ライフサイエンスコーパス: nephrotic

1 last 20 years that a substantial portion of nephrotic adults with primary FSGS do respond to treatme

2 on has been shown to decrease proteinuria in nephrotic animal models.

3 induced a more robust thrombotic response in nephrotic animals.

4 modified at a key LPL interacting site into nephrotic Buffalo Mna and Zucker Diabetic Fatty rats red

5 ed ferritin permeability was not observed in nephrotic CD2-associated protein-null (Cd2ap-/-) mice, w

6 hypothesis, we studied phosphate handling in nephrotic children and patients with CKD.

7 c phase compared with the remission phase in nephrotic children.

8 xt, the effects of plasma from patients with nephrotic conditions to non-nephrotic conditions were co

9 om patients with nephrotic conditions to non-nephrotic conditions were compared.

10 transition that appears to be common to many nephrotic conditions.

11 t, it is in patients who remain persistently nephrotic despite conservative therapy that a more aggre

12 hypercoagulopathy is highly correlated with nephrotic disease severity, but overt thrombosis may req

13 c systems enhanced proteinuria in persistent nephrotic disease.

14 In nephrotic diseases, such as membranous nephropathy and F

15 Podocytes are the key cells affected in nephrotic glomerular kidney diseases, and they respond u

16 st was shown that exposure to normal and non-nephrotic human plasma leads to a concentration of nephr

17 cardiac hypertrophy, vascular restenosis and nephrotic hypertrophy.

18 dismiss previous claims on the filtration of nephrotic levels of albumin.

19 s over the course of 5-10 years, whereas non-nephrotic patients and those entering a remission have a

20 tium (edema) and the peritoneum (ascites) of nephrotic patients is classically thought to stem from t

21 nd guiding personalized rituximab therapy in nephrotic patients with primary MN.

22 In nephrotic patients, progression to ESRD often occurs ove

23 The nephrotic phenotype was recapitulated in arhgdia-deficie

24 ed, and the relocation of nephrin induced by nephrotic plasma could be rescued back to the plasma mem

25 The effects of normal human plasma and nephrotic plasma on podocytes were tested, focusing part

26 When exposed to all nephrotic plasma samples (and a non-human serum control)

27 This work demonstrates that nephrotic plasma seems to be deficient in factors that a

28 tracellular calcium signaling was altered by nephrotic plasma, which was mediated by tyrosine kinase

29 he plasma membrane by co-incubation with non-nephrotic plasma.

30 , suggesting that thrombin may contribute to nephrotic progression.

31 ental glomerulosclerosis (FSGS) often causes nephrotic proteinuria and frequently results in end-stag

32 rotein-to-creatinine ratios became >3.5 g/g (nephrotic proteinuria cohort).

33 Of note, in both the eGFR<60 and nephrotic proteinuria cohorts, CKD cases with two APOL1

34 Rats with puromycin-aminonucleoside-induced nephrotic proteinuria displayed higher renal protein exp

35 e common morphologic feature associated with nephrotic proteinuria was diffuse visceral epithelial ce

36 ria (>/=3 g/d) and 10 from patients with non-nephrotic proteinuria.

37 ad to significant albuminuria, even reaching nephrotic range in animal models.

38 ed activity were younger (P=0.008), had less nephrotic range proteinuria (P=0.02), and exhibited a hi

39 rrence of FSGS was defined as development of nephrotic range proteinuria between days 3 and 30 posttr

40 hematuria and proteinuria (sometimes in the nephrotic range), and develop chronic kidney disease wit

41 s (FFAs) to albumin when proteinuria reached nephrotic range.

42 psies were studied, eight from patients with nephrotic-range proteinuria (>/=3 g/d) and 10 from patie

43 improved understanding of the threshold for nephrotic-range proteinuria and the pathogenesis of hype

44 ociated with the eGFR<60 cohort, but not the nephrotic-range proteinuria cohort.

