ライフサイエンスコーパス: glomerular

1 Our study revealed unprecedented details of glomerular abnormalities in Col4a3 mutants including dis

2 ropathy and inflammation to proteinuria with glomerular abnormalities.

3 We detected glomerular and peritubular capillary rarefaction, macrop

4 led a striking pattern in which genes of the glomerular and proximal tubule lineages were either unch

5 delayed development, and signs of pronephric glomerular and tubular dysfunction mimicking the early p

6 hypothesized that MCP-1 inhibition restores glomerular barrier function through influencing macropha

7 inin beta2 (LAMB2), a major component of the glomerular basement membrane (GBM).

8 rastructural thickening and splitting of the glomerular basement membrane (GBM).

9 ratus consisting of podocyte foot processes, glomerular basement membrane and endothelial cells.

10 VEGF-A165 b rescues the increase in glomerular basement membrane and podocyte slit width, as

11 ution of NETs via DNase I did not alter anti-glomerular basement membrane antibody-induced glomerular

12 -linked hereditary nephropathy (XLHN) have a glomerular basement membrane defect that leads to progre

13 Ultrastructural studies show that the glomerular basement membrane is thickened, podocyte slit

14 ous chronic glomerulonephritis (GN) and anti-glomerular basement membrane-induced nephritis.

15 on was induced using an antibody against the glomerular basement membrane.

16 levels of all inflammatory markers, restored glomerular capillaries and podocyte structure, and arres

17 The kidney glomerular capillaries are frequent sites of immune comp

18 y a pathway of neutrophil recruitment within glomerular capillaries following IgG deposition that may

19 Detailed assessment of glomerular capillaries from diabetic D2 mice demonstrate

20 utrophils, which were similar in diameter to glomerular capillaries, abruptly arrested following anti

21 lomerulonephritis, NETs are generated in the glomerular capillaries, where they are short lived and m

22 isruption under the high shear conditions in glomerular capillaries.

23 molecule in glomerular endothelial cells and glomerular capillary circumference.

24 ly increased APA staining in areas of intact glomerular capillary loops.

25 Mechanistically, both glomerular cathepsin L and heparanase expression were re

26 egulating key genes and cellular pathways in glomerular cells during development and homeostasis.

27 istal tubule, interstitial cells, and rarely glomerular cells following injection.

28 dney sections and flow cytometry analysis of glomerular cells from magnetic bead-purified glomeruli h

29 hat control inflammation and is activated in glomerular cells in glomerulonephritis (GN).

30 by RSF-induced proinflammatory signalling in glomerular cells.

31 , interstitial inflammatory infiltrates, and glomerular cells.Primary VSMCs were infected with green

32 patial scale that encompasses many different glomerular channels.

33 Neighboring glomerular columns, representing inputs from different r

34 (PN) classes form synaptic connections in 50 glomerular compartments in the antennal lobe, each of wh

35 perimental system to investigate rewiring of glomerular connectivity, we show that novel OSN synapses

36 cally fixed and found significant linkage to glomerular crescents on chromosome 2 (Crgn8, LOD = 3.8).

37 whether APA exerts a protective role against glomerular damage and during AngII-mediated hypertensive

38 in animals with polymicrobial sepsis whereas glomerular damage due to glycerol-induced kidney-injury

39 Glomerular damage mediated by glomerulus-infiltrating my

40 ch correlates with increased albuminuria and glomerular damage.

41 e), hypoalbuminemia, reduced GFR, and marked glomerular damage.

42 s assessed on CT times the biopsy-determined glomerular density).

43 xpression in diabetic nephropathy tissue and glomerular depositions of protein S.

44 with high titers of IgG1 anti-3F7.A10 led to glomerular deposits of IgG1/IgG2a complexes.

45 l but one of the patients also had segmental glomerular deposits on renal biopsy specimen.

46 h glucocorticoids ameliorate proteinuria and glomerular disease are not well understood.

47 enetic reprogramming can improve outcomes in glomerular disease by repressing the reactivation of dev

48 ctional tetraspanin CD151 is associated with glomerular disease characterised by early onset proteinu

49 with diabetic glomerulosclerosis as the only glomerular disease diagnosis (n=109).

50 H3K27me3 content of podocytes and attenuated glomerular disease in adriamycin nephrotoxicity, SNx, an

51 IgA nephropathy (IgAN) is a common chronic glomerular disease that, in most patients, slowly progre

52 eased H3K27me3 levels and sensitized mice to glomerular disease.

