ライフサイエンスコーパス: proteinuria

1 verall, 137 patients were analyzed (26% with proteinuria).

2 se 2019 (COVID-19), AKI, and nephrotic-range proteinuria.

3 spected hereditary renal disease and chronic proteinuria.

4 All patients had proteinuria.

5 , hypertension, diabetes, smoking, eGFR, and proteinuria.

6 sia, defined as gestational hypertension and proteinuria.

7 block FAK-Rac1 axis in podocyte and prevent proteinuria.

8 significantly improved survival and reduced proteinuria.

9 ntly associated with subsequent worsening of proteinuria.

10 dney, and are decreased in rats with limited proteinuria.

11 mated glomerular filtration rate (eGFR), and proteinuria.

12 unctional slit diaphragms and display severe proteinuria.

13 d nephrinuria, both of which correlated with proteinuria.

14 on in podocytes induce glomerular injury and proteinuria.

15 mes excessively permeable leading to massive proteinuria.

16 tory and tested for seven markers of tubular proteinuria.

17 erular dysfunction, frequently manifested as proteinuria.

18 erly and presented with AKI and subnephrotic proteinuria.

19 and potential targets for treating diabetic proteinuria.

20 remission after a period of nephrotic-range proteinuria.

21 nly 2 subjects developed clinically relevant proteinuria.

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

23 Pierson syndrome and unusually late onset of proteinuria.

24 relatively well preserved GFR and persistent proteinuria.

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

26 s of inherited diseases characterized by LMW proteinuria.

27 tor for podocyte foot process effacement and proteinuria.

28 , in some patients SRL may cause significant proteinuria.

29 rption in Fanconi syndrome may contribute to proteinuria.

30 labsorption of vitamin B12 and in some cases proteinuria.

31 eroid-resistant nephrotic syndrome or severe proteinuria.

32 aggravated podocytes injury and deteriorated proteinuria.

33 virus-induced renal disease with significant proteinuria.

34 ed with increases in plasmin (ogen) uria and proteinuria.

35 C3a positively correlates with the degree of proteinuria.

36 ocal segmental glomerulosclerosis (FSGS) and proteinuria.

37 ted grade 3 toxicities were hypertension and proteinuria.

38 presented with AKI; nine had nephrotic-range proteinuria.

39 te injury, effacement of foot processes, and proteinuria.

40 ytes, which results in glomerular damage and proteinuria.

41 iated with increased incidences of any-grade proteinuria (10 [21%] of 48 patients vs 0) and hypertens

42 38.8 +/- 13.3 mL/min/1.73 m, P = 0.011) and proteinuria (1280 [117 to 3752] versus 168 [83 to 1613]

43 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

44 [1%]), fatigue (27 [8%] vs eight [2%]), and proteinuria (27 [8%] vs none).

45 dverse events (AEs) were hypertension (69%), proteinuria (51%), and diarrhea and nausea (both 36%); h

46 in/1.73 m(2) , P = 0.002) and higher 24-hour proteinuria (58.5 +/- 21 versus 53.9 +/- 22 versus 42.9

47 patients with AKI and urine studies, 84% had proteinuria, 81% had hematuria, and 60% had leukocyturia

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

49 ere significantly higher among patients with proteinuria after adjustment for baseline characteristic

50 function, and that HT recipients who develop proteinuria after conversion to SRL have less attenuatio

51 ought to investigate the prognostic value of proteinuria after conversion to SRL.

52 The Robo2 cKO mice also develop less proteinuria after NTS injury.

53 s is known about potential effects of AKI on proteinuria, although proteinuria is perhaps the stronge

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

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

56 rican ancestry who developed nephrotic-range proteinuria and AKI early in the course of disease.

57 in these mice under light microscope, severe proteinuria and albuminuria were found in these podocyte

58 Mice were monitored for development of proteinuria and assessed for development of glomerular s

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

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

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

62 e are highly sensitive and PA induces severe proteinuria and collapsing FSGS.

63 ith Exoc4) knockout mice that showed massive proteinuria and died within 4 weeks of birth.

64 N gene were associated with chronic isolated proteinuria and early childhood onset.

65 led a high correlation between the amount of proteinuria and expression levels of the mechanosensor p

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

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

68 Phosphomimetic Actn4 mice developed proteinuria and glomerulosclerosis after subtotal nephre

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

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

71 s common, and can range from the presence of proteinuria and haematuria to acute kidney injury (AKI)

72 ment for CKD for years because it can reduce proteinuria and hence retard renal function decline, but

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

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

75 n of the expression of genes associated with proteinuria and injury by kidney parenchymal cells.

