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1 l tubular acidosis (RTA), aminoaciduria, and hypercalciuria.
2 y supplements and were found to have fasting hypercalciuria.
3 tients and are most commonly associated with hypercalciuria.
4 s, suppressed parathyroid hormone (PTH), and hypercalciuria.
5 pment of hypocalcemic hypoparathyroidism and hypercalciuria.
6 hysiology parallels that of human idiopathic hypercalciuria.
7 ions in urinary solute composition including hypercalciuria.
8 ity of >45% for nephrolithiasis and >50% for hypercalciuria.
9  Western diets induce metabolic acidosis and hypercalciuria.
10 ensity has been increasingly associated with hypercalciuria.
11 ns are often sufficient in the management of hypercalciuria.
12 ontribution exists in the pathophysiology of hypercalciuria.
13 ctomy did not prevent this magnesium-induced hypercalciuria.
14 eproducing the human phenotype of idiopathic hypercalciuria.
15  results from attempts in studying polygenic hypercalciuria.
16 ming rats parallels that of human idiopathic hypercalciuria.
17 citriol was associated with a higher risk of hypercalciuria.
18  restriction is only effective in absorptive hypercalciuria.
19 remature delivery, hypokalemic alkalosis and hypercalciuria.
20  (NSHPT) or autosomal dominant hypocalcaemic hypercalciuria (ADHH) for CaSR mutations and performed i
21 so show increased diuresis, albuminuria, and hypercalciuria, although the morphology of glomeruli and
22           Increasing dietary protein induces hypercalciuria and a negative calcium balance.
23 cance, significant linkage was found between hypercalciuria and a region of chromosome 1 at D1Rat169
24 oto (WKY) male rats, loci that are linked to hypercalciuria and account for a 6 to eight-fold phenoty
25  tubule dysfunction, including hyperkalemia, hypercalciuria and acidosis, often complicate their use.
26 n and CaR protein that may contribute to the hypercalciuria and calcium nephrolithiasis.
27 e in the management in patients in whom both hypercalciuria and decreased bone density are present.
28 estations, and Bartter's syndrome, featuring hypercalciuria and early presentation with severe volume
29 : Ksp-cre;Pth1r(fl/fl) Mutant mice exhibited hypercalciuria and had lower serum calcium and markedly
30                            In aldosteronism, hypercalciuria and hypermagnesuria and accompanying decr
31     Under a high-Na+ diet, KO mice exhibited hypercalciuria and increased blood pressure, which were
32                 Hydrochlorothiazide resolved hypercalciuria and increased bone mineral density at a r
33         These patients present not only with hypercalciuria and increased BTMs (mainly resorptive), b
34 d prove valuable in understanding idiopathic hypercalciuria and kidney stone disease in humans.
35 turing salt wasting, hypokalaemic alkalosis, hypercalciuria and low blood pressure.
36 ce have higher blood pressure, hyperkalemia, hypercalciuria and marked hyperplasia of the distal conv
37                 Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a human d
38                 Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is an inheri
39                 Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) was previous
40  renal disorder familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC).
41 e renal tubular acidosis are associated with hypercalciuria and nephrocalcinosis.
42 d in order to provide improved therapies for hypercalciuria and prevent kidney stone formation.
43                          They also developed hypercalciuria and renal calcium deposits and some had d
44 s a potential explanation for Cd(2+)-induced hypercalciuria and resultant renal stone formation.
45 on Ca metabolism that thus contribute to the hypercalciuria and stone formation.
46 abolism in RCTs, specifically hypercalcemia, hypercalciuria, and kidney stones, in participants who w
47 lactose-free diet, including hypercalcaemia, hypercalciuria, and nephrocalcinosis which, however, onl
48 linical and experimental monogenic causes of hypercalciuria, and outlines the initial results from at
49                                The polyuria, hypercalciuria, and proteinuria of the -/- adults and fu
50 hrosis, low plasma potassium, high blood pH, hypercalciuria, and proteinuria.
51 ndingly elevated 1,25(OH)2 vitamin D levels, hypercalciuria, and rickets/osteomalacia.
52 retention of suture material, recurrent UTI, hypercalciuria, and urinary stasis.
53 artter syndrome (diagnosis during childhood, hypercalciuria, and/or polyuria), and 26.0% had Gitelman
54                                              Hypercalciuria, as determined by the urinary calcium-to-
55 ormalization, of alkaline phosphatase and of hypercalciuria but an increase in PTH levels, while 1,25
56 late stone formation, even in the absence of hypercalciuria, but the molecular mechanisms that contro
57                                      Chronic hypercalciuria can contribute to osteoporosis, particula
58                                              Hypercalciuria can result from enhanced intestinal absor
59                                              Hypercalciuria developed in 27 percent of the patients i
60 ts in that affected individuals present with hypercalciuria due to increased serum 1,25-dihydroxyvita
61 hyroidism, patients with these mutations had hypercalciuria even at low serum calcium concentrations.
62 ecurrent calcium nephrolithiasis and fasting hypercalciuria have a higher incidence of osteopenia and
63     Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a rare disorder of autosomal re
64 use hereditary hypophosphatemic rickets with hypercalciuria (HHRH), a disorder characterized by renal
65 use hereditary hypophosphatemic rickets with hypercalciuria (HHRH).
