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1 xalate intake contributed to the severity of hyperoxaluria.
2 o 98% after multiple doses in a rat model of hyperoxaluria.
3 osis in oxalate nephropathy, such as primary hyperoxaluria.
4 d with exposure to ethylene glycol or severe hyperoxaluria.
5 aluation of LDH5 as a therapeutic target for hyperoxaluria.
6 s a potential therapeutic target for primary hyperoxalurias.
7 lyoxylate aminotransferase (AGXT) in primary hyperoxaluria 1 (PH1) patients.
8                                      Primary hyperoxaluria 1 (PH1; Online Mendelian Inheritance in Ma
9 lted in a therapeutic candidate that reduced hyperoxaluria, a cause of kidney stones, in preclinical
10 tential drug target for treatment of primary hyperoxaluria, a genetic disorder where overproduction o
11 f cinnamon and turmeric may increase risk of hyperoxaluria, a significant risk factor for urolithiasi
12                         BACKGROUND AND AIMS: Hyperoxaluria after Roux-en-Y gastric bypass (RYGB) is g
13                                              Hyperoxaluria after RYGB correlated with steatorrhea and
14 the management of metabolic diseases such as hyperoxaluria and amyloidosis.
15 stic fibrosis have an increased incidence of hyperoxaluria and calcium oxalate nephrolithiasis.
16 al absorption of oxalate, thereby preventing hyperoxaluria and calcium oxalate urolithiasis.
17 lora is associated with an increased risk of hyperoxaluria and calcium-oxalate urolithiasis.
18 sis with deafness, Bartter syndrome, primary hyperoxaluria and cystinuria, in patients attending kidn
19           Slc26a6-null mice have significant hyperoxaluria and elevation in plasma oxalate concentrat
20  promising potential therapy against genetic hyperoxaluria and ethylene glycol poisoning.
21                           The combination of hyperoxaluria and hypocitraturia can trigger Ca(2+)-oxal
22 pendent succinate uptake, as well as urinary hyperoxaluria and hypocitraturia, but no change in urina
23 spite their clinical significance in primary hyperoxaluria and idiopathic calcium oxalate nephrolithi
24 n of oxalate, thereby increasing the risk of hyperoxaluria and its complications (eg, nephrocalcinosi
25 therapy is an efficient procedure to prevent hyperoxaluria and its complications.
26 ven 0.75% ethylene glycol for 2 wk to induce hyperoxaluria and kidney calcium oxalate crystal deposit
27 ease are also associated with higher risk of hyperoxaluria and nephrolithiasis.
28             PAT1 knockout (PKO) mice exhibit hyperoxaluria and nephrolithiasis.
29  absence from the gut increases the risk for hyperoxaluria and recurrent kidney stone disease, and th
30 trol rats and experimental rats with induced hyperoxaluria and renal CaOx crystallization.
31 d caused by fat malabsorption, magnitudes of hyperoxaluria and steatorrhea should correlate.
32 pears to be a risk factor for development of hyperoxaluria and/or recurrent calcium oxalate kidney st
33 e transporter SLC26A6 develop hyperoxalemia, hyperoxaluria, and calcium-oxalate stones as a result of
34 th cystic fibrosis have an increased risk of hyperoxaluria, and of subsequent nephrocalcinosis and ca
35 ient repopulation of the liver to ameliorate hyperoxaluria, and therefore should be evaluated further
36 absence of O. formigenes and the presence of hyperoxaluria are correlated in cystic fibrosis (CF) pat
37                                      Primary hyperoxalurias are a devastating family of diseases lead
38                                      Primary hyperoxalurias are genetic diseases defined by elevated
39 e molecular aspect and management of primary hyperoxalurias as well as nephropathic cystinosis provid
40 therapeutic target for PH and other forms of hyperoxaluria associated with increased oxalate producti
41 cate an association between the induction of hyperoxaluria/CaOx nephrolithiasis and the expression of
42                                   Persistent hyperoxaluria causes nephrocalcinosis and urolithiasis,
43 lated probands with PH1 from the Mayo Clinic Hyperoxaluria Center, to date the largest with availabil
44 ad to multiple complications associated with hyperoxaluria, especially recurrent calcium oxalate urol
45 revalent, commonly driven by hypercalciuria, hyperoxaluria, hypocitraturia and low urine volume, wher
46 having a high index of suspicion for primary hyperoxaluria in patients with chronic kidney disease an
47                                 Furthermore, hyperoxaluria in the OPN wild-type mice was associated w
48                              Severe forms of hyperoxaluria, including genetic forms and those that re
49             Oxidative stress plays a role in hyperoxaluria-induced kidney injury and crystallization.
50  for the increased lipid peroxidation during hyperoxaluria-induced nephrolithiasis.
