most common lif
52                           Autosomal dominant polycystic kidney disease (ADPKD) is the most frequent g
53             Patients with autosomal dominant polycystic kidney disease (ADPKD) often need to undergo
54                           Autosomal dominant polycystic kidney disease (ADPKD) often results in ESRD
55 gression in patients with autosomal dominant polycystic kidney disease (ADPKD) remains untested.
56 etic nephropathy (DN) and autosomal-dominant polycystic kidney disease (ADPKD) served as "external" n
57        Novel therapies in autosomal dominant polycystic kidney disease (ADPKD) signal the need for ma
58             Patients with autosomal dominant polycystic kidney disease (ADPKD) typically carry a muta
59             The course of autosomal dominant polycystic kidney disease (ADPKD) varies among individua
60 er disease may complicate autosomal dominant polycystic kidney disease (ADPKD), a disease caused by m
61 lycystin-1 (PC1) leads to autosomal dominant polycystic kidney disease (ADPKD), a disorder characteri
62 hich, when mutated, cause autosomal dominant polycystic kidney disease (ADPKD), a highly prevalent hu
63 olycystin-1 (PC1) lead to autosomal-dominant polycystic kidney disease (ADPKD), a leading cause of re
64 ed Pkd1 protein result in autosomal dominant polycystic kidney disease (ADPKD), a serious inherited s
65                           Autosomal dominant polycystic kidney disease (ADPKD), characterized by the
66                        In autosomal dominant polycystic kidney disease (ADPKD), cysts accumulate and
67  compared with those with autosomal dominant polycystic kidney disease (ADPKD), in which the native k
68 idely among patients with autosomal dominant polycystic kidney disease (ADPKD), necessitating optimal
69                           Autosomal dominant polycystic kidney disease (ADPKD), one of the most commo
70 (Pkd2) gene is mutated in autosomal dominant polycystic kidney disease (ADPKD), one of the most commo
71 cally identified cases of autosomal dominant polycystic kidney disease (ADPKD), one of the most commo
72                           Autosomal dominant polycystic kidney disease (ADPKD), the most common form
73 PKD2 gene, which leads to autosomal dominant polycystic kidney disease (ADPKD).
74 ssion to renal failure in autosomal dominant polycystic kidney disease (ADPKD).
75 n genetic kidney disorder autosomal dominant polycystic kidney disease (ADPKD).
76 uses ciliopathies such as autosomal dominant polycystic kidney disease (ADPKD).
77 ain cause of mortality in autosomal-dominant polycystic kidney disease (ADPKD).
78 t for almost all cases of autosomal dominant polycystic kidney disease (ADPKD).
79 the genes responsible for autosomal dominant polycystic kidney disease (ADPKD).
80 ses, including cancer and autosomal dominant polycystic kidney disease (ADPKD).
81 polycystin-1 (PC1), cause autosomal-dominant polycystic kidney disease (ADPKD).
82 ng pathway is aberrant in autosomal-dominant polycystic kidney disease (ADPKD).
83 rthologous mouse model of autosomal dominant polycystic kidney disease (ADPKD).
84 nes, PKD1 and PKD2, cause autosomal dominant polycystic kidney disease (ADPKD).
85 escribed manifestation of autosomal dominant polycystic kidney disease (ADPKD).
86  the most common cause of autosomal dominant polycystic kidney disease (ADPKD).
87 ibute to >85% of cases of autosomal dominant polycystic kidney disease (ADPKD).
88 ed to the pathogenesis of autosomal dominant polycystic kidney disease (ADPKD).
89  concern in patients with autosomal dominant polycystic kidney disease (ADPKD).
90 olycystin-2 (PC2) lead to autosomal dominant polycystic kidney disease (ADPKD).
91 rgement of renal cysts in autosomal dominant polycystic kidney disease (ADPKD).
92 nsion and cystogenesis in autosomal dominant polycystic kidney disease (ADPKD).
93 lving patients with early autosomal dominant polycystic kidney disease (ADPKD; estimated creatinine c
94 th refractory symptoms of autosomal dominant polycystic kidney disease (APKD) in need of a renal tran
95                          Autosomal recessive polycystic kidney disease (ARPKD) is a significant hered
96                          Autosomal recessive polycystic kidney disease (ARPKD) is an important childh
97 rmation and expansion in autosomal recessive polycystic kidney disease (ARPKD) is poorly understood,
98 rats, an animal model of autosomal-recessive polycystic kidney disease (ARPKD), decreased intracellul
99                          Autosomal recessive polycystic kidney disease (ARPKD), the most common cilio
100       BACKGROUND & AIMS: Autosomal recessive polycystic kidney disease (ARPKD), the most common cilio
101                          Autosomal recessive polycystic kidney disease (ARPKD), usually considered to
102 Caroli disease (CD), and autosomal recessive polycystic kidney disease (ARPKD).
103 codes fibrocystin, cause autosomal recessive polycystic kidney disease (ARPKD).
