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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 hypothesis, we studied phosphate handling in nephrotic children and patients with CKD.
6 c phase compared with the remission phase in nephrotic children.
7 transition that appears to be common to many nephrotic conditions.
8 t, it is in patients who remain persistently nephrotic despite conservative therapy that a more aggre
9  hypercoagulopathy is highly correlated with nephrotic disease severity, but overt thrombosis may req
10 c systems enhanced proteinuria in persistent nephrotic disease.
11                                           In nephrotic diseases, such as membranous nephropathy and F
12      Podocytes are the key cells affected in nephrotic glomerular kidney diseases, and they respond u
13 cardiac hypertrophy, vascular restenosis and nephrotic hypertrophy.
14 dismiss previous claims on the filtration of nephrotic levels of albumin.
15  abundance of NHE3 and phosphorylated NCC in nephrotic mice compared with controls suggest that early
16                                              Nephrotic mice displayed decreased glomerular filtration
17 lization of gamma-ENaC persisted at day 5 in nephrotic mice when hypovolemia resolved and steady-stat
18                                      Feeding nephrotic mice with a low potassium diet prevented hyper
19 t of the tubular site of sodium retention in nephrotic mice.
20 ical localization of gamma-ENaC increased in nephrotic mice.
21 s over the course of 5-10 years, whereas non-nephrotic patients and those entering a remission have a
22 tium (edema) and the peritoneum (ascites) of nephrotic patients is classically thought to stem from t
23 nd guiding personalized rituximab therapy in nephrotic patients with primary MN.
24                                           In nephrotic patients, progression to ESRD often occurs ove
25                                          The nephrotic phenotype was recapitulated in arhgdia-deficie
26 , suggesting that thrombin may contribute to nephrotic progression.
27 ental glomerulosclerosis (FSGS) often causes nephrotic proteinuria and frequently results in end-stag
28 rotein-to-creatinine ratios became >3.5 g/g (nephrotic proteinuria cohort).
29             Of note, in both the eGFR<60 and nephrotic proteinuria cohorts, CKD cases with two APOL1
30  Rats with puromycin-aminonucleoside-induced nephrotic proteinuria displayed higher renal protein exp
31 ad to significant albuminuria, even reaching nephrotic range in animal models.
32  We evaluated the presence and timing of non-nephrotic range proteinuria (NNRP) and serum albumin mea
33 ed activity were younger (P=0.008), had less nephrotic range proteinuria (P=0.02), and exhibited a hi
34 rrence of FSGS was defined as development of nephrotic range proteinuria between days 3 and 30 posttr
35  hematuria and proteinuria (sometimes in the nephrotic range), and develop chronic kidney disease wit
36 s (FFAs) to albumin when proteinuria reached nephrotic range.
37  underlying plasma cell dyscrasia (dFLC) and nephrotic-range albuminuria (ACR).
38                                Additionally, nephrotic-range albuminuria with an albumin-to-creatinin
39 d patients of African ancestry who developed nephrotic-range proteinuria and AKI early in the course
40  improved understanding of the threshold for nephrotic-range proteinuria and the pathogenesis of hype
41 ociated with the eGFR<60 cohort, but not the nephrotic-range proteinuria cohort.
42                                              Nephrotic-range proteinuria has been known for years to
43 At diagnosis, renal disease was severe, with nephrotic-range proteinuria in 20/46 (43%) patients and
44 ng adolescence (median age, 14.1 years) with nephrotic-range proteinuria in 44% of patients and advan
45 min purified from the urine of patients with nephrotic-range proteinuria inhibits Ca(2+) uptake in TR
46 reases in circulating Angptl4 in response to nephrotic-range proteinuria reduces the degree of this p
47 re confirmed in transgenic mice that develop nephrotic-range proteinuria resulting from podocyte depl
48 s with idiopathic membranous nephropathy and nephrotic-range proteinuria using both indirect immunofl
49 D, including progressive glomerulosclerosis, nephrotic-range proteinuria, and finally kidney failure.
50                                           In nephrotic-range proteinuria, filtered plasminogen reache
51  of consanguineous parents with intermittent nephrotic-range proteinuria, we identified a homozygous
52 oronavirus disease 2019 (COVID-19), AKI, and nephrotic-range proteinuria.
53  patients (88%) presented with AKI; nine had nephrotic-range proteinuria.