45 Nephrotic-range proteinuria has been known for years to

46 At diagnosis, renal disease was severe, with nephrotic-range proteinuria in 20/46 (43%) patients and

47 ng adolescence (median age, 14.1 years) with nephrotic-range proteinuria in 44% of patients and advan

48 min purified from the urine of patients with nephrotic-range proteinuria inhibits Ca(2+) uptake in TR

49 Nephrotic-range proteinuria is considered a poor prognos

50 Nephrotic-range proteinuria is due to glomerular disease

51 reases in circulating Angptl4 in response to nephrotic-range proteinuria reduces the degree of this p

52 re confirmed in transgenic mice that develop nephrotic-range proteinuria resulting from podocyte depl

53 s with idiopathic membranous nephropathy and nephrotic-range proteinuria using both indirect immunofl

54 In nephrotic-range proteinuria, filtered plasminogen reache

55 of consanguineous parents with intermittent nephrotic-range proteinuria, we identified a homozygous

56 N who achieved a remission after a period of nephrotic-range proteinuria.

57 n of Angptl4 (NPHS2-Angptl4) in rats induced nephrotic-range, and selective, proteinuria (over 500-fo

58 nal function and prevented salt retention in nephrotic rats.

59 n, and salt retention in doxorubicin treated nephrotic rats.

60 omeruli of puromycin aminonucleotide-induced nephrotic rats.

61 t very likely extends to the duration of the nephrotic state per se.

62 5.7% vs 2.6%; aHR, 2.27; 95% CI, 1.32-3.89), nephrotic syndrome (1.3% vs 0.1%; aHR, 15.7; 95% CI, 2.9

63 logy Damage Index, the greatest frequency of nephrotic syndrome (8.9%) was observed in patients in cl

64 the underlying disease, the severity of the nephrotic syndrome (as assessed by serum albumin concent

65 Congenital nephrotic syndrome (CNS), a rare entity, is known to pre

66 omal recessive SRNS presenting as congenital nephrotic syndrome (CNS).

67 with frequently relapsing steroid-sensitive nephrotic syndrome (FR-SSNS).

68 of podocyte disorders in cases of idiopathic nephrotic syndrome (INS) are complex and remain incomple

69 ritis, type I membranoproliferative GN), and nephrotic syndrome (minimal change/FSGS, membranous neph

70 nt CGD and DM (n=1), and steroid therapy for nephrotic syndrome (n=1).

71 mutations profile in Brazilian children with nephrotic syndrome (NS) and to determine a genotype-phen

72 Nephrotic syndrome (NS) is a genetically heterogeneous g

73 Nephrotic syndrome (NS) is divided into steroid-sensitiv

74 Nephrotic syndrome (NS) occurs when the glomerular filtr

75 Rituximab induces nephrotic syndrome (NS) remission in two-thirds of patie

76 nefits of genetic screening of patients with nephrotic syndrome (NS) to diagnose monogenic causes, re

77 Glucocorticoids are the primary therapy for nephrotic syndrome (NS), but have serious side effects a

78 have been identified as monogenic causes of nephrotic syndrome (NS), but important knowledge gaps ex

79 Patients with nephrotic syndrome (NS), even with normal GFR, often dis

80 Nephrotic syndrome (NS), the association of gross protei

81 relative risk 4.79; 95% CI 2.71 to 8.46) and nephrotic syndrome (relative risk 7.78; 95% CI 1.80 to 3

82 Steroid-dependent nephrotic syndrome (SDNS) carries a high risk of toxicit

83 racterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain an

84 yme Q10 biosynthesis cause steroid-resistant nephrotic syndrome (SRNS) as part of multiorgan involvem

85 Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney d

86 Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney d

87 s reduced in patients with steroid-resistant nephrotic syndrome (SRNS) due to monogenic disorders.

88 n of single-gene causes of steroid-resistant nephrotic syndrome (SRNS) has furthered the understandin

89 Steroid-resistant nephrotic syndrome (SRNS) is a frequent cause of end-sta

90 Steroid-resistant nephrotic syndrome (SRNS) is a frequent cause of progres

91 Steroid-resistant nephrotic syndrome (SRNS) is the second most frequent ca

92 Steroid-resistant nephrotic syndrome (SRNS), a frequent cause of chronic k

93 Steroid-resistant nephrotic syndrome (SRNS), a heterogeneous disorder of t

94 cause autosomal recessive steroid-resistant nephrotic syndrome (SRNS).

95 Steroid-sensitive nephrotic syndrome (SSNS) accounts for >80% of cases of

96 ed protein (CD2AP) develop renal failure and nephrotic syndrome about 4 weeks after birth and die aro

97 hallmarks of Pierson syndrome are congenital nephrotic syndrome accompanied by ocular abnormalities,

98 Patients with biopsy-proven PMN and nephrotic syndrome after 6 months of nonimmunosuppressiv

99 Glomeruli isolated from mice with nephrotic syndrome also had increased expression of IL-1

100 ldren affected by sporadic steroid-resistant nephrotic syndrome and 38 patients who exhibited a simil

101 obtained from (1) the urine of children with nephrotic syndrome and carrying potentially pathogenic m

102 merulosclerosis (FSGS) is a leading cause of nephrotic syndrome and end-stage renal disease worldwide

103 pathologic lesion that frequently causes the nephrotic syndrome and ensuing renal failure.