104 ectomies exist for patients with symptomatic polycystic kidney disease (PCKD).
105 ious studies report a cross-talk between the polycystic kidney disease (PKD) and tuberous sclerosis c
106 insulinemic hypoglycemia (HI) and congenital polycystic kidney disease (PKD) are rare, genetically he
107 denosine monophosphate (cAMP) drives genetic polycystic kidney disease (PKD) cystogenesis.
108 s to drive the aggregation of the downstream polycystic kidney disease (PKD) domain into a melanosoma
109 ncluding the leucine-rich repeats, the first polycystic kidney disease (PKD) domain, and the C-type l
110  multimodular structure including 16 Ig-like polycystic kidney disease (PKD) domains.
111                                              Polycystic kidney disease (PKD) exhibits an inflammatory
112                                              Polycystic kidney disease (PKD) family proteins associat
113 at is defective in expression of the sensory polycystic kidney disease (PKD) gene battery and male ma
114 nd their disruption has been associated with polycystic kidney disease (PKD) genes, the majority of w
115                                              Polycystic kidney disease (PKD) in mice can arise from d
116                                              Polycystic kidney disease (PKD) is a genetic disorder th
117                                              Polycystic kidney disease (PKD) is a leading cause of ES
118                      Autosomal-dominant (AD) polycystic kidney disease (PKD) is a leading cause of re
119                                              Polycystic kidney disease (PKD) is a life-threatening di
120                                              Polycystic kidney disease (PKD) is one of the most commo
121  and interstitial fibrosis, similar to known polycystic kidney disease (PKD) models.
122 There are no proven, effective therapies for polycystic kidney disease (PKD) or polycystic liver dise
123 olysis Site (GPS) of cell-adhesion GPCRs and polycystic kidney disease (PKD) proteins constitutes a h
124 ptor potential channel polycystin (TRPP) and polycystic kidney disease (PKD) proteins, play key roles
125 eracts predominantly with the second Ig-like polycystic kidney disease (PKD) repeat domain (PKD2) pre
126                                              Polycystic kidney disease (PKD) represents a family of g
127 be an underlying cause of autosomal dominant polycystic kidney disease (PKD), and ciliary-EV interact
128 ) allele) results in proteinuria, hematuria, polycystic kidney disease (PKD), and death 3 to 4 weeks
129 ney disease (ADPKD), the most common form of polycystic kidney disease (PKD), is a disorder with char
130                                           In polycystic kidney disease (PKD), renal parenchyma is des
131                                              Polycystic kidney disease (PKD), the most common genetic
132 tro and in vivo models of autosomal dominant polycystic kidney disease (PKD).
133  is an important mediator of cystogenesis in polycystic kidney disease (PKD).
134 indicates the importance of elevated cAMP in polycystic kidney disease (PKD).
135 ding the kidney, liver and pancreas features polycystic kidney disease (PKD).
136 involved in pathological conditions, such as polycystic kidney disease (PKD).
137 s phenotype is reminiscent of human forms of polycystic kidney disease (PKD).
138 target of rapamycin (mTOR) pathway occurs in polycystic kidney disease (PKD).
139 P signaling contribute to the development of polycystic kidney disease (PKD).
140 shows beneficial effects in animal models of polycystic kidney disease (PKD); however, two clinical t
141 e (Pu-Py) mirror repeat tract from the human polycystic kidney disease (PKD1) intron 21 forms non-B D
142 ost frequently mutated in autosomal dominant polycystic kidney disease (PKD1).
143 on to the familial mutation, variation(s) in polycystic kidney disease 1 (PKD1) or HNF1 homeobox B (H
144 ng from inherited mutations in the genes for polycystic kidney disease 1 (PKD1) or polycystic kidney
145 or potential (TRP) channels Trpm, NompC, and Polycystic kidney disease 2 (Pkd2) are expressed in CIII
146                                          The Polycystic Kidney Disease 2 (Pkd2) gene is mutated in au
147 olved in osteoblast differentiation and that polycystic kidney disease 2 (Pkd2) was a downstream targ
148 es for polycystic kidney disease 1 (PKD1) or polycystic kidney disease 2 (PKD2).