54 N who achieved a remission after a period of nephrotic-range proteinuria.
55 n of Angptl4 (NPHS2-Angptl4) in rats induced nephrotic-range, and selective, proteinuria (over 500-fo
56                                           In nephrotic rat models, TCF21 expression in podocytes incr
57 nal function and prevented salt retention in nephrotic rats.
58 n, and salt retention in doxorubicin treated nephrotic rats.
59 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
60                                   Congenital nephrotic syndrome (CNS), a rare entity, is known to pre
61 omal recessive SRNS presenting as congenital nephrotic syndrome (CNS).
62  with frequently relapsing steroid-sensitive nephrotic syndrome (FR-SSNS).
63 of podocyte disorders in cases of idiopathic nephrotic syndrome (INS) are complex and remain incomple
64                                   Idiopathic nephrotic syndrome (INS) describes a group of pathologie
65 elper T-cell abnormalities in minimal-change nephrotic syndrome (MCNS), which often complicate allerg
66 ritis, type I membranoproliferative GN), and nephrotic syndrome (minimal change/FSGS, membranous neph
67 nt CGD and DM (n=1), and steroid therapy for nephrotic syndrome (n=1).
68  out of nine individuals), steroid-resistant nephrotic syndrome (nine out of 21 individuals), congeni
69 mutations profile in Brazilian children with nephrotic syndrome (NS) and to determine a genotype-phen
70     The discovery of >60 monogenic causes of nephrotic syndrome (NS) has revealed a central role for
71                                              Nephrotic syndrome (NS) is a genetically heterogeneous g
72                                              Nephrotic syndrome (NS) is divided into steroid-sensitiv
73                                              Nephrotic syndrome (NS) occurs when the glomerular filtr
74                            Rituximab induces nephrotic syndrome (NS) remission in two-thirds of patie
75 nefits of genetic screening of patients with nephrotic syndrome (NS) to diagnose monogenic causes, re
76                                              Nephrotic syndrome (NS) was the most common indication f
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    Emerging evidence has established primary nephrotic syndrome (NS), including focal segmental glome
80                                              Nephrotic syndrome (NS), the association of gross protei
81 thyroid function are common in patients with nephrotic syndrome (NS).
82 tion in kidney tubules may vary with time in nephrotic syndrome (NS).
83 relative risk 4.79; 95% CI 2.71 to 8.46) and nephrotic syndrome (relative risk 7.78; 95% CI 1.80 to 3
84                            Steroid-dependent nephrotic syndrome (SDNS) carries a high risk of toxicit
85 ified >55 genes as causing steroid-resistant nephrotic syndrome (SRNS) and localized its pathogenesis
86 racterized by the combination of early-onset nephrotic syndrome (SRNS) and microcephaly with brain an
87 yme Q10 biosynthesis cause steroid-resistant nephrotic syndrome (SRNS) as part of multiorgan involvem
88                            Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney d
89                            Steroid-resistant nephrotic syndrome (SRNS) causes 15% of chronic kidney d
90 s reduced in patients with steroid-resistant nephrotic syndrome (SRNS) due to monogenic disorders.
91 n of single-gene causes of steroid-resistant nephrotic syndrome (SRNS) has furthered the understandin
92                            Steroid-resistant nephrotic syndrome (SRNS) is a frequent cause of end-sta
93                            Steroid-resistant nephrotic syndrome (SRNS) is a frequent cause of progres
94                            Steroid-resistant nephrotic syndrome (SRNS) is characterized by high-range
95                            Steroid-resistant nephrotic syndrome (SRNS) is the second most frequent ca
96                            Steroid-resistant nephrotic syndrome (SRNS), a frequent cause of chronic k
97                            Steroid-resistant nephrotic syndrome (SRNS), a heterogeneous disorder of t
98  cause autosomal recessive steroid-resistant nephrotic syndrome (SRNS).
99  novel monogenic causes of steroid-resistant nephrotic syndrome (SRNS).
100                            Steroid-sensitive nephrotic syndrome (SSNS) accounts for >80% of cases of
101                            Steroid-sensitive nephrotic syndrome (SSNS), the most common form of nephr
102          Patients with biopsy-proven PMN and nephrotic syndrome after 6 months of nonimmunosuppressiv
103 ranous nephropathy (MN) is a common cause of nephrotic syndrome after transplantation and is associat
104 is suggested the highest TCF21 expression in nephrotic syndrome along with the urinary protein level.
