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1 ormoalbuminuric, 23 microalbuminuric, and 31 proteinuric).
2 nuric, 17 were microalbuminuric, and 19 were proteinuric.
3 n both animal models and humans exhibiting a proteinuric.
4 odels of glomerular injury and that its anti-proteinuric action may result from direct effects on cel
5 emain unknown, particularly whether the anti-proteinuric activity of AT(2)R is independent of its ant
6            Overall, AT(2)R has a direct anti-proteinuric activity, potentially via megalin regulation
7 enic mouse models of APOL1 disease, the anti-proteinuric and anti-glomerulosclerotic effects of stand
8 maller and less specific differences between proteinuric and control groups.
9 LL lesion were more often black and severely proteinuric and developed more end-stage renal disease (
10 have a proven steroidogenic-independent anti-proteinuric and glomerular protective effect.
11  injection of anti-Fx1A antiserum, rats were proteinuric and had a blunted natriuretic response to in
12         On day 7, the PHN rats were severely proteinuric, and most slit diaphragms were either absent
13 ce with the results seen in suPAR-associated proteinuric animal models, in which kidney damage is cau
14 yeloid cells was commonly found in the BM of proteinuric animals having high suPAR, and these cells e
15 vuglandin was also increased in the ileum of proteinuric animals, and intestinal epithelial cells exp
16 c patients with FSGS-CELL (n = 39) were more proteinuric at presentation than patients with FSGS-CS (
17 n the urinary side of renal tubular cells in proteinuric, but not in normal renal tissues and colocal
18              Therefore, urine from rats made proteinuric by puromycin aminoglycoside administration w
19                                              Proteinuric chronic kidney disease (CKD), once a rare af
20           In animal models and patients with proteinuric chronic kidney diseases, MMP-10 was upregula
21 patients, and studied three mouse models, of proteinuric CKD (POD-ATTAC), of ischemic CKD, and of uni
22 nce, but the long-term prognosis of residual proteinuric CKD remains guarded, indicating a need for m
23 hree-way crossover study in 27 patients with proteinuric CKD to compare the effects of the ET(A) rece
24 h renal and systemic vascular dysfunction in proteinuric CKD.
25  transfer 2 weeks after disease induction in proteinuric conditional knock-in mice demonstrated impro
26 P) are more frequent in individuals with the proteinuric disease focal and segmental glomeruloscleros
27 a dynamic actin cross-linking protein, cause proteinuric disease in humans and mice.
28 ivated in glomeruli and podocytes in several proteinuric disease models.
29 RPC6 in the pathology of nongenetic forms of proteinuric disease.
30 l perspectives on therapeutic strategies for proteinuric diseases, including diabetic nephropathy.
31 ted tubular injury can occur in MN and other proteinuric diseases.
32 athway leading to foot process effacement in proteinuric diseases.
33 er, and hence an important common pathway in proteinuric diseases.
34 meruli is observed in several human acquired proteinuric diseases.
35 r heparanase expression is increased in most proteinuric diseases.
36 trated to be a trigger mechanism for various proteinuric diseases.
37 rvention in the nephrotic syndrome and other proteinuric diseases.
38 ve therapeutic potential in the treatment of proteinuric diseases.
39 anges in these junctions are the hallmark of proteinuric diseases.
40 id target for pharmaceutical intervention in proteinuric disorders and provide an approach to investi
41 insight into molecular mechanisms underlying proteinuric disorders, highlight potentially complex int
42 es in some patients, together with the known proteinuric effect of anti-nephrin antibodies in rodent
43 ogenic-independent and MC1R-dispensable anti-proteinuric effect of melanocortin signaling.
44              Current thresholds for defining proteinuric flare appear to be set either too high or to
45 egree of proteinuria increase that defines a proteinuric flare in systemic lupus erythematosus (SLE)
46                   Ideally, the threshold for proteinuric flare should be set sufficiently high that s
47 -based approach to setting the threshold for proteinuric flare, based on quantifying the spontaneous
48 c flares (all severe except for 1) and 2 had proteinuric flares (1 in each responder group).
