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Biomedical subjects

M Mizokuchi

Publications and source records attributed to M Mizokuchi.

6 recordsLinked to original sources
PubMed1999

Plasma, urinary, and erythrocyte concentrations of guanidino compounds in patients with chronic renal failure.

Guanidino compounds are among the most likely candidates for uremic toxins. We determined the plasma, erythrocyte, and urinary concentration of guanidino compounds in 30 hemodialysis patients and 15 patients with chronic renal failure who had not undergone hemodialysis. Guanidino compounds were measured by high-performance liquid chromatography. Plasma levels of taurocyamine, guanidinosuccinic acid, alpha-N-acetyl-L-arginine, creatine, guanidinobutyric acid, guanidine, and methylguanidine were significantly increased in patients with chronic renal failure with or without hemodialysis. In contrast, plasma guanidinoacetic acid concentrations were significantly decreased. Erythrocyte concentrations of creatinine, guanidinosuccinic acid, guanidine and methylguanidine were also markedly elevated. No correlation was observed between plasma creatinine concentration and erythrocyte concentration of guanidinosuccinic acid or methylguanidine. However, there was a significant correlation between plasma and erythrocyte methylguanidine, and between plasma and erythrocyte guanidinosuccinic acid.

Adult↗
PubMed1994

A case of thin basement membrane syndrome associated with idiopathic membranous nephropathy.

A 59-year-old woman has had persistent microscopic hematuria for 10 years. A few days after the onset of upper respiratory tract infection, edema and severe proteinuria appeared. In renal biopsy, an electron micrograph revealed electron dense deposits in the subepithelial regions with diffuse thinning of the glomerular basement membrane. These glomerular findings were compatible with thin basement membrane syndrome associated with membranous nephropathy. On the basis of our review of the literature, the association of these two diseases seems to be very rare.

Basement Membrane↗
PubMed1992

Possible mechanism of impaired calcium and vitamin D metabolism in nephrotic rats.

Patients who have nephrotic syndrome and normal renal function are hypocalcemic in spite of the elevated levels of serum parathyroid hormone (PTH) caused by a low serum concentration of 1,25-dihydroxyvitamin D[1,25(OH)2D], presumably because of its loss in urine. However, it has not been established whether the conversion of 25-hydroxyvitamin D[25(OH)D] into 1,25(OH)2D is impaired in the kidney. In this study, we examined the serum levels of vitamin D metabolites, and kinetics of renal 25(OH)D-1-hydroxylase activity in vitro, and nephrogenous cyclic AMP excretion in response to exogenous PTH administration in puromycin aminonucleoside-induced nephrosis in rats. Plasma ionized calcium and the serum levels of vitamin D metabolites were lower, and conversely, the serum PTH level was higher, in nephrotic rats than in controls. Serum 1,25(OH)2D levels were higher in 25(OH)D3-treated nephrotic rats than in untreated nephrotic rats, indicating that the low 1,25(OH)2D level in nephrotic rats is partially due to the low concentration of 25(OH)D. Although PTH levels were higher in nephrotic rats than in control rats, the Vmax of renal 25(OH)D-1-hydroxylase and nephrogenous adenosine 3',5'-monophosphate (cyclic AMP) excretion in response to exogenous PTH were significantly lower in nephrotic animals than in controls. These results suggest that abnormalities in calcium and vitamin D metabolism in nephrotic rats are partially attributable to impaired proximal tubular function.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1991

Vitamin D metabolism in nephrotic rats.

It is well known that patients with nephrotic syndrome and normal renal function have hypocalcemia in spite of high PTH concentration, caused by the low serum concentration of the active vitamin D metabolite, 1,25(OH)2D, presumably due to its loss in urine. However, it has been uncertain whether the conversion of 25(OH)D into 1,25(OH)2D in the kidney is impaired. In this study, we examined the responsibility of 1,25(OH)2D in PAN-induced nephrotic rats. Sprague-Dawley rats weighing 250 g were given subcutaneous injections 1.5 mg/100 g PAN for 12 days prior to use. Some of these rats were given intraperitoneal injection of 100 IU of 25(OH)D3 for 3 days prior to use and of 10 IU of PTH. We measured Ca2+ in plasma, vitamin D metabolites and mid-molecule PTH in serum, renal 25(OH)D-1-hydroxylase activity in vitro, and response of nephrogenous cyclic AMP to exogenous PTH administration. In nephrotic rats, plasma Ca2+, serum 25(OH)D and 1,25(OH)2D were lower than in control rats, and the serum PTH level was higher than in controls. In 25(OH)D3-injected nephrotic rats, Ca2+ and 1,25(OH)2D were higher than in nephrotic rats, indicating that the decreased level of 1,25(OH)2D in nephrotic rats was partially due to the low serum level of 25(OH)D. Despite the elevation of the serum level of PTH, the Vmax of renal 25(OH)D-1-hydroxylase in nephrotic rats was lower than in controls. Response of nephrogenous cyclic AMP to PTH in nephrotic rats was lower than in controls. Although nephrotic rats had higher PTH levels than control rats, Vmax of renal 25(OH)D-1-hydroxylase and response of cyclic AMP to exogenous PTH administration in nephrotic rats were lower than in controls, suggesting that abnormalities of calcium metabolism in patients with nephrotic syndrome might be partially attributed to the impaired renal response to PTH.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