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

77 beta-PIX knockout mice developed progressive proteinuria and kidney failure with global or segmental

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

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

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

81 Studies have also observed proteinuria and microscopic hematuria in such patients.

82 ndrome (SRNS) is characterized by high-range proteinuria and most often focal and segmental glomerulo

83 teinuria rapidly reversed established severe proteinuria and nephritis and largely restored normal gl

84 TG administration is sufficient to attenuate proteinuria and podocyte injury in mouse models of diabe

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

86 ce were partially protected from LPS-induced proteinuria and recruitment of inflammatory cells.

87 idney donor candidates lacking hypertension, proteinuria and reduced kidney function after workup wil

88 Younger age and higher proteinuria and serum creatinine levels increased the li

89 giotensin system antagonists help to control proteinuria and slow the progression of fibrosis.

90 brafish causes glomerular injury with edema, proteinuria and structural changes of the glomerular fil

91 ckout of the unique TBC1D8B ortholog-induced proteinuria and that this phenotype was rescued by human

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

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

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

95 hronic renal insufficiency", "albuminuria", "proteinuria", and "randomized controlled trial"; key inc

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

97 Most patients had subnephrotic proteinuria, and approximately half had pyuria.

98 estimated glomerular filtration rate (eGFR), proteinuria, and blood pressure.

99 gressive glomerulosclerosis, nephrotic-range proteinuria, and finally kidney failure.

100 yte injury, including c-Src phosphorylation, proteinuria, and focal segmental glomerulosclerosis (FSG

101 sence of an elevated free light chain ratio, proteinuria, and hematuria.

102 type mice develop significant kidney injury, proteinuria, and kidney fibrosis after three weeks of DO

103 CXCR6 deficiency ameliorated kidney injury, proteinuria, and kidney fibrosis following treatment wit

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

105 ients with severe proteinuria than with mild proteinuria, and nephrin correlated strongly with biomar

106 28), we measured time-of-biopsy albuminuria, proteinuria, and plasmin (ogen) uria for correlations wi

107 ) and TAF9(134-144) immunized mice developed proteinuria, and their renal pathology revealed glomerul

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

109 l to mild proteinuria to about 70% in severe proteinuria, and with wider prediction intervals at lowe

110 owever, it is not clear whether all forms of proteinuria are damaging.

111 Two variants associating with proteinuria are in LRP2 and CUBN, encoding the co-transp

112 Hypertension and proteinuria are the cornerstone of the disease, though s

113 tion in PCmas(-/-) mice resulted in onset of proteinuria around postnatal day 28, accompanied by foot

114 EE-exposed mice had increased proteinuria as early as 7 weeks of age.

115 explain how loss of OCRL results in tubular proteinuria as well as the other commonly observed renal

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

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

118 more N-terminal IGS mutations, 37 of the 41 proteinuria-associated CUBN variants led to modification

119 in inducing complete or partial remission of proteinuria at 12 months and was superior in maintaining

120 rticosteroid monotherapy transiently reduced proteinuria at 12 months.

121 omposite of complete or partial remission of proteinuria at 24 months.

122 of urinary CD163 in patients with persistent proteinuria at 6 months improved the prediction of who w

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

124 quantifiable measurements of albuminuria or proteinuria at baseline and within 12 months of follow-u

125 36.3 to -10.8; P < 0.001) and higher 24-hour proteinuria (beta coefficient: 15.3; 95% CI: 1.12 to 30.

126 Proteinuria, blood urea nitrogen, and glomerular immune

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

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

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

130 e mortality (hazard ratio 3.8; P = .01) with proteinuria but similar risk of CAV-related events (P =

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

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

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

134 ney glomeruloendotheliosis with accompanying proteinuria, classic hallmarks of preeclampsia.

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

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

137 tic of a nephrotic syndrome, associated with proteinuria composed mainly of free kappa light chains.