53 Fibrillary GN (FGN) is a rare primary glomerular disease.

54 keletal apparatus results in proteinuria and glomerular disease.

55 uld be a novel therapeutic avenue in chronic glomerular disease.

56 resents the most aggressive form of acquired glomerular disease.

57 omerulopathy, which represents a spectrum of glomerular diseases characterized on fluorescent microsc

58 Therefore, neutrophil participation in glomerular diseases deserves re-evaluation.

59 y (IgAN) is the most prevalent among primary glomerular diseases worldwide.

60 features of FGN overlap with those of other glomerular diseases, and no unique histologic biomarkers

61 hannel activity of TRPC6 in association with glomerular diseases.

62 healthy glomeruli or in 19 types of non-FGN glomerular diseases.

63 tinely used to identify and classify various glomerular diseases.

64 e metabolizing role of APA in AngII-mediated glomerular diseases.

65 ts into the biology and (patho)physiology of glomerular diseases.

66 FSGS, the most common primary glomerular disorder causing ESRD, is a complex disease t

67 esis of proteinuria in primary and secondary glomerular disorders.

68 f the glomerular filtration barrier leads to glomerular dysfunction, frequently manifested as protein

69 mature myeloid cells as a key contributor to glomerular dysfunction.

70 ly elevated early on in the disease, causing glomerular endothelial cell damage.

71 I infected primary human podocytes, renal glomerular endothelial cells (GECs), and mesangial cells

72 d type, diabetic Akita mice as well as mouse glomerular endothelial cells (MGECs) were used as experi

73 ions (8-oxoguanine) exclusively localized to glomerular endothelial cells after 3 weeks of diabetes,

74 atelet endothelial cell adhesion molecule in glomerular endothelial cells and glomerular capillary ci

75 sfunction, mediated largely by Edn1-Ednra in glomerular endothelial cells representing an early event

76 lation of the VEGF activity, particularly in glomerular endothelial cells.

77 a (n=6) on the release of microvesicles from glomerular endothelial cells.

78 sed mitochondrial DNA damage associated with glomerular endothelial EDNRA expression.

79 We show that MCP-1 inhibition restores glomerular endothelial glycocalyx and barrier function a

80 MCP-1 inhibition, however, increased glomerular endothelial glycocalyx coverage, with preserv

81 ression, and suggest that cross talk between glomerular endothelial injury and podocytes leads to def

82 Glomerular endothelial mitochondrial dysfunction was ass

83 Increased glomerular endothelial phospho-p65 staining in patients

84 al dysfunction was associated with increased glomerular endothelin-1 receptor type A (Ednra) expressi

85 Visualizing the glomerular endothelium and podocyte-endothelium interfac

86 Furthermore, we detected an altered glomerular endothelium with disrupted sub-endothelial in

87 glomeruli and immunofluorescent staining of glomerular epithelial cells (podocytes) indicated that V

88 Podocytes are glomerular epithelial cells that are normally growth-arr

89 sions and recruitment of pathogenic parietal glomerular epithelial cells.

90 m creatinine concentration, albuminuria, and glomerular expression of ETS-1 and two ETS-1 targets, MC

91 ocyte injury, glomerular NF-kappaB activity, glomerular expression of inflammatory mediators, and glo

92 Finally, we validated the differential glomerular expression of select microRNAs in a second co

93 s during nephritis by microarray analysis of glomerular extract gene expression.

94 ine (Pnoninferiority = 0.0004), and measured glomerular filtration (Pnoninferiority = 0.0003).

95 ution the ultrastructural alterations of the glomerular filtration apparatus in mice lacking the crit

96 plexes in a subepithelial location along the glomerular filtration barrier 14 days after antibody inj

97 ocytes are essential components of the renal glomerular filtration barrier and podocyte dysfunction l

98 ified fatty acids (NEFAs) across the damaged glomerular filtration barrier and subsequent reabsorptio

99 Nephrotic syndrome (NS) occurs when the glomerular filtration barrier becomes excessively permea

100 to a universal end point of podocyte injury, glomerular filtration barrier disruption, and SRNS.

101 ltered podocyte differentiation and impaired glomerular filtration barrier function, with development

102 a, suggesting an important role of THSD7A in glomerular filtration barrier integrity.

103 needed to define its role in maintenance of glomerular filtration barrier integrity.

104 The glomerular filtration barrier is known as a 'size cutoff

105 Disruption of any component of the glomerular filtration barrier leads to glomerular dysfun

106 Ultrastructurally, the glomerular filtration barrier of the Gsalpha-deficient a

107 intaining the integrity of podocytes and the glomerular filtration barrier of the kidney.

