ライフサイエンスコーパス: proteinuria

1 tor for podocyte foot process effacement and proteinuria.

2 s, thereby counteracting podocyte injury and proteinuria.

3 ter treatment, especially if associated with proteinuria.

4 ement in serum creatinine and a reduction in proteinuria.

5 rse correlation between vitamin D levels and proteinuria.

6 d nephrinuria, both of which correlated with proteinuria.

7 .6+/-11.9 years, 215 (6.1%) donors developed proteinuria.

8 fested as adult-onset glomerulosclerosis and proteinuria.

9 that lead to cytoskeleton reorganization and proteinuria.

10 related with treatment-induced reductions in proteinuria.

11 rapeutic approaches to glomerular injury and proteinuria.

12 rs after biopsy) renal graft dysfunction and proteinuria.

13 uli of obese Zucker rats before the onset of proteinuria.

14 and mortality were stronger with more severe proteinuria.

15 ns, causing podocyte depletion and promoting proteinuria.

16 ined presentation of high blood pressure and proteinuria.

17 interstitial damage, glomerulosclerosis, and proteinuria.

18 ontrollable bullous pemphigoid, colitis, and proteinuria.

19 e injury, and augmented oxidative stress and proteinuria.

20 ESRD in patients with primary MN with heavy proteinuria.

21 Twenty of 43 patients (47%) had proteinuria.

22 , which culminates in glomerulosclerosis and proteinuria.

23 s increased proportionally with the level of proteinuria.

24 implicated in glomerular diseases including proteinuria.

25 wo statins in patients with diabetes who had proteinuria.

26 iltration rate and a fourfold lower level of proteinuria.

27 on in podocytes induce glomerular injury and proteinuria.

28 mes excessively permeable leading to massive proteinuria.

29 tory and tested for seven markers of tubular proteinuria.

30 erular dysfunction, frequently manifested as proteinuria.

31 erly and presented with AKI and subnephrotic proteinuria.

32 and potential targets for treating diabetic proteinuria.

33 remission after a period of nephrotic-range proteinuria.

34 nly 2 subjects developed clinically relevant proteinuria.

35 each group had >/=50% reduction in level of proteinuria.

36 Pierson syndrome and unusually late onset of proteinuria.

37 relatively well preserved GFR and persistent proteinuria.

38 sex, black race, baseline eGFR, and baseline proteinuria.

39 s of inherited diseases characterized by LMW proteinuria.

40 nterval [95% CI], 0.81 to 1.60; P=0.50), for proteinuria 0.3-1.0 g/24 h, 2.17 (95% CI, 1.49 to 3.18;

41 h, 2.17 (95% CI, 1.49 to 3.18; P<0.001), for proteinuria 1.0-3.0 g/24 h, and 3.01 (95% CI, 1.75 to 5.

42 bevacizumab were hypertension (24% v 2%) and proteinuria (11% v 0%).

43 a at 3 (n = 591) and 12 (n = 583) months (no proteinuria: 150-299 mg/24 hours, 300-999 mg/24 hours, a

44 low estimated glomerular filtration rate or proteinuria (18.7%) and those with neither of these risk

45 l-grade hypertension (320 [33%] vs 75 [8%]), proteinuria (197 [21%] vs 49 [5%]), and wound healing pr

46 r 1.73 m(2) plus ACR >/=300 mg/g or dipstick proteinuria 2+ or higher vs eGFR >/=90 mL/min per 1.73 m

47 [1%]), fatigue (27 [8%] vs eight [2%]), and proteinuria (27 [8%] vs none).

48 zone + low-dose glucocorticoids also reduced proteinuria (63%) comparably to high-dose glucocorticoid

49 nt correlated with marked reductions in both proteinuria (80%) and overall immunosuppression (64%).

50 and octreotide included hypertension (32%), proteinuria (9%), and fatigue (7%); with IFN and octreot

51 alline LCPT), renal insufficiency (83%), and proteinuria (98%).

