Carnitine metabolism changes during the first year after a successful kidney transplantation.
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Biomedical subjects
Publications and source records attributed to B Rutkowski.
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Though it is said that some immunosuppressive agents are implicated in the development of hyperlipidemia in kidney recipients, this subject is still controversial. Main plasma lipid parameters, as well as apolipoproteins A1 and B were measured periodically in 39 kidney first cadaveric, nondiabetic recipients during 24 months of clinic follow-up after transplantation. Standard triple immunosuppressive therapy: prednisone + cyclosporine + azathioprine was administrated from the beginning. After the second year of kidney transplantation, a significant reduction refers to values of TC, LDL, apo A1 and apo B. In the group with antirejection - methylprednisolone therapy, and without it only TG in the 24th month and apo B in the 1st month were statistically lower in the latter group (both p < 0.05). In the multiple regression test, a linear coincidence was observed between apo A1, apo B and prednisone cumulative dosage after the 1st month, TG and cyclosporine in the 6th month and LDL and cyclosporine in the 12th month after transplantation. It appears that steroids had an impact on lipids directly after transplantation, while cyclosporine did so thereafter.
Arterial hypertension-related renal damage is an increasingly common problem recently, because approximately 25% of patients currently treated with dialysis were hypertensive before renal replacement therapy was started. Hypertension is also known as a metabolic disease, while carbohydrate, purine and lipid disturbances are the features of this syndrome. On the other hand, the progression of renal disease depends on the extent of tubulointerstitial injury. For this reason, we undertook a study to evaluate the relationship between excretion of the markers of tubular damage (NAG) and some parameters of carbohydrate, purine and lipid metabolism in untreated essential hypertension. Both healthy volunteers (n = 15) aged 32. 6+/-7.8 and essential hypertensives (n = 25) aged 37.24+/-11.39 underwent the same tests. These tests were performed at 2-day intervals: intravenous glucose tolerance test with 0.5 g/kg b.w. as 40% glucose solution and oral fructose load test with 1.0 g/kg b.w. Area under glucose curve (GA) and serum uric acid post-fructose (PUAA) were calculated. Fasting: insulin, total cholesterol and LDL, triglycerides, free fatty acids (FFA) and urine excretion of NAG, albumin were determined. Glomerular filtration rate was estimated as creatinine clearance. Hypertensives showed statistically higher BMI (p<0.007), NAG (p<0.02), total cholesterol (p<0.01), LDL (p<0.007), FFA (p<0.007), insulin (p<0.01), PGA (p<0.01) and PUAA (p<0.03). NAG excretion correlated positively with WHR (r = 0.40), MAP (r = 0.47) and PUAA (r = 0.47) in hypertensives only. We presume that tubular injury at an early stage of renal damage in patients with essential hypertension could be a part of metabolic syndrome X.
It is known that some metabolic disturbances may modify the progression of renal disease including primary glomerulonephritis, but the role of purines in this process is still unknown. To investigate this, 13 untreated patients with primary glomerulonephritis were followed up for a mean of 17.6 months to analyze the changes in proteinuria and glomerular filtration rate. On entering the study, each patient was given an oral glucose tolerance test and an oral fructose load test. The areas under the glucose (PGA), insulin (PIA) and uric acid (PUAA, post-fructose) curves were calculated. Glomerulonephritic patients were found to have a statistically higher response to fructose than controls (782 +/- 219 vs 518 +/- 154, P < 0.005). Multiple regression analysis showed that PGA, PIA and PUAA were independently related to changes in proteinuria and glomerular filtration rate during the natural course of the disease. This preliminary study suggests that purine metabolism may modulate the progression of renal disease in proteinuric patients.
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Therapeutic electric stimulation in cases of chronic headaches was carried out in 150 patients. Migraine was diagnosed in 40 cases, common vasomotor headache in 63, cervical migraine in 24, Horton's neuralgia in 5 and complex headaches in 18 cases. The results are reported here, which were best in the cervical migraine syndrome, while in the typical migraine they were the least successful.
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Fibrates have been used clinically to treat dyslipidemias, including chronic renal failure (CRF)-related hypertriacylgliceridemia. In addition to their effects on plasma triacylglycerol concentration, fibrates also induce hepatomegaly (due to peroxisome proliferation) and increase liver malic enzyme activity. Since most experiments regarding fibrates action have been performed on healthy animals, in this paper we compare the effect of clofibrate on: a) plasma lipid concentration; b) liver weight; c) liver malic enzyme gene expression (malic enzyme activity, malic enzyme protein level and malic enzyme mRNA abundance) in control (sham-operated) animals and rats with CRF. The data presented in this paper indicate that: a) the clofibrate treatment causes a decrease in triacylglycerol concentration both in the control and rats with CRF, however the effect of the drug was more pronounced in the latter; b) administration of clofibrate induces hepatomegaly both in the control and rats with CRF; c) the liver malic enzyme gene expression is similarly affected by clofibrate in the control and rats with CRF. It is concluded that the beneficial, therapeutic effect of clofibrate on plasma lipid concentration is more pronounced in rats with CRF, but the side effects (hepatomegaly and the increase in malic enzyme gene expression) of fibrates are essentially similar in the control and rats with CRF.
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31 adult patients (15 male and 16 female) with chronic renal failure were treated for 6 months with 1-alfa-hydroxycholecalciferol on a dose 0.25-2.0 micrograms/24 h. 15 patients with not very advanced renal failure (serum creatinine level 176.8-442 mumol/l) received conservative therapy (group I), 16 patients with serum creatinine value 884-1326 mumol/l were treated by intermittent hemodialysis (group II). The statistically significant decrease of serum alkaline phosphatase activity in group I and II (p < 0.01), the rise of serum calcium level in group I (p < 0.005) were determined. Half of the patients from both the groups stated the relief or disappearance of bone and joint pains and muscle weakness. Besides in group I significant decrease of creatinine clearance (p < 0.001) and increase of serum urea and creatinine value (p < 0.01) were noticed. On the basis of these results we can conclude that the treatment with 1-alfa-hydroxycholecalciferol, produced by "Polfa", ought to be introduced gradually with increasing doses and frequent monitoring of calcium-phosphate metabolism and renal function parameters.
An effect of carnitine (Bicarnesine) on lipid metabolism in 14 patients treated with prolonged dialyses has been analysed. Carnitine has been administered orally in the dose of 30 mg/kg b.w. three times per week for 8 weeks and every day for the next 8 weeks. Carnitine, total triglycerides, total and HDL cholesterol, and glucose have been determined in serum. Blood lipoproteins have been assayed with electrophoresis in agarose gel. Total and free carnitine concentrations increased by 3.5 times within 16 weeks. Triglycerides level did not change significantly in all examined patients except a group of 6 patients with baseline hypertriglyceridemia, in which a significant but transient decrease in triglycerides level has been noted after 4 weeks of treatment. At the same time, normalization of blood lipoproteins has been observed. In the eighth week, a transient decrease in HDL-cholesterol has been noted. Result suggest, that carnitine despite an increase in total and free carnitine blood levels did not regulate lipid metabolism disorders. Moreover, its administration to patients treated with prolonged dialyses seems to be unfavourable due to several adverse reactions.
Authors discuss nephrotoxicity of aminoglycosides in patients with hepatic and biliary disorders. It may be concluded that hepatic and biliary diseases should be considered as an additional gentamycin nephrotoxicity risk factor. Administration of gentamycin to such patients require dose adjustments to renal function and--if possible--to gentamycin serum level.
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