105            Glomeruli isolated from mice with nephrotic syndrome also had increased expression of IL-1
106 ldren affected by sporadic steroid-resistant nephrotic syndrome and 38 patients who exhibited a simil
107 obtained from (1) the urine of children with nephrotic syndrome and carrying potentially pathogenic m
108 merulosclerosis (FSGS) is a leading cause of nephrotic syndrome and end-stage renal disease worldwide
109 /d were enrolled at first biopsy for primary nephrotic syndrome and followed.
110 ilial nephropathy in which steroid-sensitive nephrotic syndrome and glomerular deposits of fibrillar
111 erular disorder, manifests clinically with a nephrotic syndrome and has a high propensity for recurre
112 aracterized by early-onset steroid-resistant nephrotic syndrome and microcephaly.
113 phila orthologs of human monogenic causes of nephrotic syndrome and observed conservation of the cent
114 l target for therapeutic intervention in the nephrotic syndrome and other proteinuric diseases.
115  a clinicopathologic entity characterized by nephrotic syndrome and progression to ESRD.
116 ng anti-PLA2R antibody levels associate with nephrotic syndrome and progressive loss of kidney functi
117 se of a 61-year-old woman who presented with nephrotic syndrome and renal impairment.
118                             Common causes of nephrotic syndrome are diabetic nephropathy, minimal cha
119 naling events contributing to development of nephrotic syndrome are not well defined.
120 terations in children with sporadic forms of nephrotic syndrome associate with resistance to steroids
121 lassic pathway and the highest prevalence of nephrotic syndrome at disease onset.
122  hypercoagulopathy to identify patients with nephrotic syndrome at highest risk for thrombotic diseas
123 -LAMB2 missense mutation leads to congenital nephrotic syndrome but only mild extrarenal symptoms; th
124 e to FFAs may function in the development of nephrotic syndrome by amplifying the effects of proteinu
125 sults suggest that the R246Q mutation causes nephrotic syndrome by impairing secretion of laminin-521
126                        In children, sporadic nephrotic syndrome can be related to a genetic cause, bu
127                                Patients with nephrotic syndrome can develop nephrocalcinosis, which a
128  patients with congenital red hair color and nephrotic syndrome caused by idiopathic membranous nephr
129 insufficiency syndrome and steroid-resistant nephrotic syndrome caused by loss-of-function mutations
130                It is increasingly clear that nephrotic syndrome caused by monogenic mutations is dist
131            Here, using mouse models of human nephrotic syndrome caused by mutant laminin beta2 protei
132 l(DeltaPod) mice develop an acute congenital nephrotic syndrome characterized by focal segmental glom
133 erosis (FSGS) is a common form of idiopathic nephrotic syndrome defined by the characteristic lesions
134                    Requiring that the sum of nephrotic syndrome diagnosis codes exceed that of glomer
135 ests that immunomodulatory therapies used in nephrotic syndrome directly target the podocytes.
136 histomorphometry and sequencing of Mendelian nephrotic syndrome genes were performed.
137                            Steroid-resistant nephrotic syndrome has a poor prognosis and often leads
138         However, relevant pathomechanisms of nephrotic syndrome have not been studied in nephrocytes.
139 is of structural variation in cases of human nephrotic syndrome identified rare heterozygous deletion
140 anous nephropathy (MN) is a leading cause of nephrotic syndrome in adults and a significant cause of
141  Membranous nephropathy is a common cause of nephrotic syndrome in adults and can be primary or secon
142 nephropathy (MN) is the most common cause of nephrotic syndrome in adults, and one-third of patients
143 d as one of the leading causes of idiopathic nephrotic syndrome in adults, particularly among African
144 phropathy (MN), a relatively common cause of nephrotic syndrome in adults, were considered idiopathic
145 nephropathy (MN) is the most common cause of nephrotic syndrome in adults, with an uncertain clinical
146 ranous nephropathy (MN) is a common cause of nephrotic syndrome in adults.
147 (MCD) is the etiology of 10%-25% of cases of nephrotic syndrome in adults.
