ライフサイエンスコーパス: intrarenal

1 To determine whether endogenous intrarenal 5-hydroxytryptamine affects phosphate excreti

2 l insulin (4 mU x kg(-1) x min(-1)) and left intrarenal [6,6-2H]dextrose (14 micromol x kg(-1) x min(

3 At steady state, intrarenal accumulation of CsA and its secondary metabol

4 The intrarenal accumulation of T cells (CD4(+), CD8(+), CD4(

5 These findings suggest that intrarenal ACE-derived angiotensin II formation, even in

6 cally with losartan suggest that substantive intrarenal actions of Ang II can be maintained even when

7 d with volume homeostasis, particularly with intrarenal actions that influence pressure natriuresis.

8 hritis, CXCR3-/- and CXCL9-/- mice had fewer intrarenal activated T cells and activated macrophages.

9 roximal tubule and intercalated cells, after intrarenal administration of a rAAV vector and provide t

10 Intrarenal administration of angiotensin II receptor typ

11 ovel mechanism, Nrf2-mediated stimulation of intrarenal Agt gene expression and activation of the ren

12 ed, at least in part, via the suppression of intrarenal Agt gene expression in vivo.

13 otion that the loss of systemic AGT, but not intrarenal AGT, is responsible for death in the AGT-/- m

14 The aim of this study was to clarify the intrarenal allograft events associated with the developm

15 -, 140-, and 240-HU renal inserts containing intrarenal and exophytic 7-, 10-, and 15-mm cysts.

16 Increases in intrarenal and interstitial angiotensin (Ang) II levels

17 stent with fewer activated and proliferating intrarenal and splenic B cells in mice lacking IL-34, an

18 IL-12 "carrier cells" generated intrarenal and systemic IL-12.

19 AKI associates with intrarenal and systemic inflammation; thus, improved und

20 ty of metabolic/homeostatic processes at the intrarenal and systemic levels and are involved in drug

21 To investigate whether IL-34-dependent intrarenal and systemic mechanisms promote lupus nephrit

22 Ang II observed in wild-type mice, including intrarenal Ang II accumulation, sodium and water retenti

23 However, the precise mechanisms by which intrarenal Ang II increases blood pressure have never be

24 The resultant increased intrarenal Ang II levels contribute to the genesis of ch

25 Intrarenal AngII (1 ng) caused a 32% reduction of renal

26 njury observed in association with increased intrarenal AngII accumulation in the absence of APA sugg

27 Intrarenal AngII content, which is greater than can be e

28 produce sustained hypertension and increased intrarenal AngII contents through multiple mechanisms, w

29 It is, likely, however, that the activity of intrarenal AngII is somehow upregulated in the aging kid

30 the nonclipped kidney is renin-depleted, the intrarenal AngII levels are not suppressed, and AngII co

31 levels, thus contributing to the increase in intrarenal AngII levels.

32 nist, it is proposed that there is increased intrarenal AngII production in type 2 diabetes mellitus.

33 AngII-generating system is a major source of intrarenal AngII production, it is here reported that th

34 Simvastatin in RAS enhanced both intrarenal angiogenesis and peri-stenosis arteriogenesis

35 Hyperglycemia and high intrarenal angiotensin II (AngII) levels could contribut

36 asis and function in rats, and the impact of intrarenal angiotensin II AT(1) receptor blockade using

37 was performed to determine whether augmented intrarenal angiotensinogen may contribute to the enhance

38 creases in circulating AngII levels increase intrarenal angiotensinogen mRNA levels, which may contri

39 s point to a potential 20-HETE dependence of intrarenal angiotensinogen production and ANGII receptor

40 hese results indicate that SHR have enhanced intrarenal angiotensinogen production that contributes t

41 Risk genotype was not associated with intrarenal APOL1 mRNA expression levels.

42 We tended to augment PGI2 production by intrarenal arterial Adv-COPI administration with renal v

43 uate gene expression in the rat kidney after intrarenal arterial infusion of a rAAV (serotype 2) vect

44 and function studies before and after acute intrarenal arterial infusion of candesartan (4.2 mug kg(

45 In rats, intrarenal arterial injection of anti-glomerular endothe

46 An intrarenal arterial resistive index of less than 0.6 was

47 CC caused crystal clots occluding intrarenal arteries and a dose-dependent drop in GFR, fo

48 orm grade 3-6) was present in 19 (86%) of 22 intrarenal arteries prior to intervention, as compared w

49 Selective intrarenal artery catheters facilitate direct delivery o

50 An intrarenal artery injection technique established feasib

51 Blockade of intrarenal AT1 receptors elicited significant increases

52 Intrarenal AT2R activation prevents Na(+) retention and

53 ls of EBV DNA, although only mild persistent intrarenal atypical lymphocytic infiltrates.