104 /d were enrolled at first biopsy for primary nephrotic syndrome and followed.

105 ilial nephropathy in which steroid-sensitive nephrotic syndrome and glomerular deposits of fibrillar

106 erular disorder, manifests clinically with a nephrotic syndrome and has a high propensity for recurre

107 tified in a child with encephalomyopathy and nephrotic syndrome and in a younger sibling with only ne

108 on bilateral transperitoneal nephrectomy for nephrotic syndrome and laparoscopic nephrectomy for Wilm

109 The incidence of nephrotic syndrome and leukopenia was also lower in clus

110 phila orthologs of human monogenic causes of nephrotic syndrome and observed conservation of the cent

111 l target for therapeutic intervention in the nephrotic syndrome and other proteinuric diseases.

112 a clinicopathologic entity characterized by nephrotic syndrome and progression to ESRD.

113 ng anti-PLA2R antibody levels associate with nephrotic syndrome and progressive loss of kidney functi

114 se of a 61-year-old woman who presented with nephrotic syndrome and renal impairment.

115 Common causes of nephrotic syndrome are diabetic nephropathy, minimal cha

116 naling events contributing to development of nephrotic syndrome are not well defined.

117 terations in children with sporadic forms of nephrotic syndrome associate with resistance to steroids

118 lassic pathway and the highest prevalence of nephrotic syndrome at disease onset.

119 hypercoagulopathy to identify patients with nephrotic syndrome at highest risk for thrombotic diseas

120 -LAMB2 missense mutation leads to congenital nephrotic syndrome but only mild extrarenal symptoms; th

121 e to FFAs may function in the development of nephrotic syndrome by amplifying the effects of proteinu

122 sults suggest that the R246Q mutation causes nephrotic syndrome by impairing secretion of laminin-521

123 In children, sporadic nephrotic syndrome can be related to a genetic cause, bu

124 Patients with nephrotic syndrome can develop nephrocalcinosis, which a

125 patients with congenital red hair color and nephrotic syndrome caused by idiopathic membranous nephr

126 insufficiency syndrome and steroid-resistant nephrotic syndrome caused by loss-of-function mutations

127 Here, using mouse models of human nephrotic syndrome caused by mutant laminin beta2 protei

128 These data show that diseases that cause nephrotic syndrome change glomerular protein permeabilit

129 erosis (FSGS) is a common form of idiopathic nephrotic syndrome defined by the characteristic lesions

130 ests that immunomodulatory therapies used in nephrotic syndrome directly target the podocytes.

131 , together with the zebrafish model of human nephrotic syndrome generated by plce1 knockdown, open ne

132 histomorphometry and sequencing of Mendelian nephrotic syndrome genes were performed.

133 Steroid-resistant nephrotic syndrome has a poor prognosis and often leads

134 c, thrombotic microangiopathic syndromes and nephrotic syndrome have been described.

135 However, relevant pathomechanisms of nephrotic syndrome have not been studied in nephrocytes.

136 eral nephrectomy in patients with congenital nephrotic syndrome have permitted transplantation to be

137 anous nephropathy (MN) is a leading cause of nephrotic syndrome in adults and a significant cause of

138 Membranous nephropathy is a common cause of nephrotic syndrome in adults and can be primary or secon

139 nephropathy (MN) is the most common cause of nephrotic syndrome in adults, and one-third of patients

140 d as one of the leading causes of idiopathic nephrotic syndrome in adults, particularly among African

141 phropathy (MN), a relatively common cause of nephrotic syndrome in adults, were considered idiopathic

142 nephropathy (MN) is the most common cause of nephrotic syndrome in adults, with an uncertain clinical

143 (MCD) is the etiology of 10%-25% of cases of nephrotic syndrome in adults.

144 ranous nephropathy (MN) is a common cause of nephrotic syndrome in adults.

145 is the leading cause of steroid-unresponsive nephrotic syndrome in childhood.

146 yndrome (SSNS) accounts for >80% of cases of nephrotic syndrome in childhood.

