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1  FSGS and proteinuria (>46-fold increases in albuminuria).
2 diovascular, and safety outcomes by baseline albuminuria.
3 the glomerular filtration barrier and reduce albuminuria.
4 oint on the basis of the treatment effect on albuminuria.
5  accumulation (ELA), glomerulosclerosis, and albuminuria.
6  by mesangiolysis, capillary ballooning, and albuminuria.
7 imated glomerular filtration rate (eGFR) and albuminuria.
8 by ambulatory blood pressure monitoring) and albuminuria.
9 greatest among those with severely increased albuminuria.
10 all-cause mortality, independent of eGFR and albuminuria.
11 athways for translational research to reduce albuminuria.
12 ross trials and different levels of eGFR and albuminuria.
13  pulse rate, beta-blocker use, and sustained albuminuria.
14 duria, low molecular weight proteinuria, and albuminuria.
15 months of age or a difference in LPS-induced albuminuria.
16 by glycosuria, aminoaciduria, calciuria, and albuminuria.
17  patients with type 2 diabetes and prevalent albuminuria.
18 n, decreasing glomerular hyperfiltration and albuminuria.
19 nostic accuracy of point-of-care testing for albuminuria.
20 e and correlate with renal calcification and albuminuria.
21 pression of a highly sulfated HS domain, and albuminuria.
22 her illuminated the clinical implications of albuminuria.
23 iabetes, body mass index, baseline eGFR, and albuminuria.
24 tion and glomerular leak interact to promote albuminuria.
25 with glomerular leak can combine to increase albuminuria.
26 ns, as expected if podocyte depletion causes albuminuria.
27 induced podocyte foot process effacement and albuminuria.
28  diabetes, cardiovascular disease, eGFR, and albuminuria.
29 c kidney disease in the setting of increased albuminuria.
30 f allele-specific rat models during onset of albuminuria.
31  showed persistent glomerular hyalinosis and albuminuria 96 hours after injection, whereas wild-type
32                   Prior studies suggest that albuminuria, a biomarker of endothelial injury, is incre
33 ma cell dyscrasia (dFLC) and nephrotic-range albuminuria (ACR).
34                                              Albuminuria acts as a marker of progressive chronic kidn
35 ated with CVD and mortality, and, along with albuminuria, adds predictive discrimination to current C
36                                              Albuminuria affects millions of people, and is an indepe
37                            In the absence of albuminuria, age-related reduction in GFR with the corre
38 r filtration rate [eGFR] <60 mL/min/1.73m2), albuminuria (albumin/creatinine ratio >/=3 mg/mmol), and
39 y-induced glomerular injury, as assessed via albuminuria, although the degree of microscopic hematuri
40  showed that administration of AS-IV reduced albuminuria, ameliorated changes in the glomerular and t
41 ur study aimed to describe the prevalence of albuminuria amongst people who inject drugs in London an
42       Our findings suggest the prevalence of albuminuria amongst PWID is twice that of the general po
43 sks for secondary kidney disease end points (albuminuria and a composite of serum creatinine doubling
44 y disease, with a strong association between albuminuria and amputation.
45 ut not of the G0 allele, develop functional (albuminuria and azotemia), structural (foot-process effa
46 rted renal benefits, including inhibition of albuminuria and cellular crescent formation, similar to
47 cell injury explains the association between albuminuria and COPD, (2) CS-induced albuminuria is link
48 s suggest that phenyl sulfate contributes to albuminuria and could be used as a disease marker and fu
49 etic eNOS(-/-) mice significantly attenuated albuminuria and diabetic kidney injury, which were assoc
50 eserved in MC1R-null mice, marked by reduced albuminuria and diminished histologic signs of podocyte
51 ric type 2 diabetics UPPod:CR predicted both albuminuria and eGFR loss.
52  APOL1 risk alleles had the highest risk for albuminuria and eGFRcys decline in young adulthood, wher
53 P domain protein suppressed diabetes-induced albuminuria and enhanced M2 marker expression.
54 s and assessed for renal injury by measuring albuminuria and examining kidney histology.