54 hritis involves antibody binding to multiple intrarenal autoantigens rather than the deposition of ci

55 h histological patterns were associated with intrarenal B cell clonal expansion and ongoing somatic h

56 Intrarenal B cells in human renal allografts indicate tr

57 origins, repertoires, and functions of these intrarenal B cells remain elusive.

58 We identified intrarenal B7-1 and B7-2 expression, restricted to kidne

59 Medullary hypoxia due to intrarenal blood flow redistribution may be one of the f

60 erated and efficacious for the management of intrarenal calculi in multiple-patient populations and i

61 le in the treatment of proximal ureteral and intrarenal calculi with the development of new endoscope

62 , and Tnfr1/2-deficient mice also lacked the intrarenal CaOx deposition and tubular damage observed i

63 In mice, intrarenal CaOx deposition induced tubular damage, cytok

64 These mice had a high frequency of intrarenal CD25(+)Foxp3(+) regulatory T cells and decrea

65 However, the relative contribution of intrarenal cells and extrarenal cells to kidney regenera

66 These results show that intrarenal cells are the main source of renal repair, an

67 Since the defect is abrogated by exogenous intrarenal cGMP, the renal cGMP pathway may represent a

68 Intrarenal changes in cytoplasmic calcium levels have a

69 The focus was on intrarenal chemokine ligand/receptor pairs that were hig

70 in a transcriptional network that regulates intrarenal cholesterol metabolism.

71 e show using single-cell RNA sequencing that intrarenal class-switched B cells have an innate cell tr

72 allografts in the absence of rejection; (3) intrarenal coexpression of members of each lytic pathway

73 histological severity of acute rejection and intrarenal coexpression of mRNA encoding Fas ligand, Fas

74 ds significantly increased distention of the intrarenal collecting system and proximal ureter (P < .0

75 and overall image quality (P < .001) of the intrarenal collecting system and proximal ureter.

76 lculated on a per-renal unit (defined as the intrarenal collecting system and ureter of one kidney) b

77 instrument being employed to map the entire intrarenal collecting system.

78 portions of the urinary tract--the kidneys, intrarenal collecting systems, ureters, and bladder--and

79 ggest that salt sensitivity is determined by intrarenal collectrin, and increasing the abundance or a

80 rmation and local antibody production add to intrarenal complement activation as renal immunopatholog

81 eased from injured endothelial cells promote intrarenal complement activation.

82 ts were characterized by the upregulation of intrarenal complement regulatory genes.

83 achieved a thirty-five-fold increase in the intrarenal concentration of l-fucose following an IP bol

84 bladder, we evaluated whether measurement of intrarenal concentrations of viral DNA might serve as a

85 Intrarenal control mechanisms play an important role in

86 It has been proposed that excessive intrarenal conversion of cortisol to 6 beta-hydroxycorti

87 Intrarenal crystals trigger inflammation and renal cell

88 affects systemic CsA metabolite exposure and intrarenal CsA accumulation.

89 37), which is suggestive of CYP3A5-dependent intrarenal CsA metabolism.

90 tected in the serum or urine correlates with intrarenal CSF-1 expression and histopathology (increase

91 rine CSF-1 levels correlated with increasing intrarenal CSF-1 expression and histopathology.

92 1 levels correlated with lupus activity, and intrarenal CSF-1 expression correlated with the histopat

93 uggesting that blocking both circulating and intrarenal CSF-1 may be necessary for therapeutic effica

94 r) mice lacking IFN-gamma R, circulating and intrarenal CSF-1 were absent, TNF-alpha was markedly red

95 es and whether systemic CSF-1, as opposed to intrarenal CSF-1, promotes macrophage-dependent lupus ne

96 ong with the csCSF-1 isoform, for increasing intrarenal CSF-1.

97 of cyst diameter, occurred in 34 (38%) of 90 intrarenal cyst measurements.

98 cement is maximal when small (< or = 1.5-cm) intrarenal cysts are scanned during maximal levels of re

99 dy mass index, 31.3 kg/m(2) +/- 6.2) with 34 intrarenal cysts were included.