148 tic syndrome (SSNS), the most common form of nephrotic syndrome in childhood, is considered an autoim
149 yndrome (SSNS) accounts for >80% of cases of nephrotic syndrome in childhood.
150 is the leading cause of steroid-unresponsive nephrotic syndrome in childhood.
151                               In conclusion, nephrotic syndrome in children with truncating or homozy
152 d mutations in podocyte-specific genes cause nephrotic syndrome in humans.
153 phologic changes indicate the development of nephrotic syndrome in mice bearing the Asah1 podocyte-sp
154  or the alpha3beta1 ligand laminin result in nephrotic syndrome in murine models.
155  SGPL1, displayed a phenotype reminiscent of nephrotic syndrome in nephrocytes.
156 ed cataracts and sensorineural deafness, but nephrotic syndrome in only one case of skewed X-inactiva
157 ievable, would likely lessen the severity of nephrotic syndrome in patients carrying LAMB2 mutations.
158 glomerular diseases and induces remission of nephrotic syndrome in patients with diverse glomerulopat
159 tients, and immune-mediated pancytopenia and nephrotic syndrome in the recipient of a double UCB tran
160                   The main manifestations of nephrotic syndrome include proteinuria, hypoalbuminemia,
161                                              Nephrotic syndrome is a common disorder in adults and ch
162                               In conclusion, nephrotic syndrome is associated with an increased filtr
163                                              Nephrotic syndrome is associated with up-regulation of t
164                                              Nephrotic syndrome is characterized by massive proteinur
165                            Steroid-resistant nephrotic syndrome is characterized by podocyte dysfunct
166 nk between proteinuria and hyperlipidemia in nephrotic syndrome is not known.
167                                              Nephrotic syndrome is recognized by the presence of prot
168                          The pathogenesis of nephrotic syndrome is unclear.
169 tl4 secreted from podocytes in some forms of nephrotic syndrome lacks normal sialylation.
170 is dissociation, wild-type mice with induced nephrotic syndrome maintained an intact blood-brain barr
171 that leak through the abnormal glomerulus in nephrotic syndrome may affect tubular transport by inter
172 eatment for the initial episode of childhood nephrotic syndrome may reduce relapse rate, but whether
173 ducing remissions of proteinuria, relapse of nephrotic syndrome occurred significantly more often aft
174 of steroid-dependent or frequently relapsing nephrotic syndrome of minimal change disease (MCD), mesa
175 ce of either nephrin (as in human congenital nephrotic syndrome of the Finnish type, NPHS1) or NEPH1.
176 lomerular diseases such as steroid-resistant nephrotic syndrome or Alport syndrome were often the pri
177 rulonephritis codes identified children with nephrotic syndrome or biopsy-based minimal change nephro
178  as either primary or adjunctive therapy for nephrotic syndrome or other diseases treated with glucoc
179 ytopathies associated with steroid-resistant nephrotic syndrome or severe proteinuria.
180      PCSK9 and plasma lipids were studied in nephrotic syndrome patients before and after remission o
181 ckdown of kank2 in zebrafish recapitulated a nephrotic syndrome phenotype, resulting in proteinuria a
182 iltration, many of the disease mechanisms of nephrotic syndrome remain unresolved.
183 athogenic circulating permeability factor in nephrotic syndrome remains to be confirmed, we propose i
184                                   Idiopathic nephrotic syndrome resistant to standard treatments rema
185 months later, the patient suddenly developed nephrotic syndrome resistant to steroid therapy 1 week a
186                                              Nephrotic syndrome results from a breakdown of the kidne
187 odels of glomerular injury and patients with nephrotic syndrome revealed that calpain-induced talin1
188                                Patients with nephrotic syndrome showed a decrease in plasma cholester
189 trastructural changes (descriptors) from the Nephrotic Syndrome Study Network (NEPTUNE) Digital Patho
190 tasets derived from 90 black subjects in the Nephrotic Syndrome Study Network (NEPTUNE), stratified b
191 ogenic NS genes in 312 participants from the Nephrotic Syndrome Study Network and 61 putative control
192 f rituximab, a B cell-depleting antibody, in nephrotic syndrome suggests a pathogenic role of B cells
193  treatment strategy for those cases of human nephrotic syndrome that are caused by a primary dysfunct
194 al pattern frequently found in patients with nephrotic syndrome that often progress to end-stage kidn
195 ldren (9 months to 17 years) presenting with nephrotic syndrome to either 3 months of prednisolone fo
196 trolled trial in 31 children with idiopathic nephrotic syndrome unresponsive to the combination of ca
197  relationships among different components of nephrotic syndrome use naturally occurring pathways and
198                                              Nephrotic syndrome was reported in a highly-sensitized p
199  therapy for patients with steroid-resistant nephrotic syndrome with ADCK4 mutations.