52 Patients were divided into groups based on proteinuria (Absent(A) <150 mg/day or low-grade(P)150 mg

53 nephrin(Y3F/Y3F) mice developed progressive proteinuria accompanied by structural changes in the fil

54 ing factor(s) that lead to the recurrence of proteinuria after kidney transplantation.

55 ent clinical guidelines to routinely measure proteinuria after transplant, but illustrate the need fo

56 se controls and prevented the development of proteinuria, albuminuria, and nephrinuria.

57 arly management of the predictable risks for proteinuria among new SRL users in order to delay the pr

58 were significantly associated with new onset proteinuria among SRL users.

59 on associated with a fourfold higher risk of proteinuria and a >2-fold higher risk of ESRD.

60 We assessed the effects of proteinuria and baseline renal function on long-term ren

61 ion of LPS, pod-Shp2 KO mice exhibited lower proteinuria and blood urea nitrogen concentrations than

62 Primary outcome measures included change in proteinuria and change in eGFR.

63 t transplantation, integrating discussion of proteinuria and chronic kidney disease with emphasis on

64 determine whether vitamin D levels influence proteinuria and CKD progression in children, we performe

65 pid, glucose profiles, and 24-hour urine for proteinuria and creatinine clearance.

66 ics and non-Hispanics and may be affected by proteinuria and diabetes.

67 roteinuria and showed consistent effects for proteinuria and ESRD (TER, 0.82; 95% confidence interval

68 loss of foot process architecture results in proteinuria and FSGS.

69 chanisms by which glucocorticoids ameliorate proteinuria and glomerular disease are not well understo

70 e podocyte cytoskeletal apparatus results in proteinuria and glomerular disease.

71 eroidogenic melanocortin peptides attenuates proteinuria and glomerular injury in experimental glomer

72 echanisms responsible for the development of proteinuria and glomerulosclerosis in radiation nephropa

73 trate that PKC-deficient mice, which develop proteinuria and glomerulosclerosis, display lower beta-c

74 nephrotic syndrome, has been associated with proteinuria and hypoalbuminemia severity.

75 erapeutically, BI-BTK-1 reversed established proteinuria and improved renal histopathology.

76 in significantly delayed the onset of severe proteinuria and improved survival.

77 ) splice isoforms from the kidney results in proteinuria and increased glomerular water permeability,

78 s receiving PPAR-gamma antagonists displayed proteinuria and increased podocyte TRPC6 expression, as

79 factor for changes in the kidney leading to proteinuria and indicate a functional role for KMO and m

80 phrotic syndrome is characterized by massive proteinuria and injury of specialized glomerular epithel

81 ical for glomerular filtration, and leads to proteinuria and kidney failure.

82 Treatment of TUDCA not only attenuated proteinuria and kidney histological changes, but also am

83 as anti-CD11b and -ICAM-1 mAb inhibited both proteinuria and macrophage and PMN infiltration.

84 Glomerular injury was characterized by proteinuria and partial podocyte foot process effacement

85 gmental glomerulosclerosis, characterized by proteinuria and podocyte injury.

86 tion of dendrin delays onset and severity of proteinuria and podocyte loss.

87 h the dual FXR/TGR5 agonist INT-767 improved proteinuria and prevented podocyte injury, mesangial exp

88 c administration of AC1903 suppressed severe proteinuria and prevented podocyte loss in a transgenic

89 alling in podocytes have been shown to cause proteinuria and progressive glomerular diseases.

90 The RAS blockade also decreases proteinuria and protects renal function in non-transplan

91 Renal elasticity is associated with proteinuria and rapid renal deterioration in patients wi

92 Models predicting proteinuria and reduced eGFR performed well (C-index 0.7

93 injured renal filtration barrier, leading to proteinuria and reduced renal function.