100 ton imaging of CD11c-EYFP mice revealed that intrarenal DCs exhibited increased number and activity o

101 d TGF-beta1 protein expression and increased intrarenal display of TGF-beta1 mRNA.

102 ransduction mechanisms determined, and their intrarenal distribution mapped.

103 activating mutation of c-kit, display normal intrarenal distribution of the c-kit-positive cells at E

104 The intrarenal distribution of these prostanoid receptors ha

105 iminated between the roles of extrarenal and intrarenal dopamine in the overall regulation of renal f

106 e conditions and during hyperemia induced by intrarenal dopamine infusion (30 mug/kg).

107 rmine the effects of selective inhibition of intrarenal dopamine production, we used mice with proxim

108 Decreasing intrarenal dopamine subjects the kidney to unbuffered re

109 se results demonstrate the importance of the intrarenal dopaminergic system in salt and water homeost

110 y examined the effects of alterations in the intrarenal dopaminergic system on kidney structure and f

111 study demonstrates an important role of the intrarenal dopaminergic system to modulate the developme

112 The kidney has a local intrarenal dopaminergic system, and in the kidney, dopam

113 Intrarenal downstream effector transcripts (IFN-gamma, I

114 Standard intrarenal duplex US parameters (acceleration index [AI]

115 nal blood flow was accompanied by more rapid intrarenal dye transit time and slight increase in renal

116 The diverse intrarenal effects of the prostaglandins (PG) are mediat

117 The intrarenal etiology of lupus nephritis involves antibody

118 We found that intrarenal expression of CL-11 rapidly increases in the

119 Intrarenal expression of csCSF-1 and spCSF-1 increases w

120 ouse model of renal ischemia, an increase in intrarenal expression of CXCR3 and its ligands was obser

121 lymerase chain reaction was used to identify intrarenal expression of Fas antigen, Fas ligand, granzy

122 Our studies demonstrate that: (1) intrarenal expression of Fas ligand mRNA and of granzyme

123 ating GDF-15 levels strongly correlated with intrarenal expression of GDF15 and significantly associa

124 orrelated with early PVN grade 1 and minimal intrarenal expression of SV40-T antigen (P < 0.001).

125 Intrarenal expression of TGF-beta protein was also compa

126 Intrarenal expression of TGF-beta protein was studied by

127 Circulating levels and intrarenal expression of TGF-beta were also significantl

128 Intrarenal expression of TGF-beta, collagen, fibronectin

129 Comparisons were made of intrarenal expression of TGF-beta, collagen, fibronectin

130 Intrarenal expression of TGF-beta, collagen, fibronectin

131 AMRh associated with increased intrarenal expression of the ARHGDIB gene.

132 We investigated intrarenal expression of these molecular executors of ce

133 llagen fragments, suggesting accumulation of intrarenal extracellular matrix.

134 With increasing peripheral vasodilatation, intrarenal factors for maintenance of renal perfusion ca

135 A variety of intrarenal factors lead to progressive interstitial fibr

136 Future studies should be directed at intrarenal factors.

137 Currently, the diagnosis of intrarenal fibrosis and quantification of its developmen

138 Our findings show that CD103(+) DCs foster intrarenal FoxP3(+) Treg accumulation, thereby antagoniz

139 GDF-15 levels significantly correlated with intrarenal GDF15 transcript levels (r=0.54, P=0.01).

140 Circulating GDF-15 may be a marker for intrarenal GDF15-related signaling pathways associated w

141 The intrarenal generation of active glucocorticoid by 11beta

142 nificantly slower rate than the rejection of intrarenal grafts.

143 dehydrogenase, and hematocrit levels), acute intrarenal heme loading (cast formation), and BP during

144 renal perfusion, renal venous pressures, and intrarenal hemodynamic changes, which do not reflect str

145 Intrarenal hemodynamics and excretory function distal to

146 up, and study changes in concurrent, in vivo intrarenal hemodynamics and segmental tubular function i

147 se to injury, suggesting that a biomarker of intrarenal HO-1 activity may be useful.

148 her plasma or urinary levels of HO-1 reflect intrarenal HO-1 expression.

149 -1 levels may serve as biomarkers of AKI and intrarenal HO-1 gene activity.

150 otection associated with decreased levels of intrarenal IFN-gamma, TNF, and inflammatory chemokines a

151 s nephritis by fostering the accumulation of intrarenal IFN-gamma-secreting T cells, and 2) MRL-Fas(l

152 Although these changes in the intrarenal IGF-1 axis were distinct, it is difficult to

153 nd isotypes (G1,G2b,G3), autoantibodies, and intrarenal IgG deposits.