147 Idiopathic nephrotic syndrome in children is commonly associated wi

148 In conclusion, nephrotic syndrome in children with truncating or homozy

149 d mutations in podocyte-specific genes cause nephrotic syndrome in humans.

150 or the alpha3beta1 ligand laminin result in nephrotic syndrome in murine models.

151 SGPL1, displayed a phenotype reminiscent of nephrotic syndrome in nephrocytes.

152 ievable, would likely lessen the severity of nephrotic syndrome in patients carrying LAMB2 mutations.

153 glomerular diseases and induces remission of nephrotic syndrome in patients with diverse glomerulopat

154 tients, and immune-mediated pancytopenia and nephrotic syndrome in the recipient of a double UCB tran

155 The main manifestations of nephrotic syndrome include proteinuria, hypoalbuminemia,

156 Nephrotic syndrome is a common disorder in adults and ch

157 In conclusion, nephrotic syndrome is associated with an increased filtr

158 It has long been recognized that nephrotic syndrome is associated with an increased risk

159 Nephrotic syndrome is associated with up-regulation of t

160 Nephrotic syndrome is characterized by increased triglyc

161 Nephrotic syndrome is characterized by massive proteinur

162 Steroid-resistant nephrotic syndrome is characterized by podocyte dysfunct

163 e type of glomerular disease that causes the nephrotic syndrome is necessary for appropriate treatmen

164 nk between proteinuria and hyperlipidemia in nephrotic syndrome is not known.

165 Steroid-unresponsive nephrotic syndrome is often characterized by persistent

166 Nephrotic syndrome is recognized by the presence of prot

167 The pathogenesis of nephrotic syndrome is unclear.

168 tl4 secreted from podocytes in some forms of nephrotic syndrome lacks normal sialylation.

169 is dissociation, wild-type mice with induced nephrotic syndrome maintained an intact blood-brain barr

170 that leak through the abnormal glomerulus in nephrotic syndrome may affect tubular transport by inter

171 eatment for the initial episode of childhood nephrotic syndrome may reduce relapse rate, but whether

172 ducing remissions of proteinuria, relapse of nephrotic syndrome occurred significantly more often aft

173 of steroid-dependent or frequently relapsing nephrotic syndrome of minimal change disease (MCD), mesa

174 ce of either nephrin (as in human congenital nephrotic syndrome of the Finnish type, NPHS1) or NEPH1.

175 as either primary or adjunctive therapy for nephrotic syndrome or other diseases treated with glucoc

176 PCSK9 and plasma lipids were studied in nephrotic syndrome patients before and after remission o

177 ckdown of kank2 in zebrafish recapitulated a nephrotic syndrome phenotype, resulting in proteinuria a

178 iltration, many of the disease mechanisms of nephrotic syndrome remain unresolved.

179 athogenic circulating permeability factor in nephrotic syndrome remains to be confirmed, we propose i

180 boembolic events with oral anticoagulants in nephrotic syndrome requires a careful case-by-case analy

181 Idiopathic nephrotic syndrome resistant to standard treatments rema

182 months later, the patient suddenly developed nephrotic syndrome resistant to steroid therapy 1 week a

183 D in relapse and in remission, patients with nephrotic syndrome resulting from other glomerular disea

184 Nephrotic syndrome results from a breakdown of the kidne

185 odels of glomerular injury and patients with nephrotic syndrome revealed that calpain-induced talin1

186 Patients with nephrotic syndrome showed a decrease in plasma cholester

187 tasets derived from 90 black subjects in the Nephrotic Syndrome Study Network (NEPTUNE), stratified b

188 ogenic NS genes in 312 participants from the Nephrotic Syndrome Study Network and 61 putative control

189 f rituximab, a B cell-depleting antibody, in nephrotic syndrome suggests a pathogenic role of B cells

190 his the first report of a molecular cause of nephrotic syndrome that may resolve after therapy.

191 ldren (9 months to 17 years) presenting with nephrotic syndrome to either 3 months of prednisolone fo

192 trolled trial in 31 children with idiopathic nephrotic syndrome unresponsive to the combination of ca

193 relationships among different components of nephrotic syndrome use naturally occurring pathways and

194 Nephrotic syndrome was reported in a highly-sensitized p

195 therapy for patients with steroid-resistant nephrotic syndrome with ADCK4 mutations.

196 epsilon gene (PLCE1) as causing early-onset nephrotic syndrome with end-stage kidney disease.