108 ntified YAP as an essential component of the glomerular filtration barrier that promotes podocyte sur

109 SRNS), a heterogeneous disorder of the renal glomerular filtration barrier, results in impairment of

110 podocytes represent a key constituent of the glomerular filtration barrier.

111 percent of the participants had an estimated glomerular filtration rate >30 mL/min per 1.73 m(2).

112 We selected adult subjects with an estimated glomerular filtration rate >60 mL/min/1.73m(2), an outpa

113 ents with normal or impaired renal function (glomerular filtration rate >80 mL/min or between 80 and

114 ey disease (serum creatinine level >3 mg/dL; glomerular filtration rate <15 mL/min; acute kidney inju

115 , >1 g proteinuria, heart failure, estimated glomerular filtration rate <20 mL.min(-1).1.73 m(-2), or

116 se, renal death, development of an estimated glomerular filtration rate <30 mL/min per 1.73m(2), or d

117 oup had borderline renal function (estimated glomerular filtration rate <45 mL/min/1.73 m(2)) and hep

118 pants with chronic kidney disease (estimated glomerular filtration rate <60 mL/min per 1.73 m(2) or u

119 in patients with RD, defined as an estimated glomerular filtration rate <60 mL/min/1.73 m(2), and com

120 pnea, and any of the following: 1) estimated glomerular filtration rate <60 ml/min/1.73 m(2); 2) hypo

121 with and without renal impairment (estimated glomerular filtration rate <60mL/min/1.73m(2)).

122 (beta, 0.70; P < .001), and higher estimated glomerular filtration rate (beta, 0.03; P = .02).

123 lished cardiovascular disease, and estimated glomerular filtration rate (eGFR) >/=30 mL.min(-1).1.73

124 D Among 3 570 865 US veterans with estimated glomerular filtration rate (eGFR) >/=60 mL min(-1) 1.73

125 is of kidney function based on the estimated glomerular filtration rate (eGFR) in 110,517 European an

126 compensated cirrhosis, and with an estimated glomerular filtration rate (eGFR) of 40 mL/min or greate

127 6662 participants with a baseline estimated glomerular filtration rate (eGFR) of at least 60 mL/min/

128 oncentrations and risk of incident estimated glomerular filtration rate (eGFR) of less than 60 mL/min

129 patients with a prehospitalization estimated glomerular filtration rate (eGFR) of more than 45 mL/min

130 166 (73.1%) had diabetes, the mean estimated glomerular filtration rate (eGFR) was 33.9 +/- 15.8 ml/m

131 y the association of pre-operative estimated glomerular filtration rate (eGFR) with PPCs in laparosco

132 ion/primary nonfunction (DGF/PNF), estimated glomerular filtration rate (eGFR), and graft-survival at

133 renal outcomes: >/=30% decline in estimated glomerular filtration rate (eGFR), doubling of the serum

134 comes were HbA1c, LDL cholesterol, estimated glomerular filtration rate (eGFR), incident microalbumin

135 rectly associated with declines in estimated glomerular filtration rate (eGFR).

136 isease (CKD) is defined by reduced estimated glomerular filtration rate (eGFR).

137 Estimated glomerular filtration rate (eGFR, a marker of kidney fun

138 abetes mellitus and inversely with estimated glomerular filtration rate (eGFRcreatcysC)(all P < 0.001

139 acid (PUA) levels are associated with lower glomerular filtration rate (GFR) and higher blood pressu

140 as conducted to determine if TRPC6 regulates glomerular filtration rate (GFR) and the contractile fun

141 The glomerular filtration rate (GFR) assesses the function o

142 There was no significant change in glomerular filtration rate (GFR) before or after therapy

143 dney volume and the decline in the estimated glomerular filtration rate (GFR) but also caused more el

144 rfiltration is a risk factor for accelerated glomerular filtration rate (GFR) decline and nephropathy

145 late ion transport in response to changes in glomerular filtration rate (GFR) to maintain glomerulotu

146 inaccuracy of creatinine-based estimates of glomerular filtration rate (GFR), UK and international g

147 We tested if measured glomerular filtration rate (mGFR, by chrome-ethylenediam

148 min creatinine ratio (P < 0.01), the fall in glomerular filtration rate (P < 0.001), and improved ren

149 r SD increase; OR, 1.13; 95% CI, 1.05-1.21), glomerular filtration rate (per SD increase; OR, 0.67; 9

150 ts with baseline renal impairment (estimated glomerular filtration rate [eGFR] </= 60 mL/min) and pai

151 easures of chronic kidney disease (estimated glomerular filtration rate [eGFR] and albuminuria) with

152 1-2 chronic kidney disease (CKD) (estimated glomerular filtration rate [eGFR], >/= 60 mL/min/1.73 m(

153 redictors of BTP levels are quinolinic acid, glomerular filtration rate and age.

