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1 resistance" state (ie, resistance to further renal damage).
2 lonephritis and the development of permanent renal damage.
3 iographic contrast media fail to demonstrate renal damage.
4 aid bacterial clearance but can also lead to renal damage.
5 protein excretion, and the amount of chronic renal damage.
6 tients to reduce the incidence and extent of renal damage.
7 function and ameliorate hypertension induced renal damage.
8 e may be more susceptible to immune-mediated renal damage.
9  these compensatory pathways following acute renal damage.
10 egies that limit or prevent ischemia-induced renal damage.
11 uced in a dose-dependent fashion cardiac and renal damage.
12 e novo production of nephrons in response to renal damage.
13 CR enzyme and cholesterol accumulation after renal damage.
14 essed after in vivo ischemic and Fe-mediated renal damage.
15  urine flow protects adults from progressive renal damage.
16 peripheral vascular disease, and progressive renal damage.
17 s show that ISD protects from injury-induced renal damage.
18  after an infection actually have congenital renal damage.
19 n and glomerular hypertension eventuating in renal damage.
20  of the Th17 immune response in experimental renal damage.
21 ers cause hemodynamic process that result in renal damage.
22  after ischemia also significantly inhibited renal damage.
23 ng hypertension while preventing cardiac and renal damage.
24 ney diseases, and some show association with renal damage.
25 ce are more sensitive to tunicamycin-induced renal damage.
26 h parameters related to glycemic control and renal damage.
27 lexes improves kidney function and decreases renal damage.
28  suggesting absence of therapy-induced acute renal damage.
29  of diabetic nephropathy and obesity-induced renal damage.
30  in response to ischemia/reperfusion-induced renal damage.
31 ld overcome HFD-induced metabolic memory and renal damage.
32 utic potential for protection from ischaemic renal damage.
33 nsin II challenge and were protected against renal damage.
34 vement of IgG glycosylation in mechanisms of renal damage.
35 ompanied by a better renal function and less renal damage.
36 es metabolic memory and prevents HFD-induced renal damage.
37 pair capacity and thus, higher resistance to renal damage.
38 expression of p66Shc was linked to increased renal damage.
39 opriate activation of the AP, eventuating in renal damage.
40 ADMA metabolism protects against progressive renal damage.
41 egy for protection against cisplatin-induced renal damage.
42 d VDR-null mice from severe diabetes-related renal damage.
43  in parenchymal cells predominantly mediates renal damage.
44 tinal and systemic disease, including severe renal damage.
45 ll damage, and decreased markers of lung and renal damage.
46 ine HK-2 as an in vitro model of Stx-induced renal damage.
47 y contribute to increased blood pressure and renal damage.
48 ucial in ameliorating streptozotocin-induced renal damage.
49 l growth factor, can lead to proteinuria and renal damage.
50 kidney, improved renal function, and reduced renal damage.
51  which administration of BMP-7 may attenuate renal damage.
52 imbalance in hypertensive cardiovascular and renal damage.
53 hites, but ethnicity was not associated with renal damage (adjusted odds ratio 1.6, 95% confidence in
54  (RBF) and GFR and established the degree of renal damage after 6 weeks of RVD.
55 single therapy that effectively resolves the renal damage after ischemia.
56 synthesis also ameliorated diabetes-mediated renal damage and albuminuria in Cyp4a14KO male mice.
57 0 inhibition ameliorates diabetes-associated renal damage and atheroprogression in a mouse model of c
58 ip between the monoclonal gammopathy and the renal damage and because the significance of the monoclo
59 ittle is known about the pathogenesis of SLE renal damage and compromised renal function.
60 to discriminate only patients diagnosed with renal damage and controls with a P sensitivity of 100%,
61 rted that zinc deficiency is associated with renal damage and could increase blood pressure.
62 a useful adjunct to histology in identifying renal damage and demonstrates early and broad changes in
63  size but loss of overall tubule density; 3) renal damage and dysfunction when exposed to a Mars roun
64  and humoral pathways leading to progressive renal damage and end-stage renal disease.
65 ARC function provides a protective effect on renal damage and fibrosis associated with ANG II hyperte
66 refore evaluated the contribution of CCL5 to renal damage and fibrosis in hypertensive and normotensi
67 ned whether TRPM7 contributes to progressive renal damage and fibrosis.
68 in expression in mouse kidneys while causing renal damage and fibrosis.
69 position in the kidneys was dissociated from renal damage and from activation of renal endothelial an
70 n preclinical models of hypertension-induced renal damage and glomerulonephritis.
71 ich likely contributes to aggravation of the renal damage and hypertension in the Dahl SS rat; the ma
72 ls, histological examination revealed severe renal damage and immunohistochemical localization demons
73 L-2C-induced Treg expansion attenuates acute renal damage and improves renal recovery in vivo, sugges
74  levels were associated with accumulation of renal damage and lack of response to therapy.
75                                         Both renal damage and PARS activation were attenuated by admi
76 use of opioids, which results in hepatic and renal damage and possible addiction.