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

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

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

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

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

143 ten presenting as new-onset hypertension and proteinuria during the third trimester, preeclampsia can

144 fore analyzed standard markers of glomerular proteinuria (e.g. immunoglobulin G [IgG]), urinary nephr

145 ven at a high dose (100 mug), did not induce proteinuria, effacement of podocytes, or disruption of t

146 worsening of existing hypertension, dipstick proteinuria, epigastric or right upper-quadrant pain, he

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

148 ix [9%] patients), hypertension (five [7%]), proteinuria (four [6%]), and hypophosphataemia (four [6%

149 Add3 transgenic rats showed attenuation of proteinuria, glomerular injury, and kidney fibrosis with

150 layed AZM198 treatment significantly reduced proteinuria, glomerular thrombosis, serum creatinine, an

151 The presence of proteinuria > 200 mg/g was predictive of chronic active

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

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

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

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

156 The presence of proteinuria >200 mg/g was predictive of chronic active s

157 CKD was defined as dipstick proteinuria >=1+ and/or estimated glomerular filtration

158 Proteinuria >=1.5 g/d, hematuria, and an elevated free l

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

160 n of Coq6 in mouse podocytes caused FSGS and proteinuria (>46-fold increases in albuminuria).

161 older age (>=65 versus 45 to 64 years), more proteinuria (>=150 to <500 versus <150 mg/g), higher sys

162 Patients with proteinuria had significantly lower GFR (P = .005) but s

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

164 ividuals not responding with a resolution of proteinuria have a poor renal prognosis.

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

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

167 y the urine dipstick: glucosuria, ketonuria, proteinuria, hematuria and urine pH.

168 Patients may have proteinuria, hematuria, and/or renal dysfunction.

169 In multivariable analysis, only proteinuria (HR: 7.24; P=0.01) and the presence of missi

170 tabase (n = 192,868) reveal connections with proteinuria, hyperlipidemia, gout, and hypertension.

171 literature showed that mainly pre pregnancy proteinuria, hypertension and high SCr are risk factors

172 e literature showed that mainly prepregnancy proteinuria, hypertension, and high SCr are risk factors

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

174 (Pyr(1))-apelin-13 normalized proteinuria in association with lower renal cortical col

175 equently combine to cause various degrees of proteinuria in children and adults.

176 asing kidney function and increasing 24-hour proteinuria in children/adolescents with histologically

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

178 eractive GH signaling has been implicated in proteinuria in diabetes and acromegaly.

179 ii, a traditional herbal remedy that reduced proteinuria in diabetic patients.

180 ch beta-catenin promotes podocyte injury and proteinuria in glomerular diseases.

181 udy reveals podocyte injury as main cause of proteinuria in hantavirus patients.

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

183 Administration of Src inhibitors reduced proteinuria in msuPAR2-transgenic mice.

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

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

186 Switching from TDF to TAF improves eGFR and proteinuria in patients with renal dysfunction.

187 Studies have documented AKI with high-grade proteinuria in patients with severe acute respiratory sy

188 intaining a complete or partial remission of proteinuria in patients with this condition.

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

190 or TAZ resulted in more severe and prolonged proteinuria in response to injury, as well as worse glom

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

192 esents with new-onset hypertension and often proteinuria in the mother, which can progress to multi-o

193 characterized by new-onset hypertension and proteinuria in the second half of pregnancy) represents

194 Since the proteinuria in these patients had a high proportion of a

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

196 e in the atezolizumab monotherapy group) and proteinuria (in two [3%] patients in the atezolizumab pl

197 ses the risk of stroke by about 40% and that proteinuria increases the risk by about 70%.

198 occur only in the subgroup of patients with proteinuria, indicating podocyte damage.

199 glomerular basement membrane thickening and proteinuria induced by excess GH.

200 mplies that modulating ER stress may improve proteinuria-induced alterations of Klotho expression, an

201 r data show that dh404 significantly reduced proteinuria-induced tubular cell mitochondrial damage, s

202 Bardoxolone methyl analog attenuates proteinuria-induced tubular damage by modulating mitocho

203 r an Nrf2 activator can protect tubules from proteinuria-induced tubular damage via anti-inflammatory

204 s were higher among those with >=500 mg/g of proteinuria irrespective of eGFR.

205 Our results indicate that proteinuria is a marker of baseline renal dysfunction, a

206 Chronic inflammation and proteinuria is a risk factor for cardiovascular disease

207 Proteinuria is associated with renal function decline an

208 Proteinuria is closely associated with the progression o

209 tial effects of AKI on proteinuria, although proteinuria is perhaps the strongest risk factor for fut

210 Preeclampsia - maternal hypertension and proteinuria - is promoted by placental ischemia resultin

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

212 sion (higher GFR and lower serum creatinine, proteinuria, kidney inflammatory infiltration and nSMase

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

214 re renal disease characteristic of FSGS with proteinuria, loss of kidney function, and glomeruloscler

215 GD20, TGA-PE rats had higher blood pressure, proteinuria, lower maternal and pup weights, lower pup n

216 condition in humans that may not require any proteinuria-lowering treatment or renal biopsy.FUNDINGAT

217 is, motivating renal biopsies and the use of proteinuria-lowering treatments.