154 Changes in the estimated glomerular filtration rate and albuminuria were also ana

155 ransplant outcomes included 1-year estimated glomerular filtration rate and death-censored graft surv

156 f >50% reduction in their baseline estimated glomerular filtration rate and end stage kidney disease

157 d in those with higher BMI, higher estimated glomerular filtration rate and lower creatinine.

158 The glomerular filtration rate and plasma renin, noradrenali

159 rimary care, serum creatinine with estimated glomerular filtration rate and proteinuria measurements

160 rogressive reduction in renal blood flow and glomerular filtration rate and showed evidence of renal

161 t function had significantly lower estimated glomerular filtration rate at 12 months postbiopsy and a

162 chronic rejection, or in the mean estimated glomerular filtration rate at 15 years.

163 The changes in serum potassium and estimated glomerular filtration rate at 24, 48, 72, and 96 hours.

164 at least 100 x 10(9) platelets per L, and a glomerular filtration rate at least 60 mL/min.

165 and 30, there was no difference in estimated glomerular filtration rate between the RF study group an

166 ons in dietary Na(+) intake do not alter the glomerular filtration rate but alter the total and cell-

167 ession, administration of SRT3025 attenuated glomerular filtration rate decline and proteinuria witho

168 APOL1-associated estimated glomerular filtration rate decline was observed starting

169 ysis, transplantation, and/or >60% estimated glomerular filtration rate decline, or mortality) outcom

170 Age and basal glomerular filtration rate did not differ between groups

171 when estimated from cystatin C compared with glomerular filtration rate estimated from creatinine, 44

172 The adjusted change in mean estimated glomerular filtration rate from baseline to month 6 (Nan

173 ificant for death, 25% decrease in estimated glomerular filtration rate from baseline, major adverse

174 dney transplantation patients with estimated glomerular filtration rate greater than 90 have worse ou

175 olic blood pressure decreased, and estimated glomerular filtration rate increased (P=0.003) more in t

176 rapy discontinuation when baseline estimated glomerular filtration rate is above 44 mL/min/1.73 m.

177 Patients with mean baseline estimated glomerular filtration rate less than 45 mL/min/1.73 m we

178 rtension, 32% had LVH, and 38% had estimated glomerular filtration rate less than 60 mL/min per 1.73

179 discharge, almost twice as many patients had glomerular filtration rate less than 60 mL/min/1.73 m wh

180 with type 2 diabetes and CKD (with estimated glomerular filtration rate less than 60 mL/min/1.73 m2),

181 onic kidney disease was defined as estimated glomerular filtration rate less than 60 mL/min/1.73 m2,

182 ort study recruited adults with an estimated glomerular filtration rate of 20 to 70 mL/min/1.73 m2 fr

183 bling of creatinine or decrease in estimated glomerular filtration rate of 30% or more.

184 , lamivudine, and abacavir; and an estimated glomerular filtration rate of 50 mL/min or more.

185 V-1 RNA >/=500 copies per mL) with estimated glomerular filtration rate of at least 30 mL/min.

186 rhosis and ascites; rifaximin did not affect glomerular filtration rate or levels of vasoactive hormo

187 Estimated glomerular filtration rate was calculated using the Modi

188 No change in estimated glomerular filtration rate was noted after the procedure

189 Baseline estimated glomerular filtration rate was the only one predictor of

190 aft and patient survival, and mean estimated glomerular filtration rate were also comparable between

191 0.80; interquartile range, 0.70-1.01 mg/dL; glomerular filtration rate, 102+/-23; median, 106; inter

192 all, 1461 (10%) had CKD (mean [SD] estimated glomerular filtration rate, 49 [10] mL/min/1.73 m2).