55 hannel blocker SKF96365 markedly ameliorated albuminuria and glomerular damage in response to DOCA.
56 betes (T2D), which correlates with increased albuminuria and glomerular damage.
57           IDOL-induced dyslipidemia worsened albuminuria and glomerular macrophage accumulation but h
58 kout (KO) mice with diabetes developed worse albuminuria and glomerular pathology.
59 Darunavir and darunavir + zidovudine reduced albuminuria and histologic kidney injury and normalized
60  deletion of Drp1 in diabetic mice decreased albuminuria and improved mesangial matrix expansion and
61                Deletion of DUSP4 exacerbated albuminuria and increased mesangial expansion and glomer
62  with sham-operated controls, Px-UNx induced albuminuria and increased urine markers of kidney injury
63 i-miR-92a after disease initiation prevented albuminuria and kidney failure, indicating miR-92a inhib
64 redispose animals to hypertension-associated albuminuria and kidney injury.
65  with data on serum creatinine and change in albuminuria and more than 50 events on outcomes of inter
66 betes, phenyl sulfate administration induces albuminuria and podocyte damage.
67 h demonstrated that Shroom3 knockdown led to albuminuria and podocyte foot process effacement.
68 cy in vivo surprisingly reduced the level of albuminuria and podocyte injury in models of both diabet
69 ion of mTOR is most commonly associated with albuminuria and podocyte injury, but has also been linke
70 ups, after adjustment and stratification for albuminuria and potassium, and when modeling RAS inhibit
71  have consistently demonstrated reduction of albuminuria and preservation of kidney function.
72 dney disease, and adverse events, as well as albuminuria and progression of retinopathy in trials don
73 ted podocyte detachment, podocyte depletion, albuminuria and progression.
74 feriprone significantly delayed the onset of albuminuria and reduced blood urea nitrogen concentratio
75 e determined whether canagliflozin decreases albuminuria and reduces renal function decline independe
76  late neonatal death associated with massive albuminuria and renal failure.
77 f EVR with early CNI withdrawal after HTx on albuminuria and renal function seem dissociated; hence,
78 es available, no significant associations of albuminuria and retinal vessel diameters with depression
79 istency of the association between change in albuminuria and risk of end-stage kidney disease in a la
80 C-terminal CUBN variants are associated with albuminuria and slightly increased GFR in meta-analyses
81 mated treatment effects on 6-month change in albuminuria and the composite clinical endpoint of treat
82 se renal hyperfiltration, thereby increasing albuminuria and the progression of renal disease.
83 etween treatment effects on early changes in albuminuria and treatment effects on clinical endpoints
84                                              Albuminuria and tubular atrophy are among the highest ri
85 without diabetes, cardiovascular disease, or albuminuria and with an eGFR of 25 ml/min per 1.73 m(2)
86 ative renal hypoxia that was associated with albuminuria and with increased RPF, fat mass, and insuli
87 , 2.6; 95% CI, 1.8 to 3.8, respectively) and albuminuria and/or eGFR<60 ml/min per 1.73 m(2) (OR, 2.9
88 haemoglobin, serum uric acid, serum albumin, albuminuria, and C reactive protein as non-GFR determina
89 r filtration rate <60 mL.min(-1).1.73 m(-2), albuminuria, and diuretic use (each P interaction <0.05)
90     However, serum creatinine concentration, albuminuria, and glomerular expression of ETS-1 and two
91  but significantly attenuated hyperglycemia, albuminuria, and glomerulosclerosis and increased podocy
92 nd podocytes leads to defects and depletion, albuminuria, and glomerulosclerosis.
93 s-induced endothelial injury, podocyte loss, albuminuria, and glomerulosclerosis.