77 hat TRPM7 is upregulated during inflammatory renal damage and propose that pharmacological interventi
78 cannot generate new nephrons after postnatal renal damage and regenerative therapies for AKI are not
79 othelial HIF-2 protects from hypoxia-induced renal damage and represents a potential therapeutic targ
80 sepsis or necrotizing soft-tissue infection, renal damage and rheumatic heart disease.
81 olecular and cellular processes that lead to renal damage and to the heterogeneity of lupus nephritis
82 very effectively arrested the progression of renal damage and, in some respects, reversed renal patho
83 ctrum antibiotics whose side effects include renal damage and, strangely, tendinopathies.
84 ilateral renal artery stenosis), established renal damage, and hypertension.
85 tor has been reported in tubular cells after renal damage, and Stat3 has been implicated in CKD progr
86 lar mechanisms that lead to diabetes-induced renal damage are incompletely defined.
87 nostic capability or help determine risk for renal damage are sorely needed.
88 adicals and other factors that contribute to renal damage as well as increased retention of sodium an
89                    Lastly, we showed reduced renal damage, as determined by renal biomarkers and hist
90 xygen extraction together with a subclinical renal damage, as indicated by higher values of urinary n
91 t to body weight (HW/BW) ratios, cardiac and renal damage assessed by histological examination, PAI-1
92                Treatment with FTY720 reduced renal damage assessed histologically and also reduced ap
93  implying that macrophages contribute to the renal damage associated with HUS.
94 ulating TRAF3 levels could be a biomarker of renal damage associated with the inflammatory state.
95 ic mechanism responsible for the progressive renal damage associated with uromodulin gene mutations.
96 and renal damage (in trial 1) and those with renal damage but no decrease in the platelet count of mo
97 s, sympathetic nerve activity contributes to renal damage but the extent to which autonomic dysfuncti
98 c anti-DNA antibodies may also contribute to renal damage by directly influencing mesangial gene expr
99    Proteinuria may contribute to progressive renal damage by inducing tubulointerstitial inflammation
100 ood pressure and cause vascular remodelling, renal damage, cardiac hypertrophy, cognitive impairment
101                                              Renal damage caused by cold preservation and warm reperf
102 n extensively employed as an animal model of renal damage caused by Shiga toxins.
103 ciated with less functional and histological renal damage compared with control mice.
104 plus isoflurane anesthesia induced only mild renal damage (Cr, 0.9 +/- 0.1, minimal tubular necrosis;
105 an reverse this signature and the associated renal damage despite ongoing immune complex deposition.
106  reduced serum creatinine levels, diminished renal damage detected by histopathologic evaluation, and
107                 Endothelin-1 (ET-1) promotes renal damage during cardiovascular disease; yet, the mol
108 idase, mediates the onset of proteinuria and renal damage during experimental diabetic nephropathy.
109 n of the microbiota significantly attenuated renal damage, dysfunction, and remote organ injury and m
110 ing an important mechanism causing permanent renal damage even after an acute injury.
111                                 Differential renal damage from anti-dsDNA antibodies may be due to di
112 children at high risk for VUR or at risk for renal damage from reflux-induced scarring.
113 erstitial injury when it is given 2 wk after renal damage has been established.
114    Although immune parameters that instigate renal damage have been characterized, their link to loca
115 etal urinary tract motility defects prior to renal damage.-Hurtado, R., Bub, G., Herzlinger, D.
116 sterone in the development of myocardial and renal damage in a model with high Ang II and low nitric
117  molecular markers to measure non-invasively renal damage in children with VUR.
118                                              Renal damage in D+HUS is caused by Shiga toxin (Stx), wh
119 potent regulatory role of LXRs in preventing renal damage in diabetes.
120 E production, normalized BP, and ameliorated renal damage in diabetic Cyp4a14KO mice.
121  hypothesized that the EP1 receptor promotes renal damage in diabetic nephropathy.
122 at heparanase contributes to proteinuria and renal damage in experimental glomerulonephritis by decre
123 res of the disease and demonstrates that the renal damage in HCDD relies on the production of an isol
124 ed that a positive MCU increases the risk of renal damage in hospitalized UTI patients by about 20%,
125                          Because progressive renal damage in humans associates with proteinuria regar
126 age-specific LXR activation were analyzed on renal damage in hyperlipidemic-hyperglycemic mice.
127 t that CO itself may be protective and limit renal damage in ischemia induced ARF.
128 ssion of AM enhances cardiac hypertrophy and renal damage in male, but not female, mice with a renin
129 edly decreased the extent of albuminuria and renal damage in mouse models of DN.
130 ve protein (CRP) can prevent and reverse the renal damage in murine models of spontaneous lupus, as w
131 sis revealed a marked reduction in liver and renal damage in mutant mice treated with LPS, whereas bl
132 s suggest that IL-1beta blockade may prevent renal damage in nephrocalcinosis.