94 fic endoglucuronidase, mediates the onset of proteinuria and renal damage during experimental diabeti

95 r study shows that heparanase contributes to proteinuria and renal damage in experimental glomerulone

96 Laboratory data revealed proteinuria and severe depletion of serum IgG.

97 ven trials reported the effects on change in proteinuria and showed consistent effects for proteinuri

98 Thus both proteinuria and SHT were associated with poor graft surv

99 Low-grade proteinuria and systolic hypertension (SHT) are risk fac

100 ldenafil or pioglitazone treatment prevented proteinuria and the increased TRPC6 expression in rats w

101 and secondarily tested for association with proteinuria and time to ESRD.

102 Significant increase in proteinuria and total urinary iron was observed in the d

103 merular disease characterised by early onset proteinuria and ultrastructural thickening and splitting

104 progression of PE features (hypertension and proteinuria), and fetal/neonatal outcomes were evaluated

105 haturia, aminoaciduria, low molecular weight proteinuria, and albuminuria.

106 d in podocyte apoptosis, podocyte depletion, proteinuria, and an increase in serum creatinine.

107 ice exhibited less severe renal dysfunction, proteinuria, and fibrosis after DOCA-salt treatment comp

108 ion of TRPC5 by Englerin A did not stimulate proteinuria, and inhibition of TRPC5 by ML204 did not si

109 ne THSD7A on podocyte foot processes, induce proteinuria, and initiate a histopathological pattern th

110 hies and increased with age, blood pressure, proteinuria, and lower eGFR at baseline.

111 eeclamptic pregnancies feature hypertension, proteinuria, and placental anomalies.

112 cluding age, sex, ethnicity, renal function, proteinuria, and prior acute rejection) predicted death-

113 n in the podocyte, damage to the glycocalyx, proteinuria, and renal failure.

114 ted to blood urea nitrogen, serum uric acid, proteinuria, and supernatant IL-4; whereas positively as

115 pression in mature podocytes caused profound proteinuria, and with deep-etching freeze-fracture elect

116 Podocyte injury and the appearance of proteinuria are features of minimal-change disease (MCD)

117 Estimated glomerular filtration rate and proteinuria are predictors RRT after CF-LVAD implantatio

118 remission (CR) and partial remission (PR) of proteinuria as surrogate end points for a treatment effe

119 lone is sufficient to rescue the increase in proteinuria, as well as glomerular water permeability, i

120 not significantly improve renal function or proteinuria assessed over 1 year.

121 no difference in serum creatinine level and proteinuria at 1, 3, 6, and 12 months.

122 rticosteroid monotherapy transiently reduced proteinuria at 12 months.

123 ted at 8 wk, and 50% of the mice showed mild proteinuria at 18-24 wk due to membranous glomerulopathy

124 nalyze the effect on long-term prognosis of: proteinuria at 3 (n = 591) and 12 (n = 583) months (no p

125 during the first year in such patients with proteinuria at 3 months (reduction >/=50% of proteinuria

126 nd point of complete or partial remission of proteinuria at 6 months.

127 er transgenic model exhibited an increase in proteinuria at 8 months of age or a difference in LPS-in

128 al function, lower hemoglobin, and increased proteinuria at baseline.

129 inuria than those with less than 500 mg/g of proteinuria at the start of therapy (P < 0.001).

130 Patients with more than 500 mg/g of proteinuria at the start of treatment were significantly

131 Higher levels of proteinuria, at both 3 and 12 months, were progressively

132 therapy with intravitreal anti-VEGF agents, proteinuria be checked monthly, and there should be a lo

133 Patients with persistent proteinuria between years 1-2 and 2-3 had the poorest gr

134 ls (adjusted for demographics, measured GFR, proteinuria, body mass index, net endogenous acid produc

135 se in 25(OH)D (P=0.03), independent of eGFR; proteinuria, BP, and FGF-23 levels; and underlying renal

136 of the connexin 43 gene (connexin 43+/-) had proteinuria, BUN, and serum creatinine levels significan

137 ociated with worse renal function and higher proteinuria but did not correlate with histologic lesion

138 pared with those obtained from patients with proteinuria but without genetic mutations.