49 y podocytes of hyposialylated Angptl4, a pro-proteinuric form of the protein.
50 oom3 motif and separating this from its anti-proteinuric function.
51 ma3a gain-of-function in adult mice leads to proteinuric glomerular disease involving the three layer
52 r studies should evaluate the role of YAP in proteinuric glomerular disease pathogenesis and its pote
53 butes to the development of several types of proteinuric glomerular disease, but the involvement of i
54 ro, and thrombin generation increases during proteinuric glomerular disease.
55 e trafficking pathways may act as factors in proteinuric glomerular diseases is poorly understood.
56 olled >850 pediatric and adult patients with proteinuric glomerular diseases who have contributed to
57 n trafficking pathways may act as factors in proteinuric glomerular diseases, we focused on Rab7, a h
58  be standardized to guide prognostication of proteinuric glomerular diseases.
59                  First delineated from other proteinuric glomerular lesions in the 1980s, CG is now r
60 inuria reducing and podoprotective effect in proteinuric glomerulopathies via MC1R-independent mechan
61  contribute to a more effective treatment of proteinuric glomerulopathies with the least possible sid
62 mensional ultrastructural characteristics of proteinuric glomerulopathy in mice with CD2-associated p
63 ort for kidney podocytes-have been linked to proteinuric glomerulosclerosis in humans.
64           Examination of albumin staining of proteinuric human kidneys also showed a heterogeneous pa
65 eclampsia was assessed by the development of proteinuric hypertension.
66 ) experienced renal flares (nephritic in 33, proteinuric in 8) after a mean followup of 117 months; 3
67 or more than 2 yr or enrolling more severely proteinuric individuals.
68  rats and NEP25 transgenic mice to show that proteinuric injury expanded the intestinal lymphatic net
69 oxin-induced proteinuric injury to show that proteinuric injury expanded the kidney lymphatic network
70                   We found that animals with proteinuric injury have increased kidney lymphangiogenes
71 n the present study, we investigated whether proteinuric injury increases production of isolevuglandi
72 We used a mouse model of nephrotoxin-induced proteinuric injury to show that proteinuric injury expan
73                             In rats with one proteinuric kidney (PAN-treated) and one normal kidney (
74    Podocyte injury is a major determinant of proteinuric kidney disease and the identification of pot
75 mouse models to evaluate early biomarkers of proteinuric kidney disease and to test novel therapeutic
76 o expression in the POD-ATTAC mouse model of proteinuric kidney disease as well as in kidney epitheli
77                         Anemic patients with proteinuric kidney disease had an increased proportion o
78 the known genetic cause, therapies targeting proteinuric kidney disease in persons with two APOL1 var
79 ) gene as major contributors to a subtype of proteinuric kidney disease now referred to as APOL1-medi
80 idney disease-associated anemia in mice with proteinuric kidney disease resulting from either adminis
81 mice with adriamycin nephropathy, a model of proteinuric kidney disease that resembles human focal se
82 t podocyte-specific deletion of Yap leads to proteinuric kidney disease through increased podocyte ap
83 POL1 G2-homologous transgenic mouse model of proteinuric kidney disease was used to assess inaxaplin
84                   Podocyte injury results in proteinuric kidney disease, and genetic deletion of SD-a
85 ntal glomerulosclerosis (FSGS) is a cause of proteinuric kidney disease, compromising both native and
86        In both genetic and acquired forms of proteinuric kidney disease, dysregulation of podocyte TR
87 ully reduced proteinuria in animal models of proteinuric kidney disease, indicating that therapeutic
88                                       During proteinuric kidney disease, induction of cytoplasmic cat
89 s an appropriate therapeutic goal in chronic proteinuric kidney disease.
90  in the BM, leading to high plasma suPAR and proteinuric kidney disease.
91 iovascular risk and slows the progression of proteinuric kidney disease.
92 ed in an independent cohort of patients with proteinuric kidney disease.
93 on barrier and podocyte dysfunction leads to proteinuric kidney disease.
94 or PRDM15 were detected in six families with proteinuric kidney disease.