149 ith polycystin-2 (the protein product of the polycystic kidney disease 2 gene), and, when disrupted,
150         Here, we show that disruption of the polycystic kidney disease 2-like 1 (Pkd2l1 or Pkdl), enc
151 ociated with higher 16:1n-7, whereas PKD2L1 (polycystic kidney disease 2-like 1; P=5.7x10(-15)) and a
152 ate-dependent kinase, and the cation channel polycystic kidney disease 2.
153 and other secretory diarrheas [7] as well as polycystic kidney disease [8-10].
154                                          The polycystic kidney disease allele in this model, Bicc1, i
155 his case involves a 54-year-old patient with polycystic kidney disease and a history of hyperacute al
156 ce of renal epithelial cells is perturbed in polycystic kidney disease and apical expression of recep
157  allele significantly ameliorated the severe polycystic kidney disease and consequent runting caused
158 sing for the treatment of autosomal dominant polycystic kidney disease and have been approved in Japa
159 d Safety in Management of Autosomal Dominant Polycystic Kidney Disease and Its Outcomes) trial, tolva
160 vels of this eicosanoid are also elevated in polycystic kidney disease and may contribute to cyst for
161                    It has a critical role in polycystic kidney disease and nephronophthisis.
162  weights and cyst growth in animal models of polycystic kidney disease and PLD, and might be develope
163                                           In polycystic kidney disease and polycystic liver disease (
164     The first case is a 67-year-old man with polycystic kidney disease and recipient of a zero-antige
165 el are predicted to slow cyst enlargement in polycystic kidney disease and reduce intestinal fluid lo
166 athology resembling human autosomal dominant polycystic kidney disease and represent a useful model t
167 mbryonic development to adult progression of polycystic kidney disease and some cancers.
168 acterized internal domain is a member of the polycystic kidney disease domain family but also how the
169  potential polycystic (TRPP) channel PKD1L2 (polycystic kidney disease gene 1-like 2) underlies this
170 riched miRNA family, and upregulation of the polycystic kidney disease gene Pkd1.
171 ozygous mutations in the autosomal recessive polycystic kidney disease gene PKHD1, indicating that ad
172 f fibrocystin, the human autosomal recessive polycystic kidney disease gene product.
173 te expression of a functional complex of the polycystic kidney disease gene products, polycystin-1 an
174 lting from mutations in Pkhd1, the recessive polycystic kidney disease gene.
175                              Knockout of the polycystic kidney disease genes PKD1 or PKD2 induces cys
176 uires lov-1 and pkd-2 (homologs of the human polycystic kidney disease genes, PKD1 and PKD2), which a
177                           Autosomal dominant polycystic kidney disease has been linked to mutations i
178  or down-regulation of PKD1 or PKD2 leads to polycystic kidney disease in animal models, but their in
179                                              Polycystic kidney disease is a common genetic disorder i
180                           Autosomal dominant polycystic kidney disease is a genetic disorder associat
181                           Autosomal dominant polycystic kidney disease is caused by mutations in the
182                Recent evidence suggests that polycystic kidney disease is characterized by defects in
183                           Autosomal dominant polycystic kidney disease is the most common inherited k
184                Using human ADPKD tissues and polycystic kidney disease mouse models, we show that the
185   The most severe form of autosomal dominant polycystic kidney disease occurs in patients with mutati
186 beings, and patients with autosomal-dominant polycystic kidney disease or ARPKD.
187 fective for patients with autosomal dominant polycystic kidney disease or polycystic liver disease; e
188 m that may play a role in autosomal dominant polycystic kidney disease pathogenesis.
189 ls (NL, 42 vs. 17; US, 40 vs. 13 points) and polycystic kidney disease patients without PLD (22 point
190 es of PLD patients with general controls and polycystic kidney disease patients without PLD.
191                     Cysts and aneurysms from polycystic kidney disease patients, Pkd mouse, and zebra
192  of PCK rats and ARPKD or autosomal-dominant polycystic kidney disease patients.
193  in a disruption of renal ciliogenesis and a polycystic kidney disease phenotype in zebrafish and mic
194 unction by re-expressing survivin can rescue polycystic kidney disease phenotypes.