139 idneys of mice with GN and the inhibition of proteinuria by anti-PD-L1 mAb supported the pathogenic r

140 more, C1-Ten causes podocyte hypertrophy and proteinuria by increasing mTORC1 activity in vitro and i

141 In conclusion, CsA and FK506 inhibit proteinuria by protecting against PAN-induced podocyte i

142 ent of mice with lipidated albumin to induce proteinuria caused a decrease in the proportion of tubul

143 Proteinuria changes have a prognostic significance in pr

144 onset of hypertension; new onset/doubling of proteinuria; CKD stage shift; "general" combined outcome

145 ocyte GR knockout mice demonstrated worsened proteinuria compared to wild type.

146 r/lpr mice had significantly lower levels of proteinuria compared with female wild-type MRL-lpr/lpr m

147 Rituximab did not alter the level of proteinuria compared with that at baseline or in the con

148 Persistent and new onset proteinuria contributed to a high rate of mortality and

149 kidney under physiologic conditions and that proteinuria contributes to aberrant proteolytic activati

150 -vitamin D3 and 1,25-vitamin D2 repletion on proteinuria could not be explained by hypocalcemia, chan

151 diabetes, history of stroke, >1 g in 24 h of proteinuria daily, heart failure, estimated glomerular f

152 irmed primary IgA nephropathy and persistent proteinuria despite optimised renin-angiotensin system (

153 animals with GN reversed already established proteinuria, diminished tissue inflammation, and improve

154 sed to complement and refine the traditional proteinuria-driven approach, will improve the outcome in

155 demonstrate worsening allograft function and proteinuria during a median follow-up time of 1386 days

156 al of 6 (19.3%) of 31 patients had worsening proteinuria during or shortly after therapy.

157 hours, and >/=1 g/24 hours), and changes in proteinuria during the first year in such patients with

158 Creeping proteinuria during the first year was associated with lo

159 predefined as >/=2 of the following: tubular proteinuria, euglycemic glycosuria, increased urinary ph

160 mice with spontaneous chronic GN and severe proteinuria, few glomerulus-infiltrating PMN were found,

161 s with type 2 diabetes aged 18-75 years with proteinuria (first morning void urinary albumin to creat

162 of WT1 in podocytes of adult mice results in proteinuria, foot process effacement, and glomeruloscler

163 The predictive performance of proteinuria for graft failure was lower at 3 months afte

164 The discriminatory power of proteinuria for these intragraft injury processes was be

165 proteinuria at 3 months (reduction >/=50% of proteinuria from 3 to 12 months, variation <50%, and inc

166 Proteinuria greater than 1000 mg/24 hours developed in 2

167 Ninety subjects with proteinuria >/=0.5 g/d were enrolled at first biopsy for

168 At presentation, hematuria, proteinuria >/=1 g/d, hypertension, and renal failure we

169 STOP-IgAN) Trial, 162 patients with IgAN and proteinuria >0.75 g/d after 6 months of optimized suppor

170 uria, only those patients with time-averaged proteinuria >0.75 g/d and persistent hematuria had signi

171 Patients with time-averaged proteinuria >0.75 g/d had significantly poorer renal sur

172 (GFR>50 ml/min per 1.73 m(2)) and persistent proteinuria >1 g/d, despite 3-6 months of optimized supp

173 ients with biopsy-proven IgA nephropathy and proteinuria >1 g/d, maintained on angiotensin-converting

174 pecificity but lower sensitivity (47.8%) for proteinuria >1.0 g/24 h.

175 nd 3.01 (95% CI, 1.75 to 5.18; P<0.001), for proteinuria >3.0 g/24 h, independent of GFR and allograf

176 ration rate less than 80 mL/min; 32 (1%) had proteinuria >300 mg/day; 589 (20%) were hypertensive; 49

177 according to the magnitude of time-averaged proteinuria (>0.75 or </=0.75 g/d).