133 is instrumental, we compared the severity of renal damage in NGAL wild-type mice and NGAL-knockout mi
134            Despite advances in therapeutics, renal damage in particular continues to be an important
135             VUR is hence a weak predictor of renal damage in pediatric patients hospitalized with UTI
136 ibody-induced hypertension, proteinuria, and renal damage in pregnant mice, demonstrating that autoan
137                                              Renal damage in response to 5/6 nephrectomy was greatly
138 ay be a novel therapeutic approach to reduce renal damage in SLE.
139             Furthermore, the pathogenesis of renal damage in such patients is probably complex becaus
140 ay be important in the cascade(s) leading to renal damage in systemic Lupus erythematosus.
141 candesartan caused a significant increase in renal damage in the Dahl salt-sensitive model of hyperte
142  cilexetil significantly reduced cardiac and renal damage in the nitric oxide synthase inhibitor mode
143 pe mice, VDR-null mice developed more severe renal damage in the obstructed kidney, with marked tubul
144 te the effect of PKCalpha/beta inhibition on renal damage in this model setting, Cmpd 1 unexpectedly
145 imary VUR as an effective screening test for renal damage in this population.
146 e beneficial in ameliorating the progressive renal damage in uromodulin-associated kidney diseases.
147 ssess the influence of gestational NSAIDs on renal damage in weaning dams.
148        Patients with low platelet counts and renal damage (in trial 1) and those with renal damage bu
149       Aging of the kidney is associated with renal damage, in particular mesangial matrix expansion (
150                                         This renal damage increases in relation to the time of exposu
151 ly to improve metabolic disorder and relieve renal damage induced by diabetes.
152 systolic blood pressure, cardiac weight, and renal damage induced by DOCA-salt.
153 esized to be instrumental in the etiology of renal damage induced by proteinuria.
154 c reticulum (ER), but the pathophysiology of renal damage is unclear.
155 a-MSH significantly reduced ischemia-induced renal damage, measured by changes in renal histology and
156 administered after the development of severe renal damage (MST after proteinuria onset was 12.5 weeks
157 viewed as the major risk factor for acquired renal damage, now shares this role with nonreflux nephro
158                                              Renal damage occurred more frequently among Hispanics an
159 ere found to be protected from the liver and renal damage of tyrosinemia as hypothesized.
160 ins after AKI, and it is highly expressed in renal damage of various etiologies.
161                                              Renal damage or dysfunction was examined by immunohistoc
162 mination verified the absence of significant renal damage or immune deposition in responding mice.
163 s, and prognostic implications of persistent renal damage (RD) in patients with preexistent moderate-
164 e role of statin pre-treatment in preventing renal damage remains uncertain.
165                    Analysis of the stages of renal damage revealed that dithiothreitol-liberated poly
166 ded to either ischemic or folic acid-induced renal damage similarly to control mice.
167 y correlated with renal disease activity and renal damage (Spearman's r >/= 0.47, P < 0.0001 for both
168 of albuminuria, may indicate low-grade early renal damage supporting the utility of KIM-1 as a quanti
169 ic, but CsA has been associated with greater renal damage than Tac.
170  non-renal transplant recipients demonstrate renal damage that affects primarily the preglomerular ar
171 nephrosis compared with that in animals with renal damage that did not receive the dietary interventi
172                                              Renal damage that is characterized by activation of Ang
173 he primary virulence factors responsible for renal damage that may follow diarrheal disease.
174 olites that accurately predicted UUO-induced renal damage that was detectable by 12 h after UUO, prio
175  that includes the reduction of iron-induced renal damage, the regulation of nicotinamidase activity,
176 conditions, associated with hypertension and renal damage, the SS(NPPA-/-) rats exhibit a decrease in
177 hrectomized Wistar rats mediated the greater renal damage, the study was repeated, with Wistar rats (
178 zes to kidney tissue and eventually leads to renal damage through a process that first involves the b
179 dicated that alcohol may directly exacerbate renal damage through mitochondrial dysfunction, oxidativ
180 TLR4, these results support the concept that renal damage triggers an innate immune response, which c
181                                  In summary, renal damage upon 5/6 nephrectomy was markedly reduced i
182 nicotinic acetylcholine receptor agonists on renal damage using a mouse model of lipopolysaccharide (
183                        A predictive model of renal damage was constructed using the LASSO (least abso
184 mpact of arginase activity and expression on renal damage was evaluated in spontaneously diabetic Ins
185                                 In contrast, renal damage was significantly reduced by restricting IL
186 myocardial infarction, stroke, or persistent renal damage) was significantly lower in the statin grou
187       Urinary albumin excretion, an index of renal damage, was also lower in CDU-treated hypertensive
188 rmine susceptibility to hypertension-induced renal damage, we derived an experimental animal model in
189 ers that monitor recovery from agent-induced renal damage, we scored changes in the levels of urinary
190 sis, respectively, and all six parameters of renal damage were changed in parallel, and ARB treatment
191                         Although progressive renal damage with proteinuria only occurred in F1 mice,

 
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