154 We previously reported that 1) intrarenal IL-12 elicits nephritis by fostering the accu

155 Intrarenal IL-17A mRNA transcription and protein express

156 Intrarenal IL-34 and its two receptors increase during l

157 rvival times, 57 to >100 days) in vivo after intrarenal implant.

158 n or, alternatively, by delayed clearance of intrarenal inflammation once immunologic remission has b

159 Furthermore, PSI may decrease intrarenal inflammation through modulation of the NF-kap

160 These include glomerular hypertrophy, intrarenal inflammation, and interstitial fibrosis.

161 ostimulatory effects of histones, suppressed intrarenal inflammation, neutrophil infiltration, and tu

162 espite a similar amount of crystal deposits, intrarenal inflammation, tubular damage, and renal dysfu

163 s was unexpectedly more severe, despite less intrarenal inflammation.

164 Complex intrarenal inflammatory processes driven by lymphocytes

165 nvestigated the renal actions of K201 during intrarenal infusion in normal anesthetized dogs.

166 In hyperdynamic sepsis, intrarenal infusion of a highly selective inducible nitr

167 with RVD not treated (n=7) or 4 weeks after intrarenal infusion of ad-MSC (2.5x10(5) cells/kg; n=6),

168 The present study shows that a single intrarenal infusion of autologous EPCs preserved microva

169 n pigs with RAS, pigs with RAS 4 weeks after intrarenal infusion of autologous EPCs, and controls.

170 We, therefore, examined the effects of intrarenal infusion of selective inducible nitric oxide

171 d and denervated kidneys from CBDL rats, and intrarenal infusion of Zaprinast (10 micrograms/min) cor

172 Intrarenal injection of alpha-Syn fibrils induces the pr

173 ction, IL-4-/- mice had significantly higher intrarenal intercellular adhesion molecule-1 mRNA expres

174 idney pathology, loss of renal function, and intrarenal leukocyte infiltrates were increased in each

175 reduced serum autoantibodies, splenomegaly, intrarenal leukocyte trafficking, and end organ disease

176 F-1-deficient mice is not limited to reduced intrarenal leukocytes; circulating Igs and autoantibodie

177 type 2 diabetic nephropathy, we examined the intrarenal localization and expression of the TGF-beta1

178 A are detected in the kidney and its precise intrarenal localization is uncertain, mice with targeted

179 ediators that incite TEC death, and reducing intrarenal M phi during kidney disease diminishes TEC ap

180 The decrease in intrarenal M phi resulted from diminished recruitment an

181 IL-34 fosters intrarenal macrophage accumulation via monocyte prolifer

182 uited by chemokines into the kidney) and via intrarenal macrophage proliferation.

183 n, resulting in a more rapid accumulation of intrarenal macrophages (CD11b(+)CSF-1R(+) or CD68(+)) th

184 expression increased in both peritoneal and intrarenal macrophages in diabetic wild-type mice.

185 mmatory cytokine and chemokine expression in intrarenal macrophages.

186 ined kidney and urine samples from mice with intrarenal (maleate), prerenal (endotoxemia), or postren

187 The intrarenal mechanisms mediating adaptation to variations

188 S) by restoring angiogenesis and attenuating intrarenal microvascular (IMV) remodeling.

189 (RAS) may impair renal function by inducing intrarenal microvascular injury and remodeling.

190 uent CKD via 2 distinct mechanisms: enhanced intrarenal Mo proliferation and elevated BM myeloid cell

191 se type 2 diabetic nephropathy, only CD68(+) intrarenal monocytes expressed Cat-S mRNA, whereas Cat-S

192 necrotic cell-derived TLR4 agonists activate intrarenal mononuclear cells to secrete IL-22, which acc

193 immunity via the NLRP3/ASC/caspase-1 axis in intrarenal mononuclear phagocytes and directly damage tu

194 There are far fewer intrarenal Mphi and T cells in CSF-1-deficient MRL-Fas(l

195 e prophylaxis group had significantly higher intrarenal mRNA expression of genes involved in fibrogen

196 light microscopy, immunohistochemistry, and intrarenal mRNA expression of proinflammatory and profib

197 g the function and attenuating the damage of intrarenal MV.

