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1 concentration in blood and urine as well as nephrocalcinosis.
2 d association between hyperaldosteronism and nephrocalcinosis.
3 he proband at age 12 yrs tested negative for nephrocalcinosis.
4 familial hypercalciuric hypomagnesemia with nephrocalcinosis.
5 L-1beta blockade may prevent renal damage in nephrocalcinosis.
6 d that its loss leads to hypermagnesemia and nephrocalcinosis.
7 e metabolic acidosis, hypokalemia, and early nephrocalcinosis.
8 and deficiency in this pathway as a cause of nephrocalcinosis.
9 g of magnesium and calcium and develop renal nephrocalcinosis.
10 persistent acidosis, failure to thrive, and nephrocalcinosis.
11 re to thrive, poor growth, and in many cases nephrocalcinosis.
12 ltifactorial etiology for furosemide-related nephrocalcinosis.
13 of conditions reported to be associated with nephrocalcinosis.
14 sm play a central role in the development of nephrocalcinosis.
15 dosis are associated with hypercalciuria and nephrocalcinosis.
16 ailure to thrive, vomiting, dehydration, and nephrocalcinosis.
17 factor in the etiopathogenesis of medullary nephrocalcinosis.
18 deposits on renal biopsy are referred to as nephrocalcinosis, a condition typically associated with
24 s, particularly Tregs, in the progression of nephrocalcinosis and emphasize the fact that inflammatio
25 ycol challenge (0.7% for 1 week) resulted in nephrocalcinosis and microlithiasis in untreated Agxt-/-
26 h congenital hemihypertrophy, complicated by nephrocalcinosis and nephrolithiasis, is reported here.
31 m should be included as one of the causes of nephrocalcinosis and that our case series emphasizes the
34 ties recently reported to be associated with nephrocalcinosis are some that characteristically includ
36 ilial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a human disorder caused by m
37 ilial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is an inherited disorder caused
39 een chronic hyperaldosteronism and medullary nephrocalcinosis has rarely been made, with only a handf
40 ology demonstrated interstitial fibrosis and nephrocalcinosis in addition to absent dimorphic tubules
41 two conditions most commonly associated with nephrocalcinosis in childhood are the use of furosemide
42 ade of TNFR might delay progressive forms of nephrocalcinosis in oxalate nephropathy, such as primary
45 f the molecular cause of nephrolithiasis and nephrocalcinosis may have practical implications and mig
47 risk of kidney stone formation or medullary nephrocalcinosis, namely 46% compared with 6% observed i
48 of genotype and can guide therapy to prevent nephrocalcinosis, nephrolithiasis, and potentially, CKD.
49 hypercalciuria that may increase the risk of nephrocalcinosis, nephrolithiasis, and renal insufficien
50 ed disorder characterized by hypercalciuria, nephrocalcinosis, nephrolithiasis, low molecular weight
52 d murine kidneys with calcium oxalate (CaOx) nephrocalcinosis-related CKD compared with controls.
57 ng the period from 2000 to 2004, 31 cases of nephrocalcinosis were identified among the 7349 native r
58 familial hypomagnesemic hypercalciuria with nephrocalcinosis, whereas polymorphisms in claudin-14 ar
59 ncluding hypercalcaemia, hypercalciuria, and nephrocalcinosis which, however, only disappeared after
60 Patients with nephrotic syndrome can develop nephrocalcinosis, which animal models suggest may develo
61 mperfecta (AI) with gingival hyperplasia and nephrocalcinosis, while FAM20C mutations cause Raine syn
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