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1 0.03); 1 patient in each group had end-stage kidney failure.
2 tor for coronary artery disease, stroke, and kidney failure.
3 become the preferred treatment for end stage kidney failure.
4 attack, stroke and progression to heart and kidney failure.
5 ften associated with pain, hypertension, and kidney failure.
6 nsion, eventually culminating in progressive kidney failure.
7 dulin deficiency precedes but does not cause kidney failure.
8 ically important outcomes, such as death and kidney failure.
9 ns do not form and newborn mice die owing to kidney failure.
10 uremic syndrome may develop that can lead to kidney failure.
11 ed by renal cystic growth and progression to kidney failure.
12 corneal opacities, anemia, proteinuria, and kidney failure.
13 o our understanding and study of preterminal kidney failure.
14 s one of the most common causes of pediatric kidney failure.
15 y of bariatric surgery (BS) in patients with kidney failure.
16 long-term dialysis treatment as a result of kidney failure.
17 l for progression of diabetic nephropathy to kidney failure.
18 glomerulonephritis progressing to end-stage kidney failure.
19 nd died several weeks later, presumably from kidney failure.
20 osclerosis, tubulointerstitial fibrosis, and kidney failure.
21 include a poorly characterized risk of late kidney failure.
22 (AA) kidney donors were at greater risk for kidney failure.
23 form of primary GN and an important cause of kidney failure.
24 123) died of CVD, and 66% (n = 548) reached kidney failure.
25 ntify a locus for this common cause of human kidney failure.
26 gregate with hereditary forms of progressive kidney failure.
27 tant role in the pathophysiology of ischemic kidney failure.
28 conditions such as hypertension and chronic kidney failure.
29 erosis, are prevalent in adults with chronic kidney failure.
30 cular hemolysis, thrombocytopenia, and acute kidney failure.
31 22 years old, 11 years before his death from kidney failure.
32 baseline serum creatinine level or onset of kidney failure.
33 are particularly relevant for patients with kidney failure.
34 f hypertension in patients with diabetes and kidney failure.
35 acking CD2AP die soon after birth because of kidney failure.
36 ant severe glomerulonephritis culminating in kidney failure.
37 lar filtration, and leads to proteinuria and kidney failure.
38 regnant adults aged >/=20 y who did not have kidney failure.
39 timately leads to loss of renal function and kidney failure.
40 ey disease, an important and common cause of kidney failure.
41 d glomerular disease is the leading cause of kidney failure.
42 tinine level, acute kidney injury (AKI), and kidney failure.
43 , yet aged animals display no overt signs of kidney failure.
44 glomerular aneurysm and perinatal death from kidney failure.
45 of the glomerulus and is a leading cause of kidney failure.
46 yielding kidney injury and in some patients, kidney failure.
47 oxalate by lactate dehydrogenase, leading to kidney failure.
48 phropathy to patients at the highest risk of kidney failure.
49 emolytic anemia, thrombocytopenia, and acute kidney failure.
50 initiation of autophagy, cell apoptosis, and kidney failure.
51 hereditary glomerular disease that leads to kidney failure.
52 iscoidal LDLs and HDL particles, and develop kidney failure.
53 re proteinuria, foot process effacement, and kidney failure.
54 atients with both endstage liver disease and kidney failure.
55 ne, a hallmark of cardiovascular disease and kidney failure.
56 dult mice resulted in severe proteinuria and kidney failure.
57 tract are the most common cause of pediatric kidney failure.
58 in progressive kidney damage and ultimately kidney failure.
59 n, including a small increase in the risk of kidney failure.
60 for zero or one versus two copies of GSTM1: kidney failure, 1.66 [1.27 to 2.17]; heart failure, 1.16
61 ion cohorts included 3449 patients (386 with kidney failure [11%]) and 4942 patients (1177 with kidne
67 a 22-year-old patient who developed chronic kidney failure after receiving haploidentical HSCT from
69 pathy (IgAN) represents the leading cause of kidney failure among East Asian populations and the most
71 e proportion of patients who never developed kidney failure and (2) median number of days alive and f
72 e 0.68 (95% CI, 0.57 to 0.82; P < 0.001) for kidney failure and 0.77 (CI, 0.65 to 0.91; P = 0.0024) f
73 ephron damage and renal fibrosis, leading to kidney failure and a premature death rate of 67% by 9 we
75 de-induced increases in indexes of liver and kidney failure and concentrations of myeloperoxidase and
80 ent of proteinuria, resulting in progressive kidney failure and focal segmental glomerulosclerosis.