193 term follow-up, 1 had a normalized estimated glomerular filtration rate, and 3 (4%) had persistent CK

194 nger, with higher body mass index, estimated glomerular filtration rate, and forced expiratory volume

195 ulatory support, natriuretic peptide decile, glomerular filtration rate, and total bilirubin level we

196 ood pressure, BMI, smoking status, estimated glomerular filtration rate, LDL-cholesterol concentratio

197 daily blocks walked, diuretic use, estimated glomerular filtration rate, left ventricular mass, eject

198 , progression of retinopathy, changes in the glomerular filtration rate, lipid levels, and measures o

199 itions characterized by a sudden decrease in glomerular filtration rate, manifested by an increase in

200 thickness, other cardiovascular markers, the glomerular filtration rate, or progression of retinopath

201 No effects on the glomerular filtration rate, P = 0.14, or vasoactive horm

202 renal composite (40% reduction in estimated glomerular filtration rate, renal replacement therapy, o

203 f a sustained 40% reduction in the estimated glomerular filtration rate, the need for renal-replaceme

204 .0044), while the routinely used parameters (glomerular filtration rate, urine albumin-to-creatinine

205 atified by HbA1c, BMI, region, and estimated glomerular filtration rate.

206 l function, regardless of baseline estimated glomerular filtration rate.

207 e drugs modified according to bodyweight and glomerular filtration rate.

208 topathies and its expression correlates with glomerular filtration rate.

209 oking, elevated triglycerides, and estimated glomerular filtration rate.

210 for age, sex, body mass index, and estimated glomerular filtration rate.

211 Cr levels and glomerular filtration rates (GFRs) were grouped accordin

212 red) renal allograft survival with estimated glomerular filtration rates (mL/min per 1.73 m) of 43 to

213 censored for primary nonfunction, estimated glomerular filtration rates after 1 year and 5 years wer

214 function imaging, where blood velocities and glomerular filtration rates are simultaneously measured,

215 atients had significantly worse (P < 0.0001) glomerular filtration rates at 1, 2, 3, and 4 years post

216 In this subpopulation, estimated glomerular filtration rates at randomization were higher

217 nts of at least 200 cells per muL, estimated glomerular filtration rates of at least 70 mL per min, a

218 due to loss of podocytes, cells critical for glomerular filtration, and leads to proteinuria and kidn

219 upts precise ORN axon targeting and discrete glomerular formation.

220 lected size selectivity analogous to that of glomerular function.

221 Outer retinal and renal glomerular functions rely on specialized vasculature mai

222 th disease development, we characterised the glomerular gene expression profile at an early stage of

223 maller AuNCs are more readily trapped by the glomerular glycocalyx than larger ones.

224 d with a nephrotoxic serum showed persistent glomerular hyalinosis and albuminuria 96 hours after inj

225 nt resistance, efferent resistance (RE), and glomerular hydrostatic pressure (PGLO).

226 herapies improved renal function, decreasing glomerular hyperfiltration and albuminuria.

227 The revived interest in glomerular hyperfiltration as a prognostic and pathophys

228 This phenomenon, known as glomerular hyperfiltration, classically has been hypothe

229 al EPAS1 has a global protective role during glomerular hypertensive injuries without influencing the

230 vated levels of serum IgM and enhanced renal glomerular IgM deposition.

231 Glomerular inflammation was induced using an antibody ag

232 nct functions of the two major DC subsets in glomerular inflammation.

233 The goal was to define glomerular inflammatory events controlled by ABIN1 funct

234 1[D485N] mice, and renal pathophysiology and glomerular inflammatory phenotypes were assessed.

235 inst ErbB4 significantly suppressed diabetic glomerular injury and albuminuria in both WT and miR-146

236 ts at 2 weeks, and ES allografts showed less glomerular injury and interstitial fibrosis.

237 creased TRPC6 expression in podocytes induce glomerular injury and proteinuria.

238 ropathy progression in mice with established glomerular injury and reduced H3K27me3 levels.

239 eficiency of APA increases susceptibility to glomerular injury in BALB/c mice.

240 ed the expression of p57(Kip2) and prevented glomerular injury in RPGN.

241 one of these loci on chromosome 8, mediates glomerular injury in SS hypertension.

242 hways as likely mediators of the destructive glomerular injury in this disease.

243 However, after glomerular injury induced by either LPS or nephrotoxic s

244 c CD8(+) cells without CD4(+) cells mediated glomerular injury when MPO was planted in glomeruli.

245 lomerular basement membrane antibody-induced glomerular injury, as assessed via albuminuria, although

246 n that may be targeted by bosutinib to avert glomerular injury.

247 hort lived and make a modest contribution to glomerular injury.

248 LPAR inhibition also reduced histologic glomerular injury; decreased the expression of profibrot

249 lvement and histologically exhibited nodular glomerular involvement.

250 ys a pivotal role in hereditary and sporadic glomerular kidney disease.