200             Pierson syndrome is a congenital nephrotic syndrome with eye and neurologic defects cause
201 ients with first manifestation of idiopathic nephrotic syndrome with no immune complexes can improve
202  cause Pierson syndrome, a severe congenital nephrotic syndrome with ocular and neurologic defects.
203  cause Pierson syndrome, a severe congenital nephrotic syndrome with ocular and neurologic defects.
204             Pierson syndrome is a congenital nephrotic syndrome with ocular and neurological defects
205 THSD7A antibodies into mice induced a severe nephrotic syndrome with proteinuria, weight gain, and hy
206 100 consecutive IMN patients with persistent nephrotic syndrome with rituximab.
207                  Of children with idiopathic nephrotic syndrome, 10%-20% fail to respond to steroids
208 hose patients with available data, 92% had a nephrotic syndrome, 64% had AKI, and 67% had a documente
209                     At presentation, 49% had nephrotic syndrome, 68% had renal insufficiency, and 77%
210  have been identified as monogenic causes of nephrotic syndrome, a frequent cause of CKD.
211  gene are a major cause of steroid-resistant nephrotic syndrome, a severe human kidney disorder.
212 in steroid-dependent or frequently relapsing nephrotic syndrome, and halted disease-associated growth
213 ry diseases; 2.77 (1.49-5.15) for nephritis, nephrotic syndrome, and nephrosis; 4.08 (1.38-12.08) for
214 itis), and inflammatory (glomerulonephritis, nephrotic syndrome, and osteoarthritis) disorders.
215 odel with which to study the pathogenesis of nephrotic syndrome, and ROS formation may be a pathomech
216 ers, previous immobility, surgery or trauma, nephrotic syndrome, associated tumor, inflammatory disea
217 nt revealed a renal failure symptomatic of a nephrotic syndrome, associated with proteinuria composed
218  subset of CD2AP(-/-) mice exhibiting severe nephrotic syndrome, associated with systemic illness.
219 ) collagen developed massive albuminuria and nephrotic syndrome, because of subepithelial deposits of
220 orted to reduce proteinuria in patients with nephrotic syndrome, but mechanisms remain unknown.
221       Here, we report a phenotype comprising nephrotic syndrome, cataracts, sensorineural deafness, e
222 Lamb2(-/-) mice abrogates the development of nephrotic syndrome, correlating with a greatly extended
223                                           In nephrotic syndrome, damage to the podocytes of the kidne
224 ding patients with congestive heart failure, nephrotic syndrome, diuretic resistance, or generalized
225 were similar to those reported in congenital nephrotic syndrome, Finnish type, that is caused by muta
226 se, a major life-threatening complication of nephrotic syndrome, has been associated with proteinuria
227  search terms included amyloid, amyloidosis, nephrotic syndrome, heart failure preserved ejection fra
228 target genes, reported as possible causes of nephrotic syndrome, in a cohort of 31 children affected
229 ity and mortality associated with protracted nephrotic syndrome, including ESRD.
230 -brain barrier integrity was correlated with nephrotic syndrome, indicating that these effects are di
231 multiorgan disorder that included congenital nephrotic syndrome, interstitial lung disease, and epide
232 membranous nephropathy, a common form of the nephrotic syndrome, is an antibody-mediated autoimmune g
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            The etiology of steroid-resistant nephrotic syndrome, which manifests as FSGS, is not comp
238 anous nephropathy is a common cause of adult nephrotic syndrome, with recent evidence suggesting that
239 nhibitors may be beneficial in patients with nephrotic syndrome-associated hypercholesterolemia.
240 k4 in zebrafish and Drosophila recapitulated nephrotic syndrome-associated phenotypes.
241 nucleoside-induced injury (designed to mimic nephrotic syndrome-related injury), as determined by bot
242 direct podocyte injury drives proteinuria or nephrotic syndrome.
243 docytes increased along with the severity of nephrotic syndrome.