178 low estimated glomerular filtration rate and proteinuria had highest risk of RRT (63.6%) compared wit

179 Although change in proteinuria has been proposed as a surrogate for long-te

180 sion (AASK) Cohort Study who exhibited overt proteinuria have been reported to show high nonalbumin p

181 Men had a higher risk of proteinuria (hazard ratio [HR], 1.56; 95% confidence int

182 ment was the only factor related to creeping proteinuria (hazard ratio, 2.946; 95% confidence interva

183 e diabetes mellitus, history of stroke, >1 g proteinuria, heart failure, estimated glomerular filtrat

184 particularly fever, myalgias, pruritus, and proteinuria/hematuria, occurred in 83% vs 50% of those r

185 ey filtration barrier and is associated with proteinuria, hyperlipidemia, and edema.

186 nal disease was severe, with nephrotic-range proteinuria in 20/46 (43%) patients and chronic kidney d

187 s (primary outcome), mineral metabolism, and proteinuria in 43 consenting recipients of renal transpl

188 median age, 14.1 years) with nephrotic-range proteinuria in 44% of patients and advanced CKD in 46% o

189 he protective mechanisms of CsA and FK506 on proteinuria in a rat model of MCD induced by puromycin a

190 MDM2 knockdown caused podocyte loss and proteinuria in a zebrafish model, which was consistent w

191 WT bone marrow did not prevent the increased proteinuria in ABIN1[D845N] mice.

192 significantly lower the level of LPS-induced proteinuria in any group.

193 , prognostic significance, and management of proteinuria in both adult and pediatric transplant recip

194 omal recessive Alport syndrome and increased proteinuria in Col4a5(+/-) females that exhibit a mild f

195 loss of nephrin expression and the onset of proteinuria in diabetic mice correlate with an increased

196 expression on the slit diaphragm and reduced proteinuria in diabetic mice, whereas overexpression of

197 he use of B7-1 targeting strategies to treat proteinuria in DN.

198 evels of urinary LacCer were detected before proteinuria in lupus mice.

199 s alphavbeta3 integrin activation and causes proteinuria in mice in a suPAR-dependent manner.

200 rombin inhibition has been shown to decrease proteinuria in nephrotic animal models.

201 ay, added to optimised RAS blockade, reduced proteinuria in patients with IgA nephropathy.

202 crolimus (FK506) has been reported to reduce proteinuria in patients with nephrotic syndrome, but mec

203 gnized as key players in the pathogenesis of proteinuria in primary and secondary glomerular disorder

204 found that puromycin aminonucleoside-induced proteinuria in rats was significantly reduced by both hi

205 corticoid receptor is important for limiting proteinuria in settings of podocyte injury.

206 lar filtration rate (eGFR) and assessment of proteinuria in spot or timed urine samples, are of limit

207 ion of Sirt6 exacerbates podocyte injury and proteinuria in two independent mouse models, diabetic ne

208 inhibition of thrombin with hirudin reduced proteinuria in two rat nephrosis models, and thrombin co

209 tic apheresis reduced circulating sFlt-1 and proteinuria in women with very preterm preeclampsia and

210 d-related symptoms, such as hypertension and proteinuria, in patients with CKD, and (3) reduce interd

211 B7-1 induction in podocytes of patients with proteinuria, including those with FSGS and type 2 diabet

212 EBP-alpha in podocytes resulted in increased proteinuria, increased podocyte foot process effacement,

213 In conclusion, we show that proteinuria increases plasma phosphate concentration ind

214 Proteinuria induces elevation of both plasma phosphate a

215 Presence of proteinuria is associated with increased risk of progres

216 Proteinuria is closely associated with the progression o

217 steroids (CS) in IgA nephropathy (IgAN) when proteinuria is persistently >/=1 g/d despite 3-6 months

218 Proteinuria is routinely measured to assess renal allogr

219 Excess levels of protein in urine (proteinuria) is a hallmark of kidney disease that typica

220 Podocyte injury, manifesting as proteinuria, is the cause of many glomerular diseases.

221 membranous nephropathy (MGN), variability in proteinuria levels and lag between these changes and acc

222 (CR), partial remission (PR), and relapse as proteinuria </=0.3, 0.4-3.4, and >/=3.5 g/d after CR or

223 renal survival than those with time-averaged proteinuria </=0.75 g/d.