94 nant-negative Orai1 mutant (E108Q) increases albuminuria, and in vivo injection of BTP2 exacerbates a
95 atment also improved renal function, reduced albuminuria, and inhibited expression of profibrotic mar
96 dentified prior to onset of hyperglycemia or albuminuria, and monitored non-invasively by urinary pel
97 nd prevented the development of proteinuria, albuminuria, and nephrinuria.
98 ogression and mortality, adjusting for eGFR, albuminuria, and other confounding characteristics.
99 ris DBA resulted in improved renal function, albuminuria, and pathology, including measurements of gl
100 on, glomerular basement membrane thickening, albuminuria, and podocyte dropout.
101 o losartan, Ly normalized blood pressure and albuminuria, and prevented CKD progression more effectiv
102 ependently associated with renal impairment, albuminuria, and proximal renal tubular dysfunction.
103  resulted in reduced serum creatinine level, albuminuria, and renal histologic changes (mesangial exp
104 e leading cause of impaired kidney function, albuminuria, and renal replacement therapy globally, thu
105 evel, reduced glomerular hyperfiltration and albuminuria, and suppression of advanced glycation end-p
106 e physical stress on the filtration barrier, albuminuria, and the oxygen demand for tubular reabsorpt
107  modification by subgroups of baseline eGFR, albuminuria, and use of renin-angiotensin system (RAS) b
108 7 to -0.24 mL/min/1.73m2/year) and worsening albuminuria (aOR = 2.3; 95% CI = 1.3-4.0).
109 .1; 95% confidence interval [CI] = 1.0-4.4), albuminuria (aOR = 5.8; 95% CI = 3.7-9.0), and proximal
110                   The clinical importance of albuminuria as a predictor of kidney disease progression
111 rts, lending support to the use of change in albuminuria as a surrogate endpoint for end-stage kidney
112                                    Change in albuminuria as a surrogate endpoint for progression of c
113     Our results support a role for change in albuminuria as a surrogate endpoint for the progression
114 d surrograte endpoints, to inform the use of albuminuria as a surrogate endpoint in future randomised
115 2 inhibitors protect the kidneys by reducing albuminuria as hypothesized, people with type 2 diabetes
116    Multivariable analyses confirmed eGFR and albuminuria as key risk factors for predicting adverse a
117 mean serum creatinine concentration and less albuminuria, as well as less histologic evidence of glom
118 ng everolimus (EVR), but the significance of albuminuria associated with EVR treatment after early CN
119  (eGFR 84 +/- 11.7 ml/min/1.73m(2)) and norm-albuminuria at baseline, UPPod:CR was associated with eG
120 account for imprecision in the estimation of albuminuria at the participant level.
121 2014) with baseline measurements of eGFR and albuminuria, at least 1000 participants (this criterion
122 cluding podocytopathy, diabetic nephropathy, albuminuria, autosomal dominant polycystic kidney diseas
123 ent across patients with different levels of albuminuria, but absolute benefits are greatest among th
124                                              Albuminuria, but not estimated glomerular filtration rat
125  resulted in nephritic urine by dipstick and albuminuria by enzyme-linked immunosorbent assay, and mo
126 unction of the renal microcirculation causes albuminuria by increasing glomerular capillary wall perm
127 3-1.70), each 30% decrease in geometric mean albuminuria by the treatment relative to the control was
128 sk assessment tools that incorporate GFR and albuminuria can help guide treatment, monitoring, and re
129 minuria (increase >/=10%/year with change in albuminuria category).
130  people with GFR 45-59 ml/min/1.73 m2 and no albuminuria (CKD G3aA1).
131 rences in the other variables used to define albuminuria class transition altered the average drug ef
132                                  In the norm-albuminuria cohort (n = 75) baseline UPPod:CR was associ
133 ely to experience eGFR decline and worsening albuminuria compared with HIV-uninfected individuals.
