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nephrocalcinosis/phosphatase
Врската е зачувана во таблата со исечоци
Страница 1 од 68 резултати
[Nephrocalcinosis and alkaline kidney phosphatase].
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Nephrocalcinosis in very low birth weight infants: a single center experience.
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OBJECTIVE
To determine the incidence and risk factors of nephrocalcinosis in very low birth weight infants.
METHODS
Medical records of inborn infants with gestational age less than 32 weeks or birth weight less than 1,250 grams were collected and analyzed. All infants were born at King Chulalongkorn
Hypercalciuria and nephrocalcinosis in cystic fibrosis patients.
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The objective of this study was to determine the frequency of nephrocalcinosis and hypercalciuria in cystic fibrosis (CF) patients, and to search possible causes of this phenomenon. Forty-three CF children (24 boys, 19 girls; mean age 64.9 months, range 5 months-18 years) were included in this
Amelogenesis imperfecta with bilateral nephrocalcinosis.
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A 12-year-old patient presented with a severe delay of eruption in permanent maxillary and mandibular incisors. On examination, there was over-retained primary teeth and delayed eruption of permanent teeth. Retained primary teeth showed light yellow discolouration whereas permanent teeth were
Severe hypophosphatasia due to mutations in the tissue-nonspecific alkaline phosphatase (TNSALP) gene.
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Hypophosphatasia is a rare autosomal recessive inborn error of metabolism characterized by a defective bone mineralisation and deficiency of serum and tissue liver/bone/kidney alkaline phosphatase activity. We report the characterisation of tissue-nonspecific alkaline phosphatase (TNSALP) gene
Hyperphosphaturia after kidney transplantation in syngeneic rats: effects on nephrocalcinosis and bone metabolism?
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BACKGROUND
Studies on kidney transplantation have thus far mainly dealt with surgical techniques, immunology, and transplant tolerance. Disturbed mineral metabolism after renal denervation has not received much attention. Basic physiological research in short-term experiments has shown that
Hypercalcemia, hypercalciuria and nephrocalcinosis in a breast-fed term newborn: a rare presentation.
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Although hypercalcemia and hypercalciuria are known to occur in breast-fed pre-term infants, to the best of our knowledge, it has never been reported in a term baby previously. We report a term male baby who was followed-up during pregnancy for having bright kidneys, but a follow-up renal ultrasound
The pathogenesis and effect on renal function of nephrocalcinosis induced by different diets in female rats.
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The ability of three diets to produce nephrocalcinosis in female rats has been compared after 30, 60 and 90 days of feeding. Severe nephrocalcinosis with associated tubular damage was induced with a standard laboratory maintenance low-protein diet and with a diet containing a single-cell protein
Nephrocalcinosis and hyperlipidemia in rats fed a cholesterol- and fat-rich diet: association with hyperoxaluria, altered kidney and bone minerals, and renal tissue phospholipid-calcium interaction.
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To determine whether an "atherogenic" diet (excess of cholesterol and neutral fat) induces pathological calcification in various organs, including the kidney, and abnormal oxalate metabolism, 24 male Sprague-Dawley rats were fed either normal lab chow (controls, n = 12) or the cholesterol- and
Pyridoxine-responsive seizures as the first symptom of infantile hypophosphatasia caused by two novel missense mutations (c.677T>C, p.M226T; c.1112C>T, p.T371I) of the tissue-nonspecific alkaline phosphatase gene.
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Pyridoxine-responsive seizures (PRS) and the role of pyridoxine (PN, vitamin B(6)) in hypophosphatasia (HPP) are incompletely understood. Typically, PRS and HPP are rare, independent, metabolic disorders. In PRS, seizures resist standard anticonvulsants apart from PN, yet have a good prognosis. In
Infantile hypophosphatasia secondary to a novel compound heterozygous mutation presenting with pyridoxine-responsive seizures.
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Hypophosphatasia (HPP) is a rare metabolic disease with the hallmark finding of deficient serum tissue nonspecific alkaline phosphatase (TNSALP) activity. TNSALP is primarily known for its role in mineralization; hence, HPP is characterized by defective mineralization of bone and/or teeth. TNSALP is
Clinical Forms and Animal Models of Hypophosphatasia.
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Hypophosphatasia (HPP) is due to mutations of the tissue non-specific alkaline phosphatase (TNAP) gene expressed in the liver, kidney, and bone. TNAP substrates include inorganic pyrophosphate cleaved into inorganic phosphate (Pi) in bone, pyridoxal-5'-phosphate (PLP), the circulating form of
Improvement of bone microarchitecture parameters after 12 months of treatment with asfotase alfa in adult patient with hypophosphatasia: Case report.
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[Antenatal form of Bartter's syndrome].
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Six cases of tubular disorder of antenatal onset responsible for biological manifestations characteristic of Bartter syndrome and severe hypercalciuria are reported. In all six cases, severe hydramnios occurred during pregnancy between the 26th and 28th week after the last menstrual period. All six
Long-term clinical outcome and the identification of homozygous CYP27B1 gene mutations in a patient with vitamin D hydroxylation-deficient rickets type 1A.
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Vitamin D hydroxylation-deficient rickets type 1A (VDDR1A) is an autosomal recessively-inherited disorder caused by mutations in CYP27B1 encoding the 1α-hydroxylase enzyme. We report on a female patient with VDDR1A who presented with hypocalcemic seizure at the age of 13 months. The typical clinical
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