95 h contribute to the development of anemia in proteinuric kidney disease.
96 individuals with poorer clinical outcomes in proteinuric kidney disease.
97 eutic benefit in a rat model of hypertensive proteinuric kidney disease.
98 is of podocyte injury and the progression of proteinuric kidney disease.
99 t as anuria while others are associated with proteinuric kidney disease.
100  to podocytes is a central pathomechanism of proteinuric kidney disease.
101 ss effacement, which is a classic feature of proteinuric kidney disease.
102  strategy for the prevention or treatment of proteinuric kidney disease.
103 providing a potential therapeutic target for proteinuric kidney disease.
104 ls of biochemistry may be useful in treating proteinuric kidney disease.
105 lockade may be therapeutically beneficial in proteinuric kidney disease.
106 udy the renal involvement of HPS proteins in proteinuric kidney disease.
107 and defines a molecular mechanism underlying proteinuric kidney disease.
108  foot process effacement, and contributes to proteinuric kidney disease.
109 tial therapeutic target for the treatment of proteinuric kidney disease.Podocytes are essential compo
110 ed renal function decline in mouse models of proteinuric kidney disease: Adriamycin-induced nephropat
111 ) underlies the pathogenesis of all forms of proteinuric kidney disease; however, the specific geneti
112 ated overexpression of ShcA in several human proteinuric kidney diseases compared with normal conditi
113 docyte loss is central to the progression of proteinuric kidney diseases leading to end-stage kidney
114                                     In human proteinuric kidney diseases such as diabetic nephropathy
115    Mycophenolate mofetil (MMF) is applied in proteinuric kidney diseases, but the exact mechanism of
116 py is the standard of care for patients with proteinuric kidney diseases, but their use is challengin
117 wild-type TRPC6 is a common feature of human proteinuric kidney diseases, with highest induction obse
118 e of cytoskeletal and structural proteins in proteinuric kidney diseases.
119  provides a novel molecular target to tackle proteinuric kidney diseases.
120 c therapy in the treatment of FSGS and other proteinuric kidney diseases.
121 ssays for identifying novel therapeutics for proteinuric kidney diseases.
122  renal protection against the development of proteinuric kidney diseases.
123 rstanding of the pathogenesis of progressive proteinuric kidney diseases.
124 y represent a novel therapeutic strategy for proteinuric kidney diseases.
125 g and shed further light on the treatment of proteinuric kidney diseases.
126        CsA is also used for the treatment of proteinuric kidney diseases.
127 s increased in biopsies of early-stage human proteinuric kidney diseases.
128 mma-secretase inhibitor) protected rats with proteinuric kidney diseases.
129 ry and provides a molecular target to tackle proteinuric kidney diseases.
130 across the spectrum of primary and secondary proteinuric kidney disorders, which account for up to 90
131 ulates within the kidney interstitium during proteinuric kidney injury and elevated sodium environmen
132  renoprotective effects in three independent proteinuric kidney murine models.
133 CT01918488 and Increased Activity of ENaC in Proteinuric Kidney Transplant Recipients, NCT03036748 .
134  In vivo, we observed activated PKC-delta in proteinuric kidneys of streptozotocin-induced diabetic m
135 al tissues and colocalized with properdin in proteinuric kidneys.
136                                   The GBM of proteinuric mice appeared thickened and "moth-eaten," an
137 cant difference in allele frequencies in the proteinuric, microalbuminuric, or normoalbuminuric group
138 s under cell stress and in three independent proteinuric models (LPS, nephrotoxic serum nephritis, an
139 l agonist for KLF15 with salutary effects in proteinuric murine models through direct inhibition of i
140 romoter region of KLF15 In three independent proteinuric murine models, podocyte-specific loss of Klf
141 red human podocytes and in three independent proteinuric murine models.
142 ile of MES who were also microalbuminuric or proteinuric (n = 16) were classified as "fast-track" for
143 the renal transplant population, as it is in proteinuric nephropathies.
144 ia changes have a prognostic significance in proteinuric nephropathies.
145 mmon pathways that lead to kidney failure in proteinuric nephropathies.