198 ated mice, pyelonephritis was attenuated and intrarenal neutrophil numbers were lower in the denervat

199 e renin angiotensin system and inhibition of intrarenal nitric oxide production.

200 ations in RAP are associated with changes in intrarenal NO, suggesting a direct effect of NO to regul

201 Either intrarenal or systemic administration of C-21 prevented

202 By lowering intrarenal oxygen levels, reduced NO may contribute to s

203 ng) and molecular diagnostic tools to assess intrarenal oxygenation and perfusion, and the molecular

204 sence of a noninvasive technique to estimate intrarenal oxygenation in different zones of the kidney.

205 BOLD MRI can be used to monitor changes in intrarenal oxygenation in humans in a noninvasive fashio

206 These results suggest that marked changes in intrarenal oxygenation occur during acute transplant rej

207 opportunity for cellular repair mediated by intrarenal paracrine effects.

208 riuretic peptide and overactivity of various intrarenal paracrine systems, including vasodilator and

209 Intrarenal perfusate flows at the same time intervals we

210 ac Death (DCD) in porcine kidneys to measure intrarenal perfusion.

211 uid chromatography analysis showed increased intrarenal polyamine concentrations peaking after 24 h o

212 nal ODC protein expression and localization, intrarenal polyamine levels, and sites of proliferation

213 antly associated with clinical presentation: intrarenal polyomavirus load levels and Banff interstiti

214 al semiquantitative histologic assessment of intrarenal polyomavirus replication/load levels.

215 scular perfusion and histopathology, reduces intrarenal pro-inflammatory mediators and salvages kidne

216 is within 13 weeks, accompanied by increased intrarenal production of angiotensin (Ang) II, fibronect

217 was measured to provide an indication of the intrarenal production of NO.

218 on results from suppressed infiltration, and intrarenal proliferation, but not enhanced apoptosis.

219 Macrophages accumulated because of higher intrarenal proliferation, despite reduced monocyte recru

220 PGE2, the major intrarenal prostaglandin, interacts with at least three

221 Other intrarenal prostanoid receptors include the PGF2 alpha r

222 lation (alpha0.77-0.86) with the severity of intrarenal PV replication and disease grades.

223 of SV40-T-expressing cells as indicators of intrarenal PV replication in corresponding renal allogra

224 dicts PVN disease grades and the severity of intrarenal PV replication.

225 t correlation with disease grades or minimal intrarenal PV replication.

226 suggest that Agt-ASO effectively attenuates intrarenal RAS and therefore can be a novel and effectiv

227 , and their involvement in the regulation of intrarenal RAS thereby control blood pressure, renal inj

228 ed the predicted changes in the systemic and intrarenal RAS, while acute BK2A had no consistent effec

229 nitric oxide (NO), and the activation of the intrarenal RAS.

230 nt RAS inhibitors do not adequately suppress intrarenal RAS.

231 In DIO mice, intrarenal RCC tumor challenge in the absence of therapy

232 h advancing nephritis, thereby promoting the intrarenal recruitment of monocytes and expansion of Ly6

233 ease in cell proliferation restricted to the intrarenal region with Mfn2 deletion.

234 Since dopamine produced by the kidney is an intrarenal regulator of sodium transport, an abnormality

235 ed enhanced renal injury and exhibited fewer intrarenal regulatory T cells (Tregs) compared with gene

236 l lines, we detected a reduction of FoxP3(+) intrarenal regulatory T cells (Tregs), which protect aga

237 As a measure of intrarenal renin activity, we have examined renal plasma

238 These were accompanied by blockade of intrarenal renin and Ang II accumulation induced by hype

239 Activation of the intrarenal renin angiotensin system (RAS) is believed to

240 al microvasculature and in expression of the intrarenal renin angiotensin system.

241 masking and perhaps reflecting an activated intrarenal renin system.

242 Activation of the intrarenal renin-angiotensin system (RAS) can elicit hyp

243 The increased activity of intrarenal renin-angiotensin system (RAS) in a setting o

244 pro)renin receptor (PRR), a key regulator of intrarenal renin-angiotensin system (RAS), is predominan

245 al. present further evidence implicating the intrarenal renin-angiotensin system and take us one step

246 h our previous studies, we conclude that the intrarenal renin-angiotensin system located in the proxi

247 The intrarenal renin-angiotensin system plays a critical rol

248 The contribution of the intrarenal renin-angiotensin system to the development o

249 rtant in IFN-gamma-induced activation of the intrarenal renin-angiotensin system.

