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hypercalciuria/proljev
Veza se sprema u međuspremnik
Stranica 1 iz 19 rezultatima
The impact of sodium chloride and volume depletion in the chronic kidney disease of congenital chloride diarrhea.
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Prijava Registriraj se
Congenital chloride diarrhea is due to mutations in the intestinal Cl(-)/HCO(3)(-) exchange (SLC26A3) which results in sodium chloride and fluid depletion leading to hypochloremic and hypokalemic metabolic alkalosis. Although treatment with sodium and potassium chloride offers protection from renal
Type IV neonatal Bartter syndrome complicated with congenital chloride diarrhea.
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BACKGROUND
Pseudo-Bartter syndrome encompasses a heterogenous group of disorders similar to Bartter syndrome. Sometimes a few status may be nested, as in our case presented here.
METHODS
An 8-month-old boy was referred to our hospital with of intractable diarrhea, polyuria, persistent hypokalemia,
Congenital hypokalemia with hypercalciuria in preterm infants: a hyperprostaglandinuric tubular syndrome different from Bartter syndrome.
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Prijava Registriraj se
A congenital hypokalemic tubular disorder is described with many features resembling Bartter syndrome. Additional features include prenatal onset with polyhydramnios and premature labor; failure to thrive; episodes of fever, vomiting, diarrhea, and renal electrolyte and water wastage;
Urinary lithiasis and idiopathic hypercalciuria: the importance of dietary intake evaluation.
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OBJECTIVE
To evaluate food intake of patients with urinary lithiasis and idiopathic hypercalciuria (IH).
METHODS
Between August 2007 and June 2008, 105 patients with lithiasis were distributed into 2 groups: Group 1 (n = 55)--patients with IH (urinary calcium excretion > 250 mg in women and 300 mg
The role of salt abuse on risk for hypercalciuria.
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BACKGROUND
Elevated sodium excretion in urine resulting from excessive sodium intake can lead to hypercalciuria and contribute to the formation of urinary stones. The aim of this study was to evaluate salt intake in patients with urinary lithiasis and idiopathic hypercalciuria (IH).
METHODS
Between
Autoimmune hypoparathyroidism in a 12-year-old girl with McKusick cartilage hair hypoplasia.
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McKusick type metaphyseal chondrodysplasia, or cartilage hair hypoplasia (CHH), is a rare autosomal recessive osteochondrodysplasia secondary to a mutation in the RMRP gene. In addition to the metaphyseal chondrodysplasia and the short-limb dwarfism, patients may present with a multisystemic
Hypophosphatemic rickets accompanying congenital microvillous atrophy.
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This report concerns an 11-year-old boy who manifested hypophosphatemic rickets associated with congenital microvillous atrophy (CMA). He had been suffering from vomiting and severe diarrhea from the first day of life and had been treated with total parenteral nutrition (TPN) since he was 67 days
Two Cases of Mistaken Polyuria and Nephrocalcinosis in Infants with Glucose-Galactose Malabsorption: A Possible Role of 1,25(OH)2D3 .
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OBJECTIVE
Glucose-galactose malabsorption (GGM) is a rare and potentially fatal disorder. The autosomal recessive mutation of the SGLT1 gene interferes with the active glucose transport in the gut resulting in osmotic diarrhea and failure to thrive (FTT). Two nonrelated infants with GGM are
Metabolic risk factors in pediatric stone formers: a report from an emerging economy.
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The goal of this study was to investigate metabolic risk factors in pediatric stone formers in an emerging economy. A prospective, data collection enrolled 250 children age <1-15 years at our center. Risk factors were evaluated by gender and in age groups <1-5, 6-10 and 11-15 years. Patients were
[Gordon syndrome: The importance of measuring blood pressure in children].
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Gordon's syndrome, or type II pseudo-hypoaldosteronism, is a rare cause of arterial hypertension in children. However, it is important to diagnose this syndrome because of the spectacular efficacy of thiazide diuretics. The typical clinical picture of Gordon syndrome includes, apart from arterial
[Calcium nephrolithiasis and phosphate therapy. Long term study (65 cases) (author's transl)].
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Protected phosphate therapy was used in 65 cases of recurrent calcium nephrolithiasis. Mean duration treatment was 2 years and 1 month (more than 3 years in 17 cases). Mean lithiasis episodes by year-patients were 1,55 renal colics and 0.34 stone formation before phosphate treatment, versus 0.66
High fluid-low calcium intake: not all renal stone formers adhere to this simple treatment.
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FActors predisposing to renal stone formation have been studied in 309 patients. Dehydration before diagnosis of urolithiasis was due in 12% of the cases to frequent diarrhea and in 36% to bad working conditions. Daily fluid intake was less than 1 liter in 25% of the patients before stone formation
Biochemical profile of idiopathic uric acid nephrolithiasis.
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BACKGROUND
The objective of this study was to elucidate a biochemical profile of patients with idiopathic uric acid nephrolithiasis, without secondary causes (such as dehydration or diarrhea). Study subjects comprised 56 patients with idiopathic uric acid nephrolithiasis (UA stone group) who
Electrolyte balance in gastrointestinal disease.
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Even small losses of gastrointestinal secretions when combined with reduced intake of electrolytes may seriously disturb electrolyte balance. Knowledge of the ionic composition of secretions lost is essential in planning therapy. Loss of gastric contents usually results in excessive loss of
Pathogenetic role of cyclooxygenase-2 in hyperprostaglandin E syndrome/antenatal Bartter syndrome: therapeutic use of the cyclooxygenase-2 inhibitor nimesulide.
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Patients with hyperprostaglandin E syndrome/antenatal Bartter syndrome typically have renal salt wasting, hypercalciuria with nephrocalcinosis, and secondary hyperaldosteronism. Antenatally, these patients have fetal polyuria, leading to polyhydramnios and premature birth. Hyperprostaglandin E
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