146 in 1467 individuals with T1D (718 cases with proteinuric nephropathy and 749 controls without nephrop
147  for the development of rapidly progressive, proteinuric nephropathy.
148 or secondary membranous nephropathy or other proteinuric or autoimmune diseases and from normal contr
149       Renal flares were classified as either proteinuric or nephritic based on changes in urinary pro
150 .012) and negatively with podocyte number in proteinuric patients (r = -0.48, P = 0.040).
151 lasmin (ogen) uria, has been demonstrated in proteinuric patients and exposure of cultured podocytes
152           In contrast, 71% of glomeruli from proteinuric patients had glomerulotubular junction abnor
153 did not found any biallelic CUBN variants in proteinuric patients with reduced renal function or foca
154 nd-stage renal disease (ESRD) in a cohort of proteinuric patients with type 1 diabetes (T1D) and norm
155 otubular junction abnormalities, frequent in proteinuric patients with type 1 diabetes, may contribut
156 atients, five microalbuminuric patients, six proteinuric patients, and five control subjects were stu
157 absorption of phosphate increased during the proteinuric phase compared with the remission phase in n
158 e FHH.BN-Rab38 congenic line recapitulated a proteinuric phenotype indistinguishable from the FHH str
159                                              Proteinuric, plasmid injected G1/G1 and G2/G2 mice were
160                                              Proteinuric rats developed tubulointerstitial disease th
161                      Compared with controls, proteinuric rats exhibited significantly lower eliminati
162                                  In study A, proteinuric rats were given sheep anti-Fx1A to induce ex
163                                     In vivo, proteinuric rats were treated with vehicle or paricalcit
164 oss of renal mass and was reduced further in proteinuric rats with 0.6 kidneys.
165 hat were not different from sera pooled from proteinuric rats with HN induced with nephritogenic Fx1A
166 patients with FSGS, in single glomeruli from proteinuric rats, and in podocytes undergoing mechanical
167                Compared with vehicle-treated proteinuric rats, paricalcitol showed markedly reduced r
168 locks TRPC5 channel activity in glomeruli of proteinuric rats.
169 e may have relevance for the pathogenesis of proteinuric renal disease in human patients.
170                                  In acquired proteinuric renal disease, glomerular TRPC6 expression i
171 may have potential as a therapeutic agent in proteinuric renal disease.
172 nce will help to develop novel therapies for proteinuric renal diseases that are frequently limited t
173       Renal tubular atrophy accompanies many proteinuric renal diseases, suggesting that glomerular p
174 venting complement-derived tubular injury in proteinuric renal diseases.
175 tis flares, and evaluation of its utility in proteinuric states are needed.
176        Because podocyte injury is central to proteinuric states, such as the nephrotic syndrome, the
177 onfirm the presence of an inhibitor in other proteinuric states, the urine from two patients with pro
178 en compared with patients with other chronic proteinuric states, those with FSGS displayed a prolifer
179  albeit inhibition of albumin endocytosis in proteinuric states.
180 umin overload is linked to PTEC apoptosis in proteinuric states.
181 te glycosaminoglycans and is up-regulated in proteinuric states.
182 te TRPC6 protein expression was increased in proteinuric streptozotocin-induced diabetic rats.
183     In mouse models of Pierson's or Alport's proteinuric syndromes resulting from defects in GBM stru
184  Thus, an additional mechanism by which anti-proteinuric therapies are beneficial in the treatment of
185 nic nephrotic syndrome that responds to anti-proteinuric treatment.
186                    Renal biopsies from eight proteinuric type 1 D patients with normal to moderately
187 rial, we randomly assigned 317 patients with proteinuric type 2 diabetic nephropathy to twice-daily p
188  emerging reno-protective target and is anti-proteinuric under pathological conditions, including hig
189                                              Proteinuric urine contained a powerful specific inhibito
190                                              Proteinuric urine was fractionated by thin-layer chromat
191 ed effects on renal tubular cells exposed to proteinuric urine, equivalent levels of proteinuria were
192 and mostly occurs in patients who are highly proteinuric with early CKD.

 
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