scholarly journals A Case Study of Adult-Onset Hypophosphatemic Osteomalacia with Idiopathic Fanconi Syndrome

Nephron ◽  
1996 ◽  
Vol 72 (1) ◽  
pp. 121-122 ◽  
Author(s):  
Serran Dalmak ◽  
Ekrem Erek ◽  
Kamil Serdengeçti ◽  
Imer Okar ◽  
Uğur Ülkü ◽  
...  
Keyword(s):  
Fanconi Syndrome ◽  
Adult Onset ◽  
Hypophosphatemic Osteomalacia ◽  
Idiopathic Fanconi Syndrome

scholarly journals A case report of idiopathic Fanconi syndrome in adult onset.

1984 ◽  
Vol 33 (1) ◽  
pp. 267-270
Author(s):  
Yukihiro Kai ◽  
Yoshihira Fukuoka ◽  
Takao Hotokebuchi ◽  
Seiya Jingushi ◽  
Naotaka Ibi ◽  
...  
Keyword(s):  
Case Report ◽  
Fanconi Syndrome ◽  
Adult Onset ◽  
Idiopathic Fanconi Syndrome

Severe Hypophosphatemic Osteomalacia Secondary to Fanconi Syndrome Due to Adefovir: A Case Report

2014 ◽  
Vol 20 (12) ◽  
pp. e246-e249 ◽  
Author(s):  
Andrea Palermo ◽  
Rocky Strollo ◽  
Rocco Papalia ◽  
Luca D’Onofrio ◽  
Ernesto Maddaloni ◽  
...  
Keyword(s):  
Case Report ◽  
Fanconi Syndrome ◽  
Hypophosphatemic Osteomalacia

scholarly journals Transient acquired Fanconi syndrome with unusual and rare aetiologies: A case study of two dogs

2020 ◽  
Vol 65 (No. 1) ◽  
pp. 41-47
Author(s):  
JY Park ◽  
JH Park ◽  
HJ Han ◽  
JH Kim
Keyword(s):  
Amino Acids ◽  
Fanconi Syndrome ◽  
The Other ◽  
Babesia Gibsoni ◽  
Hepatic Copper ◽  
History Of ◽  
Underlying Causes ◽  
Laboratory Examinations ◽  
Aggressive Care

The acquired form of Fanconi syndrome is seldom identified in dogs; those cases that have been reported have been secondary to hepatic copper toxicosis, primary hypoparathyroidism, ingestion of chicken jerky treats, exposure to ethylene glycol, or gentamicin toxicity. However, to the best of our knowledge, there have been no reports of acquired Fanconi syndrome secondary to Babesia infection or ingestion of cosmetics in dogs. We here report on two dogs presented with a history of marked polyuria, polydipsia, and lethargy. Laboratory examinations showed glucosuria with normoglycaemia and severe urinary loss of amino acids. One dog was infected with Babesia gibsoni and the other dog had a history of cosmetics ingestion. The first dog received treatment for Babesia infection and the second dog received aggressive care to correct metabolic acidosis, electrolyte imbalances, and other add-on deficiencies. In both dogs, the Fanconi syndrome was successfully managed following the treatment for the underlying causes. In conclusion, both Babesia infection and cosmetics ingestion should be considered as a possible aetiology for transient acquired Fanconi syndrome in canine patients.

Hypophosphatemic Osteomalacia Due to Adefovir-Induced Fanconi Syndrome

2020 ◽  
Vol 133 (12) ◽  
pp. e687-e689
Author(s):  
Suphadetch Leungsuwan ◽  
Benjamin Hooi ◽  
Khin Saw Myint
Keyword(s):  
Fanconi Syndrome ◽  
Hypophosphatemic Osteomalacia

Electrophoretic examination of proteinuria in Lowe's syndrome and other causes of renal tubular Fanconi syndrome.