224 Compared with proteinuria <0.3 g/24 h, the hazard ratios for graft fai

225 ts with stable eGFR<30 ml/min per 1.73 m(2), proteinuria <1 g/g urinary creatinine, good nutritional

226 ith estimated glomerular filtration rate and proteinuria measurements were reported as always availab

227 ts with de novo DSA ABMR displayed increased proteinuria, more transplant glomerulopathy lesions, and

228 ation <50%, and increase >/=50% or "creeping proteinuria") (n = 283).

229 a have been reported to show high nonalbumin proteinuria (NAP), which is characteristic of a tubulopa

230 per 1.73 m(2) plus ACR <10 mg/g or dipstick proteinuria negative).

231 ial glycocalyx thickness, and development of proteinuria observed in wild-type counterparts.

232 Patients with proteinuria or lower GFR should be monitored more closel

233 y hypertension after 20 weeks' gestation and proteinuria or other evidence of multisystem involvement

234 haracterized in general by hypertension with proteinuria or other systemic disturbances.

235 isease (OR, 3.13; 95% CI, 1.51 to 6.50), and proteinuria (OR, 3.69; 95% CI, 1.63 to 8.36).

236 Tg-G2 mice did not develop kidney pathology, proteinuria, or azotemia as of 300 days of age.

237 clinical findings: reduced kidney function, proteinuria, or hematuria with other causes excluded (n

238 orrelate with age, sex, time from diagnosis, proteinuria, or serum albumin, but epitope spreading str

239 ome) in women without baseline hypertension, proteinuria, or systemic disease (OR, 1.88; 95% CI, 1.27

240 h kidney allograft which developed worsening proteinuria over the first year after transplantation.

241 younger (P=0.008), had less nephrotic range proteinuria (P=0.02), and exhibited a higher rate of spo

242 enetic deletion of Kmo in mice each led to a proteinuria phenotype.

243 background resulted in low molecular weight proteinuria, phosphaturia, and acidemia.

244 rat model of reversible podocyte injury and proteinuria, phosphorylated nephrin temporally colocaliz

245 ffects and reversed age-related increases in proteinuria, podocyte injury, fibronectin accumulation,

246 Disruption of ABIN1 function exacerbated proteinuria, podocyte injury, glomerular NF-kappaB activ

247 the selective TGR5 agonist INT-777 decreased proteinuria, podocyte injury, mesangial expansion, fibro

248 ence risk was higher in patients with higher proteinuria pretransplant [hazard ratio = 1.869 (95% con

249 ity in tests used, eligibility criteria, and proteinuria prevalence (8.7%-93.8%).

250 Here, we estimated the risk of proteinuria, reduced GFR, and ESRD in 3956 white kidney

251 suggest that melanocortin therapy confers a proteinuria reducing and podoprotective effect in protei

252 g pioglitazone could potentially enhance the proteinuria-reducing effects of glucocorticoids during N

253 We evaluated the extent of sFlt-1 removal, proteinuria reduction, pregnancy continuation, and neona

254 oorest graft survival with an improvement if proteinuria regressed (P-A), especially in the Hypertens

255 s were scarce; renal transplant function and proteinuria remained stable.

256 Vitamin D treatment to reduce proteinuria remains controversial, although there is an

257 role of pre-existing renal insufficiency and proteinuria remains unclear among LT recipients receivin

258 Positive effect of rituximab on proteinuria remission occurred after 6 months.

259 e B7-1 blocker abatacept was associated with proteinuria remission.