51                                              Hyperoxaluria is a major risk factor for kidney stones a
52                                      Primary hyperoxaluria is a rare autosomal recessive metabolic di
53                                              Hyperoxaluria is discussed relative to mutations in AGXT
54                                           If hyperoxaluria is indeed caused by fat malabsorption, mag
55 he importance of O. formigenes in regulating hyperoxaluria, laboratory rats known to be noncolonized
56        In patients with primary or secondary hyperoxaluria, nephrolithiasis, acute or chronic oxalate
57 on mediated by SLC26A6 may contribute to the hyperoxaluria observed in this mouse model of cystic fib
58 nes were hyperoxaluric, with the most severe hyperoxaluria occurring in young patients.
59 tive in the treatment of primary and enteric hyperoxaluria or even idiopathic calcium oxalate nephrol
60                                      Primary hyperoxaluria (PH) is a family of ultra-rare autosomal r
61                                      Primary hyperoxaluria (PH) is a metabolic defect that results in
62                                      Primary hyperoxaluria (PH) is a rare autosomal recessive disease
63                                      Primary hyperoxaluria (PH) is an autosomal recessive disorder of
64                                      Primary hyperoxaluria (PH) is an inherited disorder that results
65 transthyretin amyloidosis (ATTR) and primary hyperoxaluria (PH).
66  hallmark of all genetic subtypes of primary hyperoxaluria (PH).
67                                      Primary hyperoxalurias (PH) 1-3 are genetic diseases defined by
68                                      Primary hyperoxalurias (PH) are inborn errors of glyoxylate meta
69 (AGT), the metabolic error in type 1 primary hyperoxaluria (PH1).
70 ymatic defect responsible for type 1 primary hyperoxaluria (PH1).
71         Increased urinary oxalate excretion (hyperoxaluria) promotes the formation of calcium oxalate
72    Ethylene glycol poisoning also results in hyperoxaluria promoting acute renal failure and frequent
73 hepatic enzymes deficiency result in chronic hyperoxaluria, promoting end-stage renal disease in chil
74       A young girl affected by severe type I hyperoxaluria received Stiripentol for several weeks: ur
75 reatment of a single individual with primary hyperoxaluria reduced the urinary oxalate excretion.
76 ubular crystal deposition and progression of hyperoxaluria-related CKD.
77 New therapeutics being developed for primary hyperoxalurias take advantage of biochemical knowledge a
78                  Despite identical levels of hyperoxaluria, Tnfr1-, Tnfr2-, and Tnfr1/2-deficient mic
79                                      Primary Hyperoxaluria Type 1 (PH1) is a rare autosomal recessive
80                                      Primary hyperoxaluria type 1 (PH1) is a rare genetic disease cau
81                                      Primary hyperoxaluria type 1 (PH1) is an inborn error of glyoxyl
82                                      Primary hyperoxaluria type 1 (PH1) is an inborn error of metabol
83                                      Primary hyperoxaluria type 1 (PH1) is caused by defects in perox
84                                      Primary hyperoxaluria type 1 (PH1) is caused by the functional d
85                                      Primary hyperoxaluria type 1 (PH1), an inherited rare disease of
86 ion of intracellular oxalate and the primary hyperoxaluria type 1 (PH1).
87 calcium oxalate kidney stone disease primary hyperoxaluria type 1 (PH1).
88 thal hereditary kidney stone disease primary hyperoxaluria type 1 (PH1).
89                                      Primary hyperoxaluria type 1 (PHT1) treatment is mainly focused
90 t the case of a child diagnosed with primary hyperoxaluria type 1 after kidney transplant who was abl
91                                      Primary hyperoxaluria type 1 is a rare inherited disorder caused
92 g glycolate and glyoxylate levels in primary hyperoxaluria type 1 patients who have the inability to
93                  In a mouse model of primary hyperoxaluria type 1, rectal administration of O. formig
94 nal RNA interference therapeutic for primary hyperoxaluria type 1.
95 is enzyme is the underlying cause of primary hyperoxaluria type 2 (PH2) and leads to increased urinar
96                      Outcome data in primary hyperoxaluria type 3 (PH3), described as a less severe f
97                                      Primary hyperoxaluria type I (PH1) is a rare kidney disease due
98 e (PLP)-dependent enzymes, including primary hyperoxaluria type I (PH1).
99 or end-stage renal disease caused by primary hyperoxaluria type I (PH1).
100                                      Primary hyperoxaluria type I is a severe kidney stone disease ca
101 results in the kidney stone disease, primary hyperoxaluria type I, identifying mutations that specifi
102 oxylate aminotransferase, mutated in primary hyperoxaluria type I.
103                                      Primary hyperoxaluria type II (PH2) is a rare monogenic disorder
104                                      Primary hyperoxaluria type-1 (PH1) is an autosomal recessive dis
105  To determine the importance of OPN in vivo, hyperoxaluria was induced in mice targeted for the delet
106  common in obese patients before bypass, but hyperoxaluria was not caused by excess unabsorbed fatty
107 s) may be effective for treatment of primary hyperoxaluria, we propose that the methods described her
108                              Steatorrhea and hyperoxaluria were common in obese patients before bypas
109                              Steatorrhea and hyperoxaluria were defined as fecal fat >7 g/day and uri

 
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