66 ncreased the percentage of participants with hypercalciuria, hypercalcemia, and nausea by 24% (CI, 20
67                                              Hypercalciuria, hypercalcemia, and nausea were more comm
68 xhibit increased nephrocalcinosis or develop hypercalciuria, hypercalcemia, anti-KRN23 antibodies, or
69 tones are most prevalent, commonly driven by hypercalciuria, hyperoxaluria, hypocitraturia and low ur
70 ecifically, KO mice exhibited hypercalcemia, hypercalciuria, hyperphosphaturia, and osteopenia, with
71 ate abnormalities, as well as hypercalcemia, hypercalciuria, hypophosphatemia, and reduced plasma PTH
72 ight males, ages 7 to 34 yr, with idiopathic hypercalciuria (IH) served as controls.
73 from those changes encountered in idiopathic hypercalciuria (IH).
74 , hypercalcemia occurred in 2.8% to 9.0% and hypercalciuria in 12.0% to 33.0% of participants; events
75 d urine calcium excretion causing idiopathic hypercalciuria in 38%, with bone phenotypes still observ
76                           This suggests that hypercalciuria in Dent's disease is a direct consequence
77                                              Hypercalciuria in genetic hypercalciuric stone-forming (
78                                              Hypercalciuria in inbred genetic hypercalciuric stone-fo
79                                Surprisingly, hypercalciuria in RZ mice is abolished by dietary calciu
80  identifying genetic loci that contribute to hypercalciuria in the GHS rat, an F2 generation of 156 r
81   Identification of genes that contribute to hypercalciuria in this animal model should prove valuabl
82 his nephron segment, the pathogenesis of the hypercalciuria in this disease is unknown.
83 Treatment resulted in hyperphosphaturia (and hypercalciuria) in both genotypes, though mice remained
84 ome, characterized by hypokalemic alkalosis, hypercalciuria, increased serum aldosterone, and plasma
85                               This augmented hypercalciuria increases the risk of renal complications
86                                   Idiopathic hypercalciuria is a common disorder in children and can
87                                              Hypercalciuria is a complex trait.
88                                              Hypercalciuria is a major risk factor for nephrolithiasi
89                                              Hypercalciuria is an important, identifiable, and revers
90                                              Hypercalciuria is discussed relative to mutations in the
91  encountered in clinical practice, and thus, hypercalciuria is the greatest risk factor for kidney st
92                                              Hypercalciuria is the major risk factor promoting stone
93                                              Hypercalciuria is the most common risk factor for kidney
94                                              Hypercalciuria is the most common risk factor for kidney
95 ndamental step in dissecting the genetics of hypercalciuria is understanding its pathophysiology.
96 ary calcium deprivation, suggesting that the hypercalciuria may be attributable to gastrointestinal h
97                                              Hypercalciuria may promote Randall's plaque formation an
98 Although originally thought to be related to hypercalciuria, more recent studies in humans and resear
99 X-linked inherited disorder characterized by hypercalciuria, nephrocalcinosis, nephrolithiasis, low m
100 sulting in low-molecular-weight proteinuria, hypercalciuria, nephrolithiasis, and renal failure.
101                                          The hypercalciuria noted on spot testing of the urinary calc
102 ous for a SLC34A3 mutation frequently showed hypercalciuria, often in association with mild hypophosp
103 ctive of PTx: calcium >11.5 mg/dL (OR 2.27), hypercalciuria (OR 3.28, P < 0.0001), and age < 50 years
104  D supplementation on risk of hypercalcemia, hypercalciuria, or kidney stones was not modified by bas
105 f the following side effects: hypercalcemia, hypercalciuria, or kidney stones.
106 ), serum calcium >11.3 mg/dL (P < 0.01), and hypercalciuria (P = 0.02) were associated with PTx; whil
107 d osteocalcin (P </= 0.001 for each) despite hypercalciuria (P = 0.029).
108                                Their greater hypercalciuria presumably reflected activation of Ca(2+)
109 omise the attempt to dissect the genetics of hypercalciuria, summarizes the clinical and experimental
110  to CaR mutations also show disproportionate hypercalciuria that may increase the risk of nephrocalci
111          However, although WT mice developed hypercalciuria, this response was absent in Ksp-Casr mic
112 rease renal tubule Ca reabsorption and cause hypercalciuria through suppression of Ca-sensitive potas
113                    This is the first QTL for hypercalciuria to be isolated in a congenic animal.
114 lcium nephrolithiasis and idiopathic fasting hypercalciuria (urinary calcium/creatinine ratio >0.11)
115                    Gentamicin does not cause hypercalciuria via activation of the CaSR-CLDN14 pathway
116           Null mice were hypocitraturic, but hypercalciuria was absent.
117                                   Idiopathic hypercalciuria was diagnosed in 15.6%, primary hyperpara
118 esent even without alkalinisation treatment; hypercalciuria was found rarely.
119                          No hypercalcemia or hypercalciuria was observed.
120                    Similar increased risk of hypercalciuria was shown in 14 studies for the vitamin D
121                    To study human idiopathic hypercalciuria we developed an animal model, genetic hyp
122 ired Bartter syndrome or hypomagnesemia with hypercalciuria, whereas autoantibodies targeting the dis
123  adults and is most commonly associated with hypercalciuria, which may be due to monogenic renal tubu
124 lted in increased risks of hypercalcemia and hypercalciuria, which were not dose related.
125 al associations and management of idiopathic hypercalciuria will be discussed.
126 din-16 and -19 cause familial hypomagnesemic hypercalciuria with nephrocalcinosis, whereas polymorphi
127 nce of osteoporosis, renal insufficiency, or hypercalciuria with or without nephrolithiasis.
128 odel that closely resembles human idiopathic hypercalciuria, with excessive intestinal calcium absorp

 
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