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Biomedical subjects

Y Takekoshi

Publications and source records attributed to Y Takekoshi.

44 records · Page 3Linked to original sources

Pseudohypoparathyroidism type II and anticonvulsant rickets.

A patient treated with anticonvulsants showed hypocalcemia and hyperphosphatemia in association with increased serum parathyroid hormone, reduced serum 25-hydroxy D3, diminished response in phosphorus excretion to exogenous parathyroid hormone and normal response in cyclic AMP excretion. Oral administration of Vitamin D3 resulted in normalization of serum 25-hydroxy D3, calcium, and phosphorus. At this stage, phosphorus excretion after parathyroid hormone returned to normal. These findings suggest that the patient had pseudohypoparathyroidism type II with anti-convulsant medication as a complicating factor.

Adolescent↗

[Etiology of membranous nephropathy in children: Association between membranous nephropathy and hepatitis B virus infection (author's transl)].

A total of 163 Japanese children (90 boys and 73 girls, ranging in age from 3 to 15) with proteinuria and/or hematuria were studied for renal histopathology using biopsy materials by light microscopy, electron microscopy, and immunofluolescence method. Eleven patients were diagnosed as membranous nephropathy (MN) while the other 152 patients had various renal diseases other than MN. All patients with MN did not have any known predisposing of associated caused. Hepatitis B virus surface antigen (HBsAg) in the serum, as determined by a reversed passive hemagglutination method (RPHA), was positive in 100% of the patients with MN, while it was positive in 4.6% of the patients with other renal diseases. The difference was statistically significant. Of the 11 mothers of the children with MN, six were positive for HBsAg, and one of the remaining 2 was positive for antibody to HGsAg (anti-HBs) and another was not examined. These findings suggest that MN among Japanese children are mainly, if not exclusively, caused by hepatitis B virus (HBV) and that the virus is transmitted from the mother to child in most instances. In each case of HBsAg-associated glomerulonephritis reported, HBsAg was detected, by immunofluorescence, in the glomeruli, with a distribution similar to that of immunoglobulins. However deposits of HBsAg could not be demonstrated in the glomeruli of the 9 patients with MN studied. Pathogenic immune complexes in the glomerular lesions with subepithelial deposits have been shown to weigh less than 1 million daltons. Since the intact 20-nm HBsAg has a molecular weight of more than 2.4 million daltons, probably most immune complexes containing it would be very large and rapidly cleared by the reticuloendothelial system. Therefore, this failure to detect glomerular staining with anti-HBs antiserum may mean that MN is caused by some other antigen, of a lower molecular weight, associated with HBV, but not necessarily by HB surface antigen.

Adolescent↗

Strong association between membranous nephropathy and hepatitis-B surface antigenaemia in Japanese children.

Renal histology in 163 Japanese children, aged 3 to 15, with proteinuria and/or haematuria showed that 11 had membranous nephropathy (M.N) and the rest had various other renal diseases. Hepatitis-B-virus surface antigen (HBsAg) was identified, by a reversed passive haemagglutination method, in the serum of all the patients with M.N. but in only 4.6% of the patients with other renal diseases. 6 of the 11 mothers of the children with M.N. were positive for HBsAg, and 1 was positive for antibody to HBsAg (anti-HBs). These findings suggest that M.N. in Japanese children is mainly, if not exclusively, caused by hepatitis-B virus and that in most instances the virus is transmitted from mother to child.

Adolescent↗

Renal tubular acidosis and skeletal demineralization in patients on long-term anticonvulsant therapy.

Three children ranging from seven to 12 years of age from unrelated families were given long-term anticonvulsant therapy including acetazolamide (Diamox). These children had rickets and renal tubular acidosis. Investigations have suggested (1) secondary hyperparathyroidism due to hypocalcemia of rickets and (2) prolonged acetazolamide therapy were responsible for acidosis as a result of reduction of bicarbonate reabsorption in the kidney. A clear-cut recovery from acidosis and rickets was seen in two patients following medication with high doses of vitamin D, an oral supplement of phosphorus, and discontinuance of acetazolamide therapy.

Acetazolamide↗