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

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

220 and Care Excellence BP targets for CKD, and proteinuria measurement.

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

222 Diabetes and proteinuria more strongly associated with glomeruloscler

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

224 were dehydration (n=2), vomiting (n=2), and proteinuria (n=2).

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

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

227 e presence and timing of non-nephrotic range proteinuria (NNRP) and serum albumin measurements in rel

228 A remission of proteinuria occurred in 133 (89%) patients and was not d

229 us that result in the classic triad of heavy proteinuria, oedema and hypoalbuminaemia.

230 ned patients who had membranous nephropathy, proteinuria of at least 5 g per 24 hours, and a quantifi

231 Over 70% of survivors had proteinuria on long-term follow-up.

232 tion with eventual systemic autoimmunity and proteinuria onset.

233 -eclampsia was gestational hypertension plus proteinuria or a pre-eclampsia-defining complication.

234 N pathogenesis, although without significant proteinuria or hematuria.

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

236 ch direct or indirect podocyte injury drives proteinuria or nephrotic syndrome.

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

238 e between groups in terms of renal function, proteinuria, or biopsy-proven acute rejection.

239 e metabolites were not associated with eGFR, proteinuria, or blood pressure, but PA was associated wi

240 trations were also associated with decreased proteinuria over time, as measured by urinary protein:cr

241 lated strongly with biomarkers of glomerular proteinuria over time.

242 s show albuminuria proportional to patients' proteinuria, phenomenon not observed with sera from heal

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 Renal insufficiency was apparent at P21 when proteinuria presents, fibrosis of both the glomeruli and

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

249 1) mice with 201A3 after the onset of severe proteinuria rapidly reversed established severe proteinu

250 In contrast to INS, proteinuria recovered autonomously in hantavirus patient

251 ficiency, hypoglycemia, anemia, intermittent proteinuria, recurrent bloodstream infections and chroni

252 hence retard renal function decline, but the proteinuria reduction effect is still insufficient in ma

253 CKD- and proteinuria-related coding improved significantly along

254 Although proteinuria remained stable, the mean eGFR decline durin

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

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

257 assess associations with time from biopsy to proteinuria remission and time to a composite progressio

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

259 clusters of findings associated with either proteinuria remission or disease progression.

260 at 12 months and was superior in maintaining proteinuria remission up to 24 months.

261 sformation had the highest rates of complete proteinuria remission, whereas patients in clusters with

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

263 ically characterized by low molecular weight proteinuria, renal tubular acidosis (RTA), aminoaciduria

264 ne Nphs2, the consequent podocyte damage and proteinuria rendered the cells responsive to AngII and r

265 erse events were hypertension (13 [13%]) and proteinuria (seven [7%]).

266 significantly higher in patients with severe proteinuria than with mild proteinuria, and nephrin corr

267 e resulted in an increased susceptibility to proteinuria that was rescued by recombinant ICOSL.

268 ith clinical renal endpoints such as eGFR or proteinuria, there was a consistent pattern of increased

269 ate pregnancy affecting other organ systems (proteinuria, thrombocytopenia, renal insufficiency, live

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

271 signaling in podocytes, which contributes to proteinuria through EMT as well as renal fibrosis.

272 centrated on clinical (estimated GFR [eGFR], proteinuria, time posttransplant, donor-specific antibod

273 ratio increasing from <30% in normal to mild proteinuria to about 70% in severe proteinuria, and with

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

275 in female recipients with moderate to severe proteinuria, uncontrolled hypertension or reduced graft

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

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

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

279 Proteinuria was assessed in patients.

280 Proteinuria was defined as Delta urine protein >=300 mg/

281 Proteinuria was determined from a 24-hour urine collecti

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

283 Proteinuria was identified using morning dipstick result

284 Proteinuria was measured by urine protein to creatinine

285 e Bedside Schwartz equation, whereas 24-hour proteinuria was measured using a radioimmunoassay method

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 Blood pressure and dipstick proteinuria were assessed per protocol.

289 High levels of proteinuria were observed to have the largest associatio

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

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

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

293 ncing data to identify patients with chronic proteinuria who had biallelic variants in the cubilin ge

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

295 Glomerular disease presenting as proteinuria with or without AKI is an important presenta

296 D-19 and clinical features of AKI, including proteinuria with or without hematuria.

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

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

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

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