195 may predict and/or effect autosomal dominant polycystic kidney disease progression.
196                             Furthermore, the polycystic kidney disease protein IFT88 binds IFT52281-3
197 ensitive complex with the autosomal dominant polycystic kidney disease protein polycystin 2.
198                        GPS is also shared by polycystic kidney disease proteins and it precedes the f
199  who participated in the Halt Progression of Polycystic Kidney Disease Study A were categorized on th
200         For patients with autosomal dominant polycystic kidney disease that progressed more slowly, t
201 rize for Advancement in the Understanding of Polycystic Kidney Disease to participate in a forward-th
202 h G proteins are regulated in the context of polycystic kidney disease to promote abnormal epithelial
203 al mass, may accelerate progression of adult polycystic kidney disease toward end-stage renal disease
204 enal disease secondary to autosomal dominant polycystic kidney disease was referred to a quaternary c
205 , recipient employment, and the diagnosis of polycystic kidney disease were significantly associated
206 to identify patients with autosomal dominant polycystic kidney disease who are most likely to benefit
207 om GPCRs and fibrocystin (also implicated in polycystic kidney disease), we demonstrate these motifs
208 linical manifestations seen in patients with polycystic kidney disease, a cilia-associated pathology
209  a role in the pathogenesis of hypertension, polycystic kidney disease, AKI, and CKD.
210 stin-1 (PC1) give rise to autosomal dominant polycystic kidney disease, an important and common cause
211 s, diabetes, chronic interstitial nephritis, polycystic kidney disease, and 1-3 years of prior dialys
212 iseases such as ischemia/reperfusion injury, polycystic kidney disease, and congenital solitary kidne
213 C and PKD), identified in linkage studies of polycystic kidney disease, are candidate channels divide
214 ed in cancer cells, ciliopathies such as the polycystic kidney disease, as well as in the genetic dis
215 laying an important role in the formation of polycystic kidney disease, but not for Rab8 another cili
216 s the juvenile cystic kidneys (jck) model of polycystic kidney disease, but the functions of Nek8 are
217 dentical to those seen in autosomal dominant polycystic kidney disease, but without clinically releva
218                      In PCLD associated with polycystic kidney disease, cell proliferation is one of
219 utosomal recessive disorder characterized by polycystic kidney disease, central nervous system defect
220  mice, an animal model of autosomal dominant polycystic kidney disease, developed hepatic cysts.
221 erties of PC2 are lost in autosomal dominant polycystic kidney disease, emphasizing the importance of
222 APK activation, all of which are features of polycystic kidney disease, especially nephronophthisis.
223   Deletion of Lgr4 in mouse led to aniridia, polycystic kidney disease, genitourinary anomalies, and
224  a suspected diagnosis of autosomal dominant polycystic kidney disease, medullary cystic kidney disea
225                In contrast to many models of polycystic kidney disease, precystic Ift140-deleted coll
226 f a 21-year-old man with autosomal recessive polycystic kidney disease, presenting with subarachnoid
227 , and ciliary dysfunction is associated with polycystic kidney disease, retinal degeneration, polydac
228 tin 2 are responsible for autosomal dominant polycystic kidney disease, the most common heritable hum
229     To gain insights into autosomal dominant polycystic kidney disease, we performed yeast two-hybrid
230          Here we focus on autosomal dominant polycystic kidney disease, which is attributable to muta
231 ferral before dialysis were the diagnosis of polycystic kidney disease, white recipient race, referra
232                                          The polycystic kidney disease-1 (Pkd1) gene encodes a large
233 e and a downstream domain with homology to a polycystic kidney disease-1 repeat, efficiently form amy
234              Furthermore, autosomal dominant polycystic kidney disease-associated TRPP2 mutant T448K
235  G protein-coupled receptors (GPCRs) and the polycystic kidney disease-causing polycystin 1/2 complex
236 nction between the N-terminal region and the polycystic kidney disease-like domain is highly crucial
237 ithelial pancreatic neoplasia, and 1 case of polycystic kidney disease.
238 in either protein causing autosomal dominant polycystic kidney disease.
239 3 control recipients with autosomal dominant polycystic kidney disease.
240 arget in the treatment of autosomal dominant polycystic kidney disease.
241 trarenal manifestation in autosomal dominant polycystic kidney disease.
242 g therapeutic strategy in autosomal dominant polycystic kidney disease.
243 ions to human PC2 (hPC2) are associated with polycystic kidney disease.