1989 ◽  
Vol 35 (11) ◽  
pp. 2231-2233 ◽  
Author(s):  
N M Papadopoulos ◽  
R Costello ◽  
L Charnas ◽  
M D Adamson ◽  
W A Gahl
Keyword(s):  
Metabolic Disorders ◽  
Fanconi Syndrome ◽  
Gamma Globulin ◽  
Urine Samples ◽  
Agarose Gel ◽  
Urinary Proteins ◽  
Urine Protein ◽  
Zone Electrophoresis ◽  
Idiopathic Fanconi Syndrome ◽  
Renal Tubular

Abstract Urine samples from 26 patients with five different causes of renal tubular Fanconi syndrome were examined by zone electrophoresis on agarose gel and immunofixation. The tubular disorders associated with Lowe's syndrome, cystinosis, and idiopathic Fanconi syndrome exhibited urine protein electrophoretic characteristics that differentiated them from normal and from each other. In particular, Lowe's syndrome urine exhibited four discrete bands in the gamma globulin zone. Electrophoresis of urinary proteins may be useful in distinguishing among the different metabolic disorders causing renal tubular Fanconi syndrome.

scholarly journals Adult-onset hypophosphatemic osteomalacia.

2005 ◽  
Vol 94 (11) ◽  
pp. 2391-2393
Author(s):  
Ruri Honda ◽  
Yuko Nakasone ◽  
Ryo Morikawa ◽  
Rithuko Ishihara ◽  
Tomoko Nomura ◽  
...  
Keyword(s):  
Adult Onset ◽  
Hypophosphatemic Osteomalacia

Hypercalciuria in idiopathic fanconi syndrome

1979 ◽  
Vol 131 (4) ◽  
pp. 247-254 ◽  
Author(s):  
K. Kruse ◽  
H. Bartels
Keyword(s):  
Fanconi Syndrome ◽  
Idiopathic Fanconi Syndrome

scholarly journals Urinary Megalin Deficiency Implicates Abnormal Tubular Endocytic Function in Fanconi Syndrome

2002 ◽  
Vol 13 (1) ◽  
pp. 125-133
Author(s):  
Anthony G. W. Norden ◽  
Marta Lapsley ◽  
Takashi Igarashi ◽  
Catherine L. Kelleher ◽  
Philip J. Lee ◽  
...  
Keyword(s):  
Fanconi Syndrome ◽  
Autosomal Dominant ◽  
Apical Cell ◽  
Sodium Dodecyl ◽  
Tubular Proteinuria ◽  
Renal Fanconi Syndrome ◽  
Dent’S Disease ◽  
Mean Values ◽  
Dent's Disease ◽  
Idiopathic Fanconi Syndrome

ABSTRACT. Normal reabsorption of glomerular filtrate proteins probably requires recycling of the endocytic receptors megalin (gp330) and cubilin. Both receptors are located on the luminal surface of the renal proximal tubule epithelium. Whether abnormal amounts of receptor are present in the urine of patients with Dent’s disease, Lowe’s syndrome, or autosomal dominant idiopathic Fanconi syndrome was explored. They are all forms of the renal Fanconi syndrome and are associated with tubular proteinuria. Urine samples of equal creatinine contents were dialyzed, lyophilized, and subjected to electrophoresis on nonreducing sodium dodecyl sulfate-5% polyacrylamide gels. Proteins were blotted and probed with anti-megalin IgG, anti-cubilin IgG, or receptor-associated protein. Megalin and cubilin levels detected by immunochemiluminescence were measured as integrated pixels and expressed as percentages of the normal mean values. A striking deficiency of urinary megalin, compared with normal individuals (n = 42), was observed for eight of nine families with Dent’s disease (n = 10) and for the two families with Lowe’s syndrome (n = 3). The family with autosomal dominant idiopathic Fanconi syndrome (n = 2) exhibited megalin levels within the normal range. The measured levels of cubilin were normal for all patients. These results are consistent with defective recycling of megalin to the apical cell surface of the proximal tubules and thus decreased loss into urine in Dent’s disease and Lowe’s syndrome. This defect would interfere with the normal endocytic function of megalin, result in losses of potential ligands into the urine, and produce tubular proteinuria.

Sign in / Sign up

Export Citation Format

Share Document