134                                     eGFR and albuminuria contributed multiplicatively (eg, adjusted H
135 er, only Podo-GC-A KO mice developed massive albuminuria (controls: 35-fold; KO: 5400-fold versus bas
136                                              Albuminuria could identify patients with COPD in whom an
137                              Taken together, albuminuria decreases Klotho expression through increase
138                                              Albuminuria due to reduced cubilin function could be an
139 ardiovascular outcomes were glycohemoglobin, albuminuria, duration of diabetes mellitus, systolic blo
140                             Glycohemoglobin, albuminuria, duration of diabetes mellitus, systolic blo
141 ars or older, they had a repeated measure of albuminuria during an elapsed period of 8 months to 4 ye
142 m restriction substantially reduced residual albuminuria during fixed dose angiotensin-converting enz
143                        Reduction of residual albuminuria during single-agent renin-angiotensin-aldost
144 l/min/1.73m(2)/year showed that UPPod:CR and albuminuria each improved the AUC similarly such that co
145 and blood pressure management), treatment of albuminuria (eg, angiotensin-converting enzyme inhibitor
146 or to development of either hyperglycemia or albuminuria, fa/fa rats were hyperinsulinemic with high
147  particularly in patients with high baseline albuminuria; for patients with low baseline levels of al
148          In the intention-to-treat analysis, albuminuria (geometric mean) was 1060 (95% confidence in
149 a in these patients had a high proportion of albuminuria, glomerular diseases such as steroid-resista
150 ity lipoprotein cholesterol, hemoglobin A1c, albuminuria, glomerular filtration rate, smoking, and ex
151 ervention with a NOX1/NOX4 inhibitor reduced albuminuria, glomerular hypertrophy, and mesangial matri
152 evelop diabetic nephropathy, exhibiting less albuminuria, glomerular hypertrophy, podocyte injury, an
153 sex, higher baseline serum creatinine value, albuminuria, greater severity of acute kidney injury, an
154  CKD-Epidemiology Collaboration equation, or albuminuria &gt;30 mg/g, and CKD stages 3-5 was defined as
155 patients with nondiabetic CKD stages 1-3 and albuminuria &gt;300 mg/24 h despite ramipril at 10 mg/d and
156 a man with diabetes, cardiovascular disease, albuminuria &gt;300 mg/d, and an eGFR of 20 ml/min per 1.73
157  filtration rate [GFR] <60 mL/min/1.73 m2 or albuminuria &gt;=30 mg per 24 hours) for more than 3 months
158 ssion (eg, estimated GFR <30 mL/min/1.73 m2, albuminuria &gt;=300 mg per 24 hours, or rapid decline in e
159                         Podocyte markers and albuminuria had overlapping AUC contributions, as expect
160                                    Change in albuminuria has strong biological plausibility as a surr
161            However, the true significance of albuminuria has yet to be fully defined.
162  with chronic kidney disease with or without albuminuria have not been well studied.
163 gliflozin with respect to the progression of albuminuria (hazard ratio, 0.73; 95% CI, 0.67 to 0.79) a
164 d traits such as glomerular filtration rate, albuminuria, hypertension, electrolyte and metabolite le
165 flozin decreases HbA1c, body weight, BP, and albuminuria, implying that canagliflozin confers renopro
166 in moderate and severe stages of CKD-related albuminuria improved the most at 12-month follow-up (by
167 ting the NPY2R in vivo significantly reduced albuminuria in adriamycin-treated glomerulosclerotic mic
168 ly suppressed diabetic glomerular injury and albuminuria in both WT and miR-146a(-/-) animals.
169 ) and dietary sodium restriction on residual albuminuria in CKD.
170 ed into phenyl sulfate in the liver, reduces albuminuria in diabetic mice.
171 ular endothelial cell (GEnC) dysfunction and albuminuria in diabetic nephropathy.
172 ic kidneys appears to be a primary driver of albuminuria in fa/fa rats and thereby an under-recognize
173                                              Albuminuria in maintenance heart transplantation (HTx) i
174 in ER-stressed podocytes, as well as inhibit albuminuria in our NS model.
175 th basal and predicted 2-year progression of albuminuria in patients with microalbuminuria.