197 Pierson syndrome is a congenital nephrotic syndrome with eye and neurologic defects cause

198 ients with first manifestation of idiopathic nephrotic syndrome with no immune complexes can improve

199 cause Pierson syndrome, a severe congenital nephrotic syndrome with ocular and neurologic defects.

200 cause Pierson syndrome, a severe congenital nephrotic syndrome with ocular and neurologic defects.

201 Pierson syndrome is a congenital nephrotic syndrome with ocular and neurological defects

202 THSD7A antibodies into mice induced a severe nephrotic syndrome with proteinuria, weight gain, and hy

203 100 consecutive IMN patients with persistent nephrotic syndrome with rituximab.

204 Of children with idiopathic nephrotic syndrome, 10%-20% fail to respond to steroids

205 hose patients with available data, 92% had a nephrotic syndrome, 64% had AKI, and 67% had a documente

206 At presentation, 49% had nephrotic syndrome, 68% had renal insufficiency, and 77%

207 Nephrotic syndrome, a malfunction of the kidney glomerul

208 gene are a major cause of steroid-resistant nephrotic syndrome, a severe human kidney disorder.

209 scribe an infant with severe Leigh syndrome, nephrotic syndrome, and CoQ(10) deficiency in muscle and

210 in steroid-dependent or frequently relapsing nephrotic syndrome, and halted disease-associated growth

211 ry diseases; 2.77 (1.49-5.15) for nephritis, nephrotic syndrome, and nephrosis; 4.08 (1.38-12.08) for

212 itis), and inflammatory (glomerulonephritis, nephrotic syndrome, and osteoarthritis) disorders.

213 odel with which to study the pathogenesis of nephrotic syndrome, and ROS formation may be a pathomech

214 ers, previous immobility, surgery or trauma, nephrotic syndrome, associated tumor, inflammatory disea

215 subset of CD2AP(-/-) mice exhibiting severe nephrotic syndrome, associated with systemic illness.

216 ) collagen developed massive albuminuria and nephrotic syndrome, because of subepithelial deposits of

217 orted to reduce proteinuria in patients with nephrotic syndrome, but mechanisms remain unknown.

218 Lamb2(-/-) mice abrogates the development of nephrotic syndrome, correlating with a greatly extended

219 In nephrotic syndrome, damage to the podocytes of the kidne

220 ding patients with congestive heart failure, nephrotic syndrome, diuretic resistance, or generalized

221 proteinuria, edema and, in steroid-resistant nephrotic syndrome, end-stage kidney disease.

222 were similar to those reported in congenital nephrotic syndrome, Finnish type, that is caused by muta

223 se, a major life-threatening complication of nephrotic syndrome, has been associated with proteinuria

224 target genes, reported as possible causes of nephrotic syndrome, in a cohort of 31 children affected

225 in the epidemiology of steroid-unresponsive nephrotic syndrome, in particular focal segmental glomer

226 ity and mortality associated with protracted nephrotic syndrome, including ESRD.

227 g nephrin lead to proteinuria and congenital nephrotic syndrome, indicating that nephrin is essential

228 -brain barrier integrity was correlated with nephrotic syndrome, indicating that these effects are di

229 multiorgan disorder that included congenital nephrotic syndrome, interstitial lung disease, and epide

230 membranous nephropathy, a common form of the nephrotic syndrome, is an antibody-mediated autoimmune g

231 cation of patients with steroid-unresponsive nephrotic syndrome, severity of disease, progression and

232 s central to proteinuric states, such as the nephrotic syndrome, the murine adriamycin nephrosis mode

233 ong the glomerular basement membranes, and a nephrotic syndrome, two additional immunizations were ne

234 CD2AP(-/-) mice normally die by 6 weeks from nephrotic syndrome, we used mice that also express a CD2

235 n during organogenesis results in congenital nephrotic syndrome, whereas VEGF164 overexpression after

236 be single-gene defects-eg, steroid-resistant nephrotic syndrome, which is caused by podocin mutations

237 anous nephropathy is a common cause of adult nephrotic syndrome, with recent evidence suggesting that

238 nhibitors may be beneficial in patients with nephrotic syndrome-associated hypercholesterolemia.

239 k4 in zebrafish and Drosophila recapitulated nephrotic syndrome-associated phenotypes.

240 nucleoside-induced injury (designed to mimic nephrotic syndrome-related injury), as determined by bot

241 a severity, consistent with reports in human nephrotic syndrome.