244 mutation is an important cause of hereditary nephrotic syndrome.
245 th frequently relapsing or steroid-dependent nephrotic syndrome.
246  rats with puromycin aminonucleoside-induced nephrotic syndrome.
247 contribution of PCSK9 to the dyslipidemia of nephrotic syndrome.
248 ameliorates dyslipidemia in a mouse model of nephrotic syndrome.
249 SK9 in mediating the hypercholesterolemia of nephrotic syndrome.
250 eful for predicting relapse in patients with nephrotic syndrome.
251 philia due to a factor VIII autoantibody and nephrotic syndrome.
252 KANK1), KANK2, and KANK4 in individuals with nephrotic syndrome.
253 C, leading to nodular glomerulosclerosis and nephrotic syndrome.
254 merular capillary tuft, podocyte injury, and nephrotic syndrome.
255 everity of the acquired hypercoagulopathy of nephrotic syndrome.
256 cytes that is dysfunctional in some types of nephrotic syndrome.
257 a severity, consistent with reports in human nephrotic syndrome.
258 aminonucleoside and adriamycin rat models of nephrotic syndrome.
259 markers or therapeutic targets in persistent nephrotic syndrome.
260 and provide insight into the pathogenesis of nephrotic syndrome.
261 e in podocytes might promote pathogenesis of nephrotic syndrome.
262  deteriorating renal function or untreatable nephrotic syndrome.
263  4 (ADCK4) gene that cause steroid-resistant nephrotic syndrome.
264 ot benefit clinical outcome in children with nephrotic syndrome.
265 ed structure, the disruption of which causes nephrotic syndrome.
266 tal interstitial lung disease and congenital nephrotic syndrome.
267  glomeruli, mimicking the phenotype of human nephrotic syndrome.
268 -based consortium studying steroid-resistant nephrotic syndrome.
269 and of patients with Finnish-type congenital nephrotic syndrome.
270 bitors in children with resistant idiopathic nephrotic syndrome.
271 rarenal defects but still exhibit congenital nephrotic syndrome.
272 eading to the filtration barrier defects and nephrotic syndrome.
273  podocyte-secreted Angptl4 has a key role in nephrotic syndrome.
274 ases the risk for high-grade proteinuria and nephrotic syndrome.
275 s of proteinuria and rates of progression to nephrotic syndrome.
276 ide (LPS)-treated mice, a model of transient nephrotic syndrome.
277  mg/dl); three (30%) patients presented with nephrotic syndrome.
278 d, lead to inherited FSGS and/or the related nephrotic syndrome.
279 ltrastructural changes and steroid-sensitive nephrotic syndrome.
280 sclerosis as a cause of steroid-unresponsive nephrotic syndrome.
281  as to the treatment of steroid-unresponsive nephrotic syndrome.
282 mulation in podocytes to cellular damage and nephrotic syndrome.
283 fficking plays a role in the pathogenesis of nephrotic syndrome.
284 ycocalyx have been correlated with models of nephrotic syndrome.
285 ns in the gene TBC1D8B in five families with nephrotic syndrome.
286 ypothesized to be the cause of the patient's nephrotic syndrome.
287 s with idiopathic membranous nephropathy and nephrotic syndrome.
288 e in children with primary steroid-resistant nephrotic syndrome.
289 ectively, in children with steroid-resistant nephrotic syndrome.
290  model in which to study the pathogenesis of nephrotic syndrome.
291 ceptors may be novel therapeutic targets for nephrotic syndrome.
292 th lupus nephritis, diabetic nephropathy, or nephrotic syndrome.
293 o heart disease, cancer, diabetes, nephritis/nephrotic syndrome/nephrosis, chronic lower respiratory
294 vents; partial and complete remission of the nephrotic syndrome; and a composite of doubling of serum
295  differential diagnosis of adult nondiabetic nephrotic syndrome; heart failure with preserved ejectio
296  described as unifying feature in idiopathic nephrotic syndromes (INS).
297 ive genes have been found to cause inherited nephrotic syndromes and FSGS.
298                  Two patients presented with nephrotic syndromes and one patient with an IgG4-related
299 diseases and in other human pathologies with nephrotic syndromes such as HIV and Hantavirus infection
300 the urine is a common biomarker of a variety nephrotic syndromes.

 
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