nephrocalcinosis/potassium

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Greater effect of dietary potassium tripolyphosphate than of potassium dihydrogenphosphate on the nephrocalcinosis and proximal tubular function in female rats from the intake of a high-phosphorus diet.

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We examined whether a difference in potassium dihydrogenphosphate (KH2PO4) and potassium tripolyphosphate (K5P3O10) as dietary phosphorus sources could differentially effect the nephrocalcinosis and proximal tubular function in female rats. Rats were fed on a diet containing KH2PO4 or K5P3O10, at

Isolated nephrocalcinosis due to compound heterozygous mutations in renal outer medullary potassium channel.

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Identification of a monogenic etiology is possible in a proportion of patients with childhood-onset nephrolithiasis or nephrocalcinosis. Bartter syndrome (BS), a hereditary tubulopathy characterized by polyuria, hypokalemic alkalosis and growth retardation that rarely presents with isolated

The production of secondary potassium depletion, sodium retention, nephrocalcinosis and hypercalcaemia by magnesium deficiency.

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Renal tubular acidosis and renal potassium wasting acquired as a result of hypercalcemic nephropathy.

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Renal hypomagnesemia, hypercalciuria and nephrocalcinosis in a middle-aged man.

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We report a 41-year-old man with hypomagnesemia, hypercalciuria, nephrocalcinosis, myopia and horizontal nystagmus. The hypomagnesemia was due to primary renal magnesium loss. He was diagnosed as having the syndrome of renal hypomagnesemia, hypercalciuria and nephrocalcinosis. This is a rare

Does citrate prevent nephrocalcinosis in preterm neonates?

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Nephrocalcinosis (NC) occurs frequently in preterm neonates. A high U-calcium/citrate is one of the contributing factors to the development of NC. In stone-forming children and adults citrate supplementation is a successful preventive therapy. In this randomized controlled trial the effect of

Renal function and kidney length in preterm infants with nephrocalcinosis: a longitudinal study.

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Renal injury in early life may lead to hypertension and renal disease in adulthood. In this prospective study, we estimated renal glomerular and tubular function and kidney length (KL) during the first 2 years of life of preterm infants with nephrocalcinosis (NC) associated with prematurity. The

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis: unusual clinical associations and novel claudin16 mutation in an Egyptian family.

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BACKGROUND Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare autosomal recessive tubular disorder that eventually progresses to renal failure, depending upon the extent of nephrocalcinosis. Its basic pathogenesis is impaired tubular resorption of magnesium and

Nephrocalcinosis in pre-term neonates: a study of incidence and risk factors.

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The objective of this study was to determine the incidence and risk factors of nephrocalcinosis (NC) in pre-term neonates in the neonatal intensive care unit (NICU) at the Al-Minya University, Egypt. The study included 97 pre-term neonates with a gestational age 34 weeks. Data on duration of

Hypomagnesemia with Hypercalciuria Leading to Nephrocalcinosis, Amelogenesis Imperfecta, and Short Stature in a Child Carrying a Homozygous Deletion in the CLDN16 Gene

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Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare autosomal recessive disease caused by mutations in the CLDN16 or CLDN19 gene; however, few cases develop classical amelogenesis imperfecta. Herein, we report the case of a boy with early clinical renal manifestations

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis.

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Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare autosomal recessive tubular disorder that is frequently associated with progressive renal failure. The primary defect is related to impaired tubular reabsorption of magnesium (Mg) and calcium (Ca) in the thick

Prematurity-associated nephrocalcinosis and kidney function in early childhood.

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To assess the impact of prematurity-associated nephrocalcinosis on kidney function later in life, 20 premature children with neonatal nephrocalcinosis and 20 controls, matched for birth weight and postnatal age but without nephrocalcinosis, were examined (birth weight 905+/-209 vs. 957+/-226 g;

[Accidentally diagnosed distal renal tubular acidosis with nephrocalcinosis - a case report].

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Distal renal tubular acidosis is a defect of acidification of urine in distal tubule. Full-blown form is characterized by polyuria, growth deficiency, nephrolithiasis or nephrocalcinosis. Mutations in genes encoding Cl-/HCO3 - exchanger (autosomal dominant) or H+-ATPase (autosomal

[Polyhydramnios, prematurity, dystrophy, polyuria, constipation, nephrocalcinosis and renal tumor: presentation of a classic tubulopathy].

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BACKGROUND A diagnostic workup of a renal mass will rarely lead to the diagnosis of a tubulopathy. We would like to stress the importance of taking a detailed history and of evaluating these findings in the context of the clinical symptoms. METHODS A 3 year old boy with a renal mass, diagnosed due

[Effect of calcium antagonists (nifedipine) on nephrocalcinosis and calcium excretion in the rat].

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An animal model was established to test the effect of a calcium antagonist on nephrocalcinosis, which was induced by an atherogenous diet, and its effect on the excretion of calcium and other parameters relevant for stone formation. With the administration of nifedipine (Adalat), the grade of

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