Erythrocytosis in type I renal tubular acidosis with nephrocalcinosis.
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Biomedical subjects
Publications and source records attributed to H Yatzidis.
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Tubulin is an intracellular protein whose in vivo polymerization leads to the formation of microtubules (MT). MT are essential component of axons of nerve cells. This reaction is the limiting factor in the growth of axons. Uremic neuropathy is characterized in part by an axonal degeneration. A chromatographic fraction from uremic plasma (2-5 fraction) inhibits in vitro the tubulin polymerization and thus MT formation and therefore may be implicated in the occurrence of uremic neuropathy. In vitro, biotin counteracts the inhibitory effect of 2-5 fraction on MT formation. This effect could be a partial explanation of the possible clinical improvement brought on by biotin in uremic neuropathy.
We studied the feasibility of treating refractory anemia and post-transfusional serious hemochromatosis in a patient undergoing hemodialysis (3x4 h weekly) for fourteen years, with recombinant human erythropoietin (r-HuEPO) associated with blood-letting. Blood transfusion previously received by the patient at a rate of two units of packed red cells every month for nine years was stopped and r-HuEPO (80 U/kg b.w.) was administered i.v. at the end of each hemodialysis. When Hct increased over 30%, approximately 40 ml of blood was removed per hemodialysis session in an attempt to accelerate iron loss. Excellent control of anemia and hemochromatosis was achieved after seven months of treatment. The patient's general condition and skin pigmentation were significantly improved.
This paper describes the use of glycylglycine to prepare dialysis solution containing bicarbonate, calcium and magnesium. Bicarbonate with glycylglycine form a buffer with a constant pH of 7.35, which prevents reaction with calcium or magnesium and the formation of insoluble carbonate salts. This bicarbonate-based solution is stable over long periods and can be used with the same simplicity and convenience as lactate solution for peritoneal dialysis (PD) in humans.
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Fifteen normal pregnant women were studied. Serial measurements of serum total, free and bound uric acid and their clearances were done in early (10-20 weeks), mid- (20-30 weeks) and advanced (30-40 weeks) pregnancy, and after delivery (4-5 weeks). The following was observed. 1. A decrease in early and mid-pregnancy of total and free uric acid (p less than 0.001). 2. A gradual increase from the early to advanced pregnancy of bound uric acid (p less than 0.001). 3. An increase in early and mid-pregnancy of total uric acid clearance and a similar but more pronounced increase of free uric acid clearance (p less than 0.001). These findings explain many differences in previous conflicting reports concerning the metabolic behavior of uric acid, and place future investigation thereof on a more promising basis in normal and abnormal pregnancy.
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In 92 uremic patients under chronic hemodialysis without ascorbic acid supplementation, serum ascorbic acid was measured before hemodialysis and between two sessions. The results indicated a more serious ascorbic acid deficiency of patients than in previous studies. This difference might be explained by the highly specific enzymatic method applied in the present study, excluding any potential interference of various serum reducing substances.
Serum ferroxidase I (ceruloplasmin) and ferroxidase II activities were studied in 49 uremic patients under conservative treatment, in 79 patients undergoing hemodialysis and in 56 healthy subjects, as controls. Ferroxidase I was significantly higher in both groups of patients. Ferroxidase II was significantly elevated only in patients undergoing chronic hemodialysis. The cause of this difference is not clear, but seems to be of considerable interest.
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Thirty-four idiopathic rapid calcium stone formers (24 male/10 female) were studied. Their ages ranged from 20 to 60 years (40 +/- 11) and all had good renal function. The trial comprised two consecutive periods of 3 years and 4 years duration respectively. In the first (control period), the patients were maintained on a customary diet with an adequate fluid intake sufficient to produce about 2 liters of urine daily. In the second (treatment period), they received a similar diet plus 20 mmol of sodium thiosulphate daily. New stone development fell from 100 in the control period to 15 in the treatment period, corresponding to a rate of 0.98 and 0.11 per year (p less than 0.001). It is suggested that the benefit from sodium thiosulphate results from calcium thiosulphate formation in urine, a salt with a molar solubility of 250 to 100.000-fold greater than that of other urinary calcium salts.
In 9 patients undergoing chronic hemodialysis for 2-10 years and suffering from encephalopathy (dialysis dementia) and peripheral neuropathy, 10 mg of biotin was given daily in three doses for 1-4 years. Within 3 months there was a marked improvement in all patients in respect to disorientation, speech disorders, memory failure, myoclonic jerks, flapping tremor, restless legs, paresthesia and difficulties in walking. It is recommended to start giving biotin regularly in any patient with advanced renal failure before severe neural or muscular lesions become manifest. The correlation of biotin with uremic neurologic disorders and the possible mechanism of its therapeutic action are discussed.
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Total urinary protein is rapidly precipitated at room temperature by tannic acid. The tannic acid/protein precipitate, dissolved in aqueous triethanolamine/ferric chloride solution, gives a purple-violet color of high absorptivity. Absorbance at 510 nm is linearly related to concentration from 0.05 to 1.50 A for a protein content of 0.05 to 1.50 g/liter, and less than 5 mg/liter can be detected. The CV and analytical recovery ranged from 0.5 to 1.8% and 98 to 103%, respectively. Nonprotein urinary constituents do not interfere.