242 aminonucleoside and adriamycin rat models of nephrotic syndrome.

243 markers or therapeutic targets in persistent nephrotic syndrome.

244 and provide insight into the pathogenesis of nephrotic syndrome.

245 e in podocytes might promote pathogenesis of nephrotic syndrome.

246 deteriorating renal function or untreatable nephrotic syndrome.

247 4 (ADCK4) gene that cause steroid-resistant nephrotic syndrome.

248 s with idiopathic membranous nephropathy and nephrotic syndrome.

249 ot benefit clinical outcome in children with nephrotic syndrome.

250 ed structure, the disruption of which causes nephrotic syndrome.

251 tal interstitial lung disease and congenital nephrotic syndrome.

252 glomeruli, mimicking the phenotype of human nephrotic syndrome.

253 -based consortium studying steroid-resistant nephrotic syndrome.

254 and of patients with Finnish-type congenital nephrotic syndrome.

255 bitors in children with resistant idiopathic nephrotic syndrome.

256 rarenal defects but still exhibit congenital nephrotic syndrome.

257 eading to the filtration barrier defects and nephrotic syndrome.

258 podocyte-secreted Angptl4 has a key role in nephrotic syndrome.

259 ases the risk for high-grade proteinuria and nephrotic syndrome.

260 s of proteinuria and rates of progression to nephrotic syndrome.

261 ide (LPS)-treated mice, a model of transient nephrotic syndrome.

262 mg/dl); three (30%) patients presented with nephrotic syndrome.

263 d, lead to inherited FSGS and/or the related nephrotic syndrome.

264 ltrastructural changes and steroid-sensitive nephrotic syndrome.

265 sclerosis as a cause of steroid-unresponsive nephrotic syndrome.

266 as to the treatment of steroid-unresponsive nephrotic syndrome.

267 ocytes in a number of experimental models of nephrotic syndrome.

268 increased in patients with steroid-sensitive nephrotic syndrome.

269 e in children with primary steroid-resistant nephrotic syndrome.

270 ss effacement and lipopolysaccharide-induced nephrotic syndrome.

271 ch model Pierson syndrome, a rare congenital nephrotic syndrome.

272 pathophysiology and treatment mechanisms of nephrotic syndrome.

273 te gene expression during the development of nephrotic syndrome.

274 ectively, in children with steroid-resistant nephrotic syndrome.

275 several months, but they developed a lethal nephrotic syndrome.

276 e pathogenesis of proteinuria and congenital nephrotic syndrome.

277 ted in autosomal recessive steroid-resistant nephrotic syndrome.

278 model in which to study the pathogenesis of nephrotic syndrome.

279 foot process (FP) effacement and LPS-induced nephrotic syndrome.

280 s are the standard of care for most forms of nephrotic syndrome.

281 lex, and this connection is disrupted in the nephrotic syndrome.

282 ceptors may be novel therapeutic targets for nephrotic syndrome.

283 th lupus nephritis, diabetic nephropathy, or nephrotic syndrome.

284 ypothesized to be the cause of the patient's nephrotic syndrome.

285 mutation is an important cause of hereditary nephrotic syndrome.

286 th frequently relapsing or steroid-dependent nephrotic syndrome.

287 rats with puromycin aminonucleoside-induced nephrotic syndrome.

288 contribution of PCSK9 to the dyslipidemia of nephrotic syndrome.

289 ameliorates dyslipidemia in a mouse model of nephrotic syndrome.

290 SK9 in mediating the hypercholesterolemia of nephrotic syndrome.

291 eful for predicting relapse in patients with nephrotic syndrome.

292 philia due to a factor VIII autoantibody and nephrotic syndrome.

293 KANK1), KANK2, and KANK4 in individuals with nephrotic syndrome.

294 merular capillary tuft, podocyte injury, and nephrotic syndrome.

295 everity of the acquired hypercoagulopathy of nephrotic syndrome.

296 cytes that is dysfunctional in some types of nephrotic syndrome.

297 o heart disease, cancer, diabetes, nephritis/nephrotic syndrome/nephrosis, chronic lower respiratory

298 vents; partial and complete remission of the nephrotic syndrome; and a composite of doubling of serum

299 ive genes have been found to cause inherited nephrotic syndromes and FSGS.

300 Two patients presented with nephrotic syndromes and one patient with an IgG4-related

301 diseases and in other human pathologies with nephrotic syndromes such as HIV and Hantavirus infection