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.