260 ker with higher affinity, and did not induce proteinuria remission.

261 ealed time-averaged hematuria, time-averaged proteinuria, renal function at baseline, and the presenc

262 a(-/-) mice showed significantly exacerbated proteinuria, renal macrophage infiltration, glomerular h

263 Dipstick proteinuria showed smaller improvement than ACR.

264 l treatment (including extensive PE) reduced proteinuria significantly (from 5.3 [2.0-7.8] to 1.0 [0.

265 stabilizes synaptopodin, reduced LPS-induced proteinuria significantly in wild-type mice but to a les

266 activated (M2b) macrophages, correlated with proteinuria status.

267 ression of podocyte proteins at the onset of proteinuria suggested that the primary cause of podocyte

268 gnificantly more likely to develop worsening proteinuria than those with less than 500 mg/g of protei

269 athway results in low molecular weight (LMW) proteinuria that can progress to end-stage kidney diseas

270 FSGS is a CKD with heavy proteinuria that eventually progresses to ESRD.

271 l, estimated glomerular filtration rate, and proteinuria, the hazard ratios associated with per 1 SD

272 fil ameliorates podocyte injury and prevents proteinuria through cGMP- and PKG-dependent binding of P

273 litazone + high-dose glucocorticoids reduced proteinuria to almost control levels (97%).

274 reafter, a 25% rise in serum Cr or new-onset proteinuria triggered graft biopsy (index biopsy, IBx),

275 ficantly ameliorated serum creatinine level, proteinuria, tubular injury, and kidney inflammation.

276 ith preeclampsia, negatively correlated with proteinuria, urinary podocin(+) EVs-to-nephrin(+) EVs ra

277 r filtration rate (<40 mL/min/1.73 m(2)) and proteinuria (urine protein to creatinine ratio >/=0.55 m

278 howed that CsA and FK506 treatment decreased proteinuria via a mechanism associated to a reduction in

279 e level (range) was 1.4 (0.8-2.4) mg/dl, and proteinuria was 2.1 (0.6-5.3) g/d.

280 Dipstick proteinuria was also a significant predictor of RRT afte

281 Proteinuria was also measured in ABIN1[D485N] mice trans

282 e with eGFR>/=60 ml/min per 1.73 m(2) and no proteinuria was cancer (38.1%); the most common cause of

283 ment b (C3b) deposition was reduced, whereas proteinuria was diminished.

284 as more prevalent (83% vs 53%, P < .001) and proteinuria was higher (7.3 g/L vs 5.0 g/L, P < .001).

285 Proteinuria was identified using morning dipstick result

286 tly affect the podocytes in the treatment of proteinuria, we created a mouse model with podocyte-spec

287 ice induced a severe nephrotic syndrome with proteinuria, weight gain, and hyperlipidemia.

288 psy samples with concomitant data on 24-hour proteinuria were included in the analyses (n=2274).

289 y a good surrogate for ESRD, whereas data on proteinuria were limited.

290 Hypertension and proteinuria were present in 19% and 28% of these patient

291 Independent determinants of proteinuria were repeat transplantation, mean arterial p

292 suPAR, and these cells efficiently transmit proteinuria when transferred to healthy mice.

293 ll as bone marrow plasma cell percentage and proteinuria; whereas positively associated with estimate

294 The loss of podocytes causes proteinuria, which is involved in the pathogenesis of di

295 rom indolent nephropathy and inflammation to proteinuria with glomerular abnormalities.

296 umin-to-creatinine ratio (ACR), and dipstick proteinuria with the incidence of peripheral artery dise

297 Complete and partial remission of proteinuria within 12 months of disease onset occurred i

298 After adjustments, new onset proteinuria within the first year after the initiation o

299 uated glomerular filtration rate decline and proteinuria without affecting blood pressure.

300 Sodium intake influences blood pressure and proteinuria, yet the impact on long-term outcomes is unc