81 skin disorder that develops in patients with kidney failure and has been linked to exposure to gadoli
82 a new mechanism of pathologic thrombosis and kidney failure and have immediate implications for treat
83 copy of GSTM1 associated with higher risk of kidney failure and heart failure (adjusted hazard ratio
84 ss of GSTM1 is also associated with incident kidney failure and heart failure, we estimated GSTM1 cop
85 cipients.The incidence of dialysis-dependent kidney failure and infection in the liver transplant pat
86 d their physicians that their early onset of kidney failure and longer period of transplantation and
87 increasingly recognized among patients with kidney failure and may be driven by left heart failure,
89 scular events, graft loss and progression of kidney failure and mortality in renal transplant recipie
92 icated Stx2 as the sole contributor to acute kidney failure and other systemic complications in human
94 downward spiral of injury toward progressive kidney failure and should, therefore, be investigated.
95 period, 102 previous kidney donors developed kidney failure and were listed for kidney transplantatio
96 sociated with neurological abnormalities and kidney failure and, as an acid glucocerebrosidase recept
97 urred in 5715 participants without prevalent kidney failure, and 1028 heart failure events occurred i
98 ction, associated with a significant risk of kidney failure, and an abnormal facial expression upon s
99 re autoimmune crescentic glomerulonephritis, kidney failure, and lung hemorrhage due to binding of pa
101 procedure in the treatment of patients with kidney failure, and requires collaboration of experts fr
102 ir in models of myocardial infarction, acute kidney failure, and stroke through the action of trophic
103 renal donation because of their own risk of kidney failure; and consideration of genetic testing to
107 creatinine associated with a higher risk for kidney failure but a lower risk for all-cause mortality.
108 s of chronic kidney disease include not only kidney failure but also complications of decreased kidne
109 tein, each remained directly associated with kidney failure but differed with respect to their associ
110 Renal ciliopathies are a leading cause of kidney failure, but their exact etiology is poorly under
111 prevent or delay serious sequelae, including kidney failure, cardiovascular disease, and premature de
112 dney disease (CKD) are at increased risk for kidney failure, cardiovascular events, and all-cause mor
113 ast 1-year follow-up; and outcomes of death, kidney failure, cardiovascular events, change in kidney
114 orted on a model that predicted the risk for kidney failure, cardiovascular events, or all-cause mort
115 n monogenetic disorders, is characterized by kidney failure caused by bilateral renal cyst growth.
117 Ia) are reported in four of 17 children with kidney failure caused by renal adysplasia in the absence
118 wheat flour causes a dose-dependent chronic kidney failure characterized by renal tubulointerstitial
119 adverse outcomes (death, dialysis-dependent kidney failure (DDKF), and cardiovascular outcomes) for
120 te increased significantly as their risk for kidney failure decreased, as the payment offered increas
121 After the randomized trial was completed, kidney failure (defined as initiation of dialysis or kid
124 utcome measure was either death or end-stage kidney failure (dependence on dialysis) at 90 days after
125 , all-cause mortality, or dialysis-dependent kidney failure despite significant reduction in homocyst
127 Over a median follow-up of 24.6 years, 256 kidney failure events occurred in 5715 participants with
129 (2) median number of days alive and free of kidney failure for patients who did not survive, who exp
130 rulonephritis is an important cause of human kidney failure for which the underlying molecular basis
135 gadolinium contrast agents in patients with kidney failure has markedly decreased, patients with exp
136 l status, myocardial or mesenteric ischemia, kidney failure, hypotension, cardiac tamponade, and limb
138 icantly increased the rate of progression to kidney failure in a Col4a3(-/-) mouse model of autosomal
139 United States and the leading cause of acute kidney failure in children who develop hemolytic uremic
140 bstructive nephropathy, the leading cause of kidney failure in children, can be anatomic or functiona
141 olytic uremic syndrome, the leading cause of kidney failure in children, often follows infection with
147 ensin-converting enzyme slows progression to kidney failure in patients with Alport syndrome but is n
148 lly validated models for predicting risk for kidney failure in patients with CKD are available and re
150 antation plays an important role in treating kidney failure in patients with end-stage liver disease.