250 an infusion of angiotensin II (assessment of intrarenal renin-angiotensin-aldosterone system [RAAS])

251 with stimulation of both the circulating and intrarenal renin-angiotensin-aldosterone system.

252 Despite early-onset hypertension and intrarenal renin/angiotensin II (AngII) activation, angi

253 ry resulted in a significant decrease in the intrarenal resident dendritic cell (DC; CD45(+)MHCII(+)C

254 erfusion conditions were maintained with low intrarenal resistance and normal electrolyte and pH para

255 ctional area suggests that adenosine affects intrarenal resistance blood vessels rather than large co

256 Intrarenal resistance decreased over the course of perfu

257 Increased intrarenal resistance index (RI) has been associated wit

258 During NP intrarenal resistance remained lower (P < 0.0001) in the

259 During reperfusion, intrarenal resistance was significantly lower in the HMP

260 The intrarenal resistive index is routinely measured in many

261 of senescence, and it discusses the role of intrarenal senescent cells in the pathogenesis of AKI; t

262 , these observations suggest that endogenous intrarenal serotonin enhances phosphate reabsorption in

263 Intrarenal signal intensity variations were correlated w

264 lated phosphate metabolism by identifying an intrarenal signaling axis for FGF23.

265 ncy, with flank or back pain associated with intrarenal sludging, and with the classic syndrome of re

266 latter syndrome had radiographic evidence of intrarenal sludging.

267 iflozin caused substantial redistribution of intrarenal sodium delivery and reabsorption, providing m

268 the kidney cortex processed antigen for the intrarenal stimulation of T helper cells, a function imp

269 ed as a routine option for the management of intrarenal stone disease.

270 ues to improve as a method for management of intrarenal stone disease.

271 f stone fragment retrieval during retrograde intrarenal stone surgery, potentially improving stone-fr

272 ckwave rate improves stone fragmentation for intrarenal stones.

273 mmation, T cell glomerular infiltration, and intrarenal synthesis of TNF-alpha, IL-1beta, and VCAM-1.

274 scular hypertension has been linked to other intrarenal systems, the lipoxygenase pathway, and renin

275 here is an amplification of the frequency of intrarenal T cells generating IFN-gamma and TNF-alpha in

276 a cohort of patients with C3 glomerulopathy, intrarenal terminal pathway activation was associated wi

277 termined the relative level of expression of intrarenal TGFbeta protein in transplant biopsies.

278 These findings indicate intrarenal TNFalpha contributes to the development of hy

279 Characterization of the intrarenal transcription profile associated with I/RI wa

280 opsy taken 3 months posttransplantation, the intrarenal transcriptome differed in patients treated wi

281 ective single-center study characterized the intrarenal transcriptome during I/RI as a means of ident

282 ression of APOL1 mRNA levels with a group of intrarenal transcripts that together were associated wit

283 Intrarenal urate crystal deposition was absent in all gr

284 The mechanism does not involve intrarenal uric acid crystal deposition and appears to i

285 mmol/L, overlapping with clinically relevant intrarenal/urinary levels after fluorinated anesthetic u

286 , oxonic acid (OA), results in hypertension, intrarenal vascular disease, and renal injury.

287 hypertrophy may significantly influence the intrarenal vascular resistance measured using Doppler so

288 The intrarenal vasculature was normal in the mutant mice.

289 s and by the thickening and hyalinization of intrarenal vasculature.

290 duction was observed in the glomeruli or the intrarenal vasculature.

291 e (CsA)-induced nephrotoxicity may be due to intrarenal vasoconstriction and glomerular hypoperfusion

292 with chronic tubulointerstitial disease and intrarenal vasoconstriction raised the hypothesis that h

293 n to modify acute cyclosporine (CsA)-induced intrarenal vasoconstriction.

294 stulated to play a major role in the intense intrarenal vasospasm and hypertension provoked by cyclos

295 ominantly in the endothelium of coronary and intrarenal vessels and in renal tubular epithelium.

296 The vascular endothelium of proliferating intrarenal vessels from patients with antiphospholipid s

297 DSA, whereas the visibility of the hilar and intrarenal vessels was significantly worse (P = 0.0001).

298 A in cases that do not require assessment of intrarenal vessels.

299 These observations indicate that intrarenal viral replication in sustained viruria is fre

300 iments were conducted in three tumor models: intrarenal VX2 sarcoma in 27 rabbits, RCC 786-0 human re