176 rm and long-term effects of empagliflozin on albuminuria in patients with type 2 diabetes and establi
177 er-2 (SGLT2) inhibitor empagliflozin reduced albuminuria in patients with type 2 diabetes and prevale
178 (GLP)-1 analogs such as liraglutide improved albuminuria in patients with type 2 diabetes in large ra
179  as well as blood pressure, body weight, and albuminuria in people with diabetes.
180 841K/E1841K) mice exhibited mildly increased albuminuria in response to high salt; severe albuminuria
181 neralocorticoid receptor antagonist, reduced albuminuria in short-term trials involving patients with
182 a, and in vivo injection of BTP2 exacerbates albuminuria in streptozotocin-induced and Akita diabetic
183 ce of reduced glomerular filtration rate and albuminuria in the Fontan population; however, the long-
184 ociated; hence, the clinical significance of albuminuria in this setting is uncertain and should not
185               Furthermore, the prevention of albuminuria in treated mice was associated with preserva
186             The main outcome measure was any albuminuria including both microalbuminuria and macroalb
187  by clinically relevant eGFR subgroups or by albuminuria, including patients with eGFR as low as 20 m
188 iated with greater eGFR decline or worsening albuminuria (increase >/=10%/year with change in albumin
189                      Each SD log-transformed albuminuria increased hazards of incident COPD-related h
190 ive pulmonary disease (COPD) frequently have albuminuria (indicative of renal endothelial cell injury
191                                              Albuminuria is a hallmark of kidney disease of various e
192                                              Albuminuria is a key biomarker for cardiovascular diseas
193                                              Albuminuria is an independent risk factor for the progre
194 discovering signaling pathways that modulate albuminuria is desirable.
195                                              Albuminuria is high amongst people who inject drugs comp
196 ssociation between capillary rarefaction and albuminuria is lacking.
197 between albuminuria and COPD, (2) CS-induced albuminuria is linked to increases in the oxidative stre
198                   The key cell that prevents albuminuria is the terminally differentiated glomerular
199  DKD phenotypes, including glycemic control, albuminuria, kidney function, and kidney function declin
200 c nephropathy" progressing through stages of albuminuria, leading to decline in glomerular filtration
201 onsistent with recent studies reporting that albuminuria leads to impairment of kidney function.
202 afety outcomes were mostly consistent across albuminuria levels including increased risks for amputat
203 , followed by higher mean HbA(1c), sustained albuminuria, longer duration of type 1 diabetes, higher
204 sion reduced the development of hypertrophy, albuminuria, loss of GEnC fenestrations and protected ag
205 ivity, males had progressive glomerulopathy, albuminuria, loss of podocytes, and tubulointerstitial f
206                              We assessed the albuminuria-lowering effect of the sodium-glucose co-tra
207 ve glucose control can be renoprotective and albuminuria-lowering treatments can slow the deteriorati
208     Likewise, compared with patients with no albuminuria (&lt;30 mg/g), those microalbuminuria and those
209                                              Albuminuria may be a biomarker of generalized (i.e., mic
210 vel data and quantified percentage change in albuminuria, measured as change in urine albumin-to-crea
211 ts with preserved lung function, mean age at albuminuria measurement was 60 years, 51% were never-smo
212 UK routine primary care database and limited albuminuria measurements.
213 ion: plasma markers of endothelial function, albuminuria, measurements of skin and muscle microcircul
214 oethidium oxidation, and increased levels of albuminuria, mesangial matrix accumulation, and urinary
215 albuminuria in response to high salt; severe albuminuria, nephrinuria, FSGS, and podocyte foot efface
216 feration did not translate into a decline of albuminuria nor in a sustained reduction in sclerotic le
217  APA-KO mice developed a significant rise in albuminuria not observed in AngII-treated wild-type mice
218 nteraction), with a decreasing prevalence of albuminuria observed only among adults younger than 65 y
219                                  Progressive albuminuria occurred in Gsalpha-deficient mice.
220 0 copies) were significantly associated with albuminuria (odds ratio [OR], 3.2; 95% confidence interv
221 stricting analyses to patients with baseline albuminuria of more than 30 mg/g (ie, 3.4 mg/mmol; R(2)
222 n criteria were quantifiable measurements of albuminuria or proteinuria at baseline and within 12 mon
223      Late sirolimus treatment did not reduce albuminuria or the progression of glomerulosclerosis.
224    End points were annual change in eGFR and albuminuria over 2 years of follow-up.
225 d to eGFR slope were UPPod:CR (P < 0.01) and albuminuria (P < 0.01).
