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1 ailure to thrive, vomiting, dehydration, and nephrocalcinosis.
2 factor in the etiopathogenesis of medullary nephrocalcinosis.
3 concentration in blood and urine as well as nephrocalcinosis.
4 d association between hyperaldosteronism and nephrocalcinosis.
5 he proband at age 12 yrs tested negative for nephrocalcinosis.
6 familial hypercalciuric hypomagnesemia with nephrocalcinosis.
7 L-1beta blockade may prevent renal damage in nephrocalcinosis.
8 d that its loss leads to hypermagnesemia and nephrocalcinosis.
9 e metabolic acidosis, hypokalemia, and early nephrocalcinosis.
10 and deficiency in this pathway as a cause of nephrocalcinosis.
11 g of magnesium and calcium and develop renal nephrocalcinosis.
12 persistent acidosis, failure to thrive, and nephrocalcinosis.
13 re to thrive, poor growth, and in many cases nephrocalcinosis.
14 ltifactorial etiology for furosemide-related nephrocalcinosis.
15 of conditions reported to be associated with nephrocalcinosis.
16 sm play a central role in the development of nephrocalcinosis.
17 te in humans may lead to nephrolithiasis and nephrocalcinosis.
18 osteomalacia in adults, nephrolithiasis and nephrocalcinosis.
19 st plasma creatinine, and greatest amount of nephrocalcinosis.
20 dosis are associated with hypercalciuria and nephrocalcinosis.
21 deposits on renal biopsy are referred to as nephrocalcinosis, a condition typically associated with
27 s, particularly Tregs, in the progression of nephrocalcinosis and emphasize the fact that inflammatio
29 oxalate, leading to recurrent kidney stones, nephrocalcinosis and eventually kidney failure; the subs
31 ycol challenge (0.7% for 1 week) resulted in nephrocalcinosis and microlithiasis in untreated Agxt-/-
32 h congenital hemihypertrophy, complicated by nephrocalcinosis and nephrolithiasis, is reported here.
37 m should be included as one of the causes of nephrocalcinosis and that our case series emphasizes the
41 ties recently reported to be associated with nephrocalcinosis are some that characteristically includ
43 ilial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a human disorder caused by m
44 ilial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is an inherited disorder caused
45 ilial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) was previously considered to be
47 een chronic hyperaldosteronism and medullary nephrocalcinosis has rarely been made, with only a handf
48 ology demonstrated interstitial fibrosis and nephrocalcinosis in addition to absent dimorphic tubules
49 two conditions most commonly associated with nephrocalcinosis in childhood are the use of furosemide
50 e, vomiting, constipation, hypercalcemia and nephrocalcinosis in infancy, while biallelic SLC34A3 car
51 ade of TNFR might delay progressive forms of nephrocalcinosis in oxalate nephropathy, such as primary
54 tion of oxalate that leads to kidney stones, nephrocalcinosis, kidney failure, and systemic oxalosis.
55 an diseases such as amelogenesis imperfecta, nephrocalcinosis, lethal and nonlethal forms of Raine sy
56 f the molecular cause of nephrolithiasis and nephrocalcinosis may have practical implications and mig
58 risk of kidney stone formation or medullary nephrocalcinosis, namely 46% compared with 6% observed i
59 of genotype and can guide therapy to prevent nephrocalcinosis, nephrolithiasis, and potentially, CKD.
60 hypercalciuria that may increase the risk of nephrocalcinosis, nephrolithiasis, and renal insufficien
61 ed disorder characterized by hypercalciuria, nephrocalcinosis, nephrolithiasis, low molecular weight
62 in patients with chronic kidney disease and nephrocalcinosis/nephrolithiasis or with end stage kidne
63 ltrasound, persistent hyperechoic kidneys or nephrocalcinosis on ultrasound, and persistent metabolic
66 While the disorder typically presents with nephrocalcinosis, recurrent nephrolithiasis, and/or earl
67 d murine kidneys with calcium oxalate (CaOx) nephrocalcinosis-related CKD compared with controls.
72 pomagnesemia, hypokalemia, salt wasting, and nephrocalcinosis, we identified heterozygous missense va
73 ng the period from 2000 to 2004, 31 cases of nephrocalcinosis were identified among the 7349 native r
74 familial hypomagnesemic hypercalciuria with nephrocalcinosis, whereas polymorphisms in claudin-14 ar
75 ncluding hypercalcaemia, hypercalciuria, and nephrocalcinosis which, however, only disappeared after
76 Patients with nephrotic syndrome can develop nephrocalcinosis, which animal models suggest may develo
77 mperfecta (AI) with gingival hyperplasia and nephrocalcinosis, while FAM20C mutations cause Raine syn
78 osis, hypophosphatemia and, less frequently, nephrocalcinosis, while the prevalences of kidney stones