244 hannel that is mutated in autosomal dominant polycystic kidney disease.
245 2), respectively, lead to autosomal dominant polycystic kidney disease.
246 plains both renal and vascular phenotypes in polycystic kidney disease.
247 l diseases, such as diabetic nephropathy and polycystic kidney disease.
248  pathway result in deranged ciliogenesis and polycystic kidney disease.
249 humans and mice, nephronophthisis (NPHP) and polycystic kidney disease.
250 st, urine podocyte mRNAs did not increase in polycystic kidney disease.
251 a Ca(2+)-dependent channel with relevance to polycystic kidney disease.
252 obulin A nephropathy, and autosomal dominant polycystic kidney disease.
253        Persons with early autosomal dominant polycystic kidney disease.
254 2, the protein mutated in autosomal dominant polycystic kidney disease.
255  for approximately 15% of autosomal dominant polycystic kidney disease.
256 ice, a model that mimics autosomal recessive polycystic kidney disease.
257 C1) is the major cause of autosomal dominant polycystic kidney disease.
258 aintenance of tubule diameter correlate with polycystic kidney disease.
259 also suggest insight into the development of polycystic kidney disease.
260 cium signaling and causes autosomal dominant polycystic kidney disease.
261 ssociates with accelerated cyst formation in polycystic kidney disease.
262 ction has been linked to the pathogenesis of polycystic kidney disease.
263 kinesis defects in both mice and humans with polycystic kidney disease.
264 y mutated or truncated in autosomal dominant polycystic kidney disease.
265 ne proteins implicated in autosomal dominant polycystic kidney disease.
266 disorders, such as Bardet-Biedl Syndrome and Polycystic Kidney Disease.
267 mation and enlargement in autosomal dominant polycystic kidney disease.
268 1 +/- 1 years) with PLD, 117 had concomitant polycystic kidney disease.
269  in a neonatal kidney organ culture model of polycystic kidney disease.
270 ecessive disorder characterized by bilateral polycystic kidney disease.
271 d to preserve renal function in experimental polycystic kidney disease.
272  Dysfunction of renal primary cilia leads to polycystic kidney disease.
273 umerous disease models, including cancer and polycystic kidney disease.
274  have utility in diagnosis and monitoring of polycystic kidney disease.
275 s on renal function and favor cyst growth in polycystic kidney disease.
276  as a possible therapy for heart failure and polycystic kidney disease.
277      Ectopic cAMP signaling is pathologic in polycystic kidney disease; however, its spatiotemporal a
278 ) mice, a mouse model of autosomal recessive polycystic kidney disease; this gene encodes cystin, a 1
279 s of inherited disorders, autosomal dominant polycystic kidney diseases (ADPKD), a significant cause
280                                              Polycystic kidney diseases (PKD) are a group of inherite
281                                              Polycystic kidney diseases (PKD) are genetic disorders c
282 g is a key feature in the pathophysiology of polycystic kidney diseases (PKD).
283                                              Polycystic kidney diseases (PKDs) are genetic disorders
284                                              Polycystic kidney diseases (PKDs) comprise a subgroup of
285                             Genetic forms of polycystic kidney diseases (PKDs), including nephronopht
286                                              Polycystic kidney diseases are characterized by numerous
287                                              Polycystic kidney diseases are the most common genetic d
288 e autosomal dominant and autosomal recessive polycystic kidney diseases, are incurable pathological c
289 ons in genes encoding polycystin-1 and -2 in polycystic kidney diseases.
290           However, automatic segmentation of polycystic kidneys is a challenging task due to severe a
291                                              Polycystic kidneys of Pkd2WS25/- mice, an orthologous mo
292                                       In the polycystic kidney (PCK) rat model, activation of STAT3 i
293                                           In polycystic kidney (PCK) rats, an animal model of autosom
294 ession was analyzed in livers of control and polycystic kidney (PCK) rats, control and polycystic kid
295 ation of both SEC63 and XBP1 exacerbated the polycystic kidney phenotype in mice by markedly suppress
296  examined hepatic cystogenesis in OA-treated polycystic kidney rats and after genetic elimination of
297                 OA increased cystogenesis in polycystic kidney rats by 35%; in contrast, hepatic cyst
298                                    In Wistar polycystic kidney rats with hydrocephalus, alteration of
299     All patients received general health and polycystic kidney symptom surveys.
300 neal injection is preferentially targeted to polycystic kidneys whereas injected IgG is not.

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