251 150 ms after stimulation and are mediated by glomerular layer circuits.

252 L-dSAC axons arborize extensively across the glomerular layer to provide highly divergent yet selecti

253 al TCs (eTCs), which are a TC subtype in the glomerular layer with large, direct OSN signals and capa

254 e, we identify the first selective marker of glomerular layer-projecting deep short-axon cells (GL-dS

255 synaptic nicotinic and GABAergic currents in glomerular layer-projecting interneurons.

256 s, are due to weaker excitation and stronger glomerular-layer-mediated inhibition.

257 nduced dyslipidemia worsened albuminuria and glomerular macrophage accumulation but had no effect on

258 xpression of PD-L1 by CD11b(+)F4/80(-)I-A(-) glomerular macrophages in kidneys of mice with GN and th

259 Glomerular mesangial cell (GMC) proliferation and matrix

260 n rate (GFR) and the contractile function of glomerular mesangial cells (MCs).

261 tion in approximately 5000 gene promoters in glomerular mesangial cells, including those of Tgfb1, Tg

262 tubulointerstitial collagen deposition, but glomerular mesangial expansion was unaffected.

263 stolic BP and were the only group to exhibit glomerular mesangial hypercellularity.

264 s suggest that VEGF protects the retinal and glomerular microvasculature, not only through VEGFR2-med

265 CONTROLS: A random forest analysis based on glomerular miRNAs identified 18/20 DSA+ and 8/10 control

266 d cells belonging to clusters of at least 15 glomerular modules, providing a potential mechanism to i

267 er, monocyte depletion significantly reduced glomerular necrosis and crescent formation and abrogated

268 important role of monocytes/macrophages for glomerular necrosis and crescent formation in a renal AN

269 with bosutinib reduced FcgammaRIIA-mediated glomerular neutrophil accumulation and renal injury in e

270 on exacerbated proteinuria, podocyte injury, glomerular NF-kappaB activity, glomerular expression of

271 nephrotoxic nephritis, whereas reduction in glomerular numbers occurred much later.

272 Changes in miRNA expression glomerular of capillaries during antibody-mediated rejec

273 at glucocorticoids act directly on activated glomerular parietal epithelial cells in crescentic nephr

274 reover, mechanisms underpinning all acquired glomerular pathologies converge on disruption of the cyt

275 (R246Q) in LMX1B was reported as a cause of glomerular pathologies without extra-renal manifestation

276 ith diabetes developed worse albuminuria and glomerular pathology.

277 /peptidomic analyses suggest that changes in glomerular permselectivity and tubular reabsorption acco

278 filtration barrier, results in impairment of glomerular permselectivity.

279 signs of tubular dysfunction but lacking the glomerular phenotype.

280 owever, the functional role of the TJ in the glomerular podocyte is unclear.

281 Aminopeptidase A (APA) is expressed in glomerular podocytes and tubular epithelia and metaboliz

282 ated phenotype of ordinarily quiescent adult glomerular podocytes.

283 orm 6 (TRPC6) channels in cardiomyocytes and glomerular podocytes.

284 ion by RNA interference decreases markers of glomerular proinflammatory macrophage activation.

285 The glomerular proteome of fibrillary GN cases also containe

286 ar expression of inflammatory mediators, and glomerular recruitment and retention of neutrophils in a

287 Ts1Rhr mice do not demonstrate a defect in glomerular refinement, suggesting that distinct genes or

288 Acute tubular and glomerular renal injury was accompanied by nonheme iron

289 Podocyte and glomerular research is center stage for the development

290 odel of diabetic nephropathy showed enhanced glomerular ROS production, accelerated glomerulosclerosi

291 to inflammatory-mediated podocyte death and glomerular scarring.

292 dence of CKD, through common changes such as glomerular sclerosis, tubular atrophy, and interstitial

293 To examine this issue, we used single glomerular stimulation in mouse olfactory bulb slices to

294 opically, but the axon terminals fuse into a glomerular structure in the central brain where retinoto

295 n (ARMD), choriocapillaris degeneration, and glomerular thrombotic microangiopathy (TMA).

296 iRNA induction in epithelial cells can break glomerular tolerance to immune injury.

297 preparations, although minor differences in glomerular tuft contractility and macula densa cell calc

298 y showed strong and specific staining of the glomerular tufts in a distribution that mimicked that of

299 teins and small bioactive molecules from the glomerular ultrafiltrate to maintain essentially protein

300 scue the increase in proteinuria, as well as glomerular water permeability, in the context of progres