151 itial Jak/Stat expression and progression of kidney failure in patients with type 2 diabetic nephropa
153 higher rates of both hyperkalemia and acute kidney failure in the early (1.3% and 2.7%, respectively
155 disease (DKD) is the single leading cause of kidney failure in the U.S., for which a cure has not yet
158 disease initiation prevented albuminuria and kidney failure, indicating miR-92a inhibition as a poten
161 nformation regarding risk for progression to kidney failure is required for clinical decisions about
162 ns, which usually results in proteinuria and kidney failure, is caused by mutations to the COL4A3, CO
163 D), the most common genetic cause of chronic kidney failure, is characterized by the presence of nume
164 ysis is used in less than 17% of adults with kidney failure, it is the preferred dialysis treatment f
169 1.04 [0.86 to 1.26]), or dialysis-dependent kidney failure (n=343 events; 1.15 [0.93 to 1.43]) compa
170 e dysfunction, glaucoma, insulin resistance, kidney failure, neuronal degeneration, and osteoporosis.
172 E (risk for renal dysfunction, injury to the kidney, failure of kidney function, loss of kidney funct
176 the impact of control of diabetes as well as kidney failure on hypertension by combined kidney and pa
177 ients lost pancreatic function subsequent to kidney failure, one secondary to noncompliance and the o
178 transplantation) and a composite outcome of kidney failure or all-cause mortality were ascertained t
179 predictors of risk and the composite outcome kidney failure or creatinine doubling, was developed and
180 The 24-hr urinary samples of patients with kidney failure or on renal replacement therapy were excl
181 (OR, 2.97; 95% CI, 1.83 to 4.81; P<0.0001), kidney failure (OR, 4.77; 95% CI, 1.80 to 12.6; P=0.002)
182 atients who did not survive, who experienced kidney failure, or both was 9 days (interquartile range
184 d-stage renal disease, death attributable to kidney failure, or the need for renal-replacement therap
185 or phrases "nephrotoxicity," "nephropathy," kidney failure," or "renal failure." The identified publ
188 contrast to the dramatic increase in treated kidney failure, overall CKD prevalence in the U.S. popul
190 velop a recessive phenotype characterized by kidney failure, proteinuria, glomerulosclerosis, and ret
191 d its presence in all moribund mice suggests kidney failure rather than the fibrotic heart lesions as
192 ric reflux accounts for approximately 10% of kidney failure requiring dialysis or transplantation, an
195 ntravital microscopy of animals with chronic kidney failure showed that FGF23 inhibits chemokine-acti
196 7.4 %, of life-threatening bleeding 7.4%, of kidney failure stage III 7.4%, and of major access site
197 in excretion is an important risk factor for kidney failure, stroke, and cardiovascular disease, perh
199 97,451 (5.36%) died, 3295 (0.18%) developed kidney failure that was treated and 3116 (0.17%) develop
201 etween patients with or without a history of kidney failure, the allelic or genotypic distributions f
202 the impact of the SNPs on dialysis-dependent kidney failure, the incidence of infections and patient
204 rticipants' risk for subsequently developing kidney failure themselves, and who would receive the don
208 The number of survivors who never developed kidney failure was 94 of 165 patients (57.0%) in the vas
209 Within each eGFR stratum the rate of treated kidney failure was higher in younger compared with older
211 athogenesis provoking glomerulonephritis and kidney failure was nonhematopoietic in origin, independe
212 process effacement leads to proteinuria and kidney failure, we studied the function of FAK in podocy
214 9 mL/min/1.73 m2), adjusted rates of treated kidney failure were more than 10-fold higher among the y
215 mL/min/1.73 m2, adjusted rates of untreated kidney failure were more than 5-fold higher among the ol
216 rosis is responsible for chronic progressive kidney failure, which is present in a large number of ad
217 n heavy albuminuria, glomerulosclerosis, and kidney failure, which led to animal death beginning at 1
218 of secondary hyperparathyroidism in chronic kidney failure with calcium and active vitamin D is pote
219 this is related directly to the treatment of kidney failure with HD or to the higher prevalence of ob
222 st formation, kidney enlargement, and severe kidney failure, with a mean survival time of 2 months.
223 with type 2 diabetes is the leading cause of kidney failure, with both inflammation and oxidative str
224 nockout (KO) mice, which develop spontaneous kidney failure, with that of Col4a3;Tsp1 double-knockout
226 kidney disease (DKD) is the leading cause of kidney failure worldwide and the single strongest predic
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