226  UPPod:CR was associated with development of albuminuria (P = 0.007) and, in the tertile with both no
227 those with moderately and severely increased albuminuria (P heterogeneity<0.001).
228 rved in participants with severely increased albuminuria (P heterogeneity=0.004).
229 ts in participants with moderately increased albuminuria (P heterogeneity=0.03), but no effect modifi
230 tent across studies irrespective of baseline albuminuria (p(trend)=0.66) and use of RAS blockade (p(h
231 ions in participants with severely increased albuminuria (placebo-subtracted difference 3.01 ml/min p
232                           BIO alone improved albuminuria, podocyte density in superficial and juxtame
233                                    Levels of albuminuria, podocyte injury and podocyte number were si
234  exhibited significantly increased levels of albuminuria, podocyte injury, and loss of podocytes comp
235 proliferation, basement membrane thickening, albuminuria, podocyte loss, and aspects of FSGS during a
236 anti-podocyte autoantibodies, the chips show albuminuria proportional to patients' proteinuria, pheno
237 ey disease", "chronic renal insufficiency", "albuminuria", "proteinuria", and "randomized controlled
238 cohort (n = 128), we measured time-of-biopsy albuminuria, proteinuria, and plasmin (ogen) uria for co
239 inute per 1.73 m(2) of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], >3
240 emapticap pegol (NOX-E36) shows long-lasting albuminuria-reducing effects in diabetic nephropathy.
241 h study medication, PARI did provide further albuminuria reduction (P=0.04 LS + PARI versus LS + PLAC
242 tio, C-reactive protein, angiotensin II, and albuminuria reduction and with increased glucose disposa
243 mean albuminuria to 0.7 (ie, 30% decrease in albuminuria) relative to the control will provide an ave
244 ver, mean serum creatinine concentration and albuminuria remained lower in ES allograft recipients th
245       Kallistatin overexpression exacerbated albuminuria, renal fibrosis, inflammation, and oxidative
246 ype 1 diabetes (T1D) and relate the ratio to albuminuria, renal plasma flow (RPF), fat mass, and insu
247  type 2 diabetes mellitus (T2DM) with higher albuminuria should benefit more.
248                 Neither approaches decreased albuminuria significantly, whereas diuretics did signifi
249 eks of age led to a significant reduction in albuminuria, similar to that observed with renin-angiote
250  at target: glycohemoglobin, blood pressure, albuminuria, smoking, and low-density lipoprotein choles
251  and chronic kidney disease, with or without albuminuria, sotagliflozin resulted in a lower risk of t
252 ntermediate renal outcomes of transitions in albuminuria stages (ie, transitions between normoalbumin
253 agliflozin group versus placebo according to albuminuria status at baseline (normoalbuminuria: UACR <
254 albumin excretion, irrespective of patients' albuminuria status at baseline.
255  or subpopulations based on baseline eGFR or albuminuria status were analyzed or an eGFR decline of >
256 lar disease, according to patients' baseline albuminuria status.
257 luding increased risks for amputation across albuminuria subgroups (P heterogeneity=0.66).
258 ed the annual loss of kidney function across albuminuria subgroups, with greater absolute reductions
259 re for the comprehensive analysis of a major albuminuria susceptibility locus detected in these model
260 GEC(HO-1) rats older than 6 months developed albuminuria that was detectable at 6 months and became s
261 estimated glomerular filtration rate, (micro)albuminuria, the use of lipid-modifying and blood pressu
262      For each SD increase in log-transformed albuminuria, there was 2.81% greater FEV(1) decline (95%
263 ia; for patients with low baseline levels of albuminuria this association is less certain.
