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Results for “AMINOACIDURIA, RENAL”

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At least 37 records · Page 2Linked to original sources
PubMed1980

Aminoaciduria in chronic renal failure--its relationship to vitamin D and parathyroid status.

Fractional clearances of amino acids in 24 patients with chronic renal failure indicate that aminoaciduria is common and often severe. Eleven studies have also been carried out in ten patients with stable renal failure before and during treatment with different metabolites of vitamin D. Sequential measurements of fractional clearance of amino acids, plasma 25-hydroxy-vitamin D (25-(OH)D) and serum parathyroid hormone were made. All patients initially had hyperaminoaciduria, secondary hyperparathyroidism and osteomalacia. Treatment with 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) or 1 alpha-hydroxycholecalciferol (1 alpha(OH)D3) significantly improved amino acid reabsorption irrespective of the initial degree of aminoaciduria. Cholecalciferol or 25-hydroxycholecalciferol(25(OH)D3) improved amino acid transport in patients with initially mild hyperaminoaciduria, but not in patients with severe hyperaminoaciduria. Reduction in aminoaciduria during treatment with 25(OH)D3 may have depended on a variable ability to synthesize 1,25(OH)2D3. Changes in amino acid transport did not correlate with changes in serum parathyroid hormone. It is suggested that defective amino acid reabsorption in patients with chronic renal failure is due at least in part to deficiency of 1,25(OH)2D3.

Amino Acids↗
PubMed1977

Renal glucosuria and aminoaciduria.

A follow-up examination of five patients in whom renal glucosuria had been diagnosed 7-15 years previously, showed that the condition was unchanged. There was no indication of hormonal abnormalities. Oral glucose tolerance test, with determination of insulin, growth hormone and free fatty acids, showed no difference between the patients and a group of normal subjects. The urinary excretion of insulin and albumin was normal, but two patients turned out to have an increased excretion of certain amino acids, aspartic acid in one and glutamic acid, citrulline and alanine in the other.

Adult↗
PubMed1995

A prospective evaluation of ifosfamide-related nephrotoxicity in children and young adults.

BACKGROUND: Ifosfamide has been associated with proximal renal tubular dysfunction resembling Fanconi-like syndrome and leading to rickets in young children. The characteristic manifestations of this nephrotoxicity include phosphaturia and hypophosphatemia, glycosuria, aminoaciduria, renal tubular acidosis, and urinary loss of low molecular weight serum proteins. However, the relationship between acute ifosfamide nephrotoxicity, which is frequently subclinical, and long term renal damage is unclear. In this prospective study, the laboratory features of ifosfamide-induced acute nephrotoxicity were characterized further and correlated with the development of chronic nephropathy. METHODS: The renal function of newly diagnosed children and young adults with high risk sarcomas was followed during therapy with a high dose ifosfamide-containing regimen. Serum and urine were collected regularly immediately before and after 5-day cycles of ifosfamide throughout treatment for determination of the fractional excretion of electrolytes (sodium, potassium, phosphate, magnesium, calcium) and glucose and urinary excretion of amino acids and beta 2-microglobulin. RESULTS: Significant changes in the renal threshold of phosphate excretion, the fractional excretion of calcium and glucose, and the urinary excretion of beta 2-microglobulin were observed when comparing pretreatment values with those at the end of a 5-day treatment cycle. The median renal threshold of phosphate excretion decreased from 1.22 to 0.82 mmol/L (P < 0.0001). The median fractional excretions of calcium and glucose increased from 1.05% to 1.68% (P < 0.0001) and 0.05% to 0.08% (P = 0.0006), respectively. Beta 2-microglobulin excretion increased by 70-fold from 0.02 to 1.42 mg/mmol (P < 0.0001). Except for glucose and beta 2-microglobulin excretion, renal parameters returned to baseline before the next ifosfamide treatment cycle. Acute aminoaciduria was observed in 21 of 23 patients. Chronic nephrotoxicity, as defined by the development of a Fanconi-like syndrome or chronic tubular electrolyte loss requiring oral supplementation, developed in the three patients with the highest urinary excretion of beta 2-microglobulin after ifosfamide therapy. CONCLUSIONS: Prospectively, high dose ifosfamide was associated with a 4% incidence of Fanconi-like syndrome; however, evidence of acute reversible subclinical nephrotoxicity was observed for all patients. Severe beta 2-microglobulinuria appeared to be a prognostic laboratory indicator for the development of chronic nephrotoxicity.

Adolescent↗
PubMed1985

[Acute interstitial nephritis and uveitis: a recently recognized syndrome].

The case is described of a 14-year-old boy who presented with a 6-week history of fatigue, severe weight loss (15 kg) and glycosuria. On admission he was in non-oliguric renal failure (serum creatinine 1360 mumol/l) with moderate proteinuria (1.3 g per 24 h), glycosuria (9.5 g per 24 h) and generalized aminoaciduria. Renal biopsy showed acute interstitial nephritis (AIN) with severe mononuclear cell infiltration. No etiology was found. The patient required hemodialysis (5 times) and responded dramatically to therapy with prednisone (initially 75 mg per day), which was discontinued after 2 months. He presented again 11 weeks after admission with iridocyclitis of the right eye, and 2 months later with the same condition in the left eye. Response to local application of steroids was slow. The association of AIN with uveitis has so far been reported in 12 other pediatric patients aged 10 to 16 years, and in one adult patient; 64% were female. Uveitis often recurred, in contrast to nephritis. The etiology of the syndrome is unknown, a transient defect in cell-mediated immunity being postulated.

Acute Disease↗
PubMed2005

A patient with symptomatic osteomalacia associated with Fanconi syndrome.

We report a patient with renal tubulointerstitial fibrosis and symptomatic osteomalacia associated with Fanconi syndrome. A 55-year-old woman was hospitalized because of an inability to walk. Beginning approximately 2 years previously, she had experienced gradually worsening pain in the hips, shoulders, and trunk, culminating in a bedridden state. Serum urea nitrogen was 38 mg/dl; creatinine, 2.6 mg/dl; uric acid. 3.6 mg/dl; phosphate, 2.3 mg/dl; and alkaline phosphatase, 2111 IU/l. Urinary beta2 microglobulin was 72 331 microg/day. Aminoaciduria, renal glucosuria, and proximal renal tubular acidosis with a normal anion gap were also noted. The patient was diagnosed with Fanconi syndrome. Radiography demonstrated typical Looser zones in the proximal portion of the left and especially the right femoral shaft, and at several other sites. A renal biopsy specimen disclosed severe tubulointerstitial fibrosis with little cellular infiltration. Glomeruli were largely intact. A bone biopsy specimen indicated osteomalacia; no tetracycline labeling could be seen along most trabecular bone surfaces, and the ratio of total osteoid volume to bone volume was increased (71.8%). Bicarbonate administration (9 g/day) gradually lessened most symptoms, permitting ambulation. Calcitriol administration decreased excessive intact-parathyroid hormone emerging after 2 months of acidosis correction. Thus, severe acidosis associated with Fanconi syndrome can induce osteomalacia showing serious skeletal complications, but also responsiveness to bicarbonate therapy.

Journal Article↗
PubMed1964

MYOGLOBINURIA.

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Adolescent↗