264  treatments that decrease the geometric mean albuminuria to 0.7 (ie, 30% decrease in albuminuria) rel
265 001 versus RS + PLAC), and LS + PARI reduced albuminuria to 683 (95% confidence interval, 502 to 929)
266                            LS + PLAC reduced albuminuria to 717 (95% confidence interval, 512 to 1005
267  analysis to relate the treatment effects on albuminuria to those on the clinical endpoint across stu
268 mg/g) and 760 (7.5%) with severely increased albuminuria (UACR >300 mg/g) at baseline.
269 of podocytes, key cells in the prevention of albuminuria, under diabetic conditions.
270 ccelerated development of glomerulopathy and albuminuria upon streptozotocin (STZ)-induced hyperglyce
271     In type 2 diabetics with micro- or macro-albuminuria UPPod:CR and albuminuria were equally good a
272 rticipants (22.3%) with moderately increased albuminuria (urinary albumin/creatinine ratio [UACR] 30-
273 GFR) <60 mL.min(-1).1.73 m(-2) and 19.0% had albuminuria (urinary albumin:creatinine ratio >=30 mg/g)
274 MTP-131 significantly inhibited increases in albuminuria, urinary H(2)O(2), and mesangial matrix accu
275                                              Albuminuria (urine albumin-to-creatinine ratio >/=30 mg/
276  known history of type 2 diabetes, increased albuminuria (urine albumin-to-creatinine ratio [UACR] 30
277                                              Albuminuria (urine albumin-to-creatinine ratio) was meas
278 was 60 years, 51% were never-smokers, median albuminuria was 5.6 mg/g, and mean FEV(1) decline was 31
279 ratio (95% confidence interval) for incident albuminuria was 5.71 (3.64-8.94) for high-risk blacks an
280                                              Albuminuria was associated with greater lung function de
281  In RARE-LacZ mice, Adriamycin-induced heavy albuminuria was associated with reduced RA/RAR activity
282                                    Change in albuminuria was consistently associated with subsequent
283 d by iohexol and p-aminohippurate clearance; albuminuria was estimated by urine albumin-to-creatinine
284 ramatic reduction was found in diuresis, and albuminuria was evident after administration of 1% NaCl
285 but no effect modification was observed when albuminuria was fitted as a continuous variable (P heter
286 cant heterogeneity in the temporal trend for albuminuria was noted by age (P = .049 for interaction)
287 the estimated glomerular filtration rate and albuminuria were also analyzed.
288 ith micro- or macro-albuminuria UPPod:CR and albuminuria were equally good at predicting eGFR loss.
289 der light microscope, severe proteinuria and albuminuria were found in these podocyte-specific knocko
290                 Risk factors associated with albuminuria were HIV (aOR 4.11 [95% CI 1.37-12.38]); fol
291 ms for CKD account for both reduced eGFR and albuminuria; whether each measure associates with greate
292                Additionally, nephrotic-range albuminuria with an albumin-to-creatinine-ratio (ACR) >2
293                        Canagliflozin lowered albuminuria with greater proportional reductions in thos
294           Previously we demonstrated massive albuminuria with hypertension in uninephrectomized, aldo
295 ial-specific Epas1 gene deletion accentuated albuminuria with severe podocyte lesions and recruitment
296 ntified associations of percentage change in albuminuria with subsequent end-stage kidney disease usi
297 imated glomerular filtration rate [eGFR] and albuminuria) with the incidence of peripheral artery dis
298 e with the mouse-specific NOX-E36 attenuated albuminuria without any change in systemic hemodynamics,
299 lin A receptor antagonist atrasentan reduces albuminuria without causing significant sodium retention
300  alterations of Klotho expression induced by albuminuria, yet the underlying mechanisms are unclear.

 
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