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Biomedical subjects

K Stefíková

Publications and source records attributed to K Stefíková.

17 recordsLinked to original sources
PubMed2004

[Intensive vitamin D supplementation in the treatment of osteoporosis].

Vitamin D deficiency is not possible to correct with the nutritional vitamin D doses in postmenopausal women with decreased bone mineral density. The aim of study was to evaluated the effectivity and safety of 15,000 IU/week vitamin D administrated in 52 postmenopausal women with osteopenia or osteoporosis. Patients were divided into two groups. Treated group was supplemented by calcium 0.5 g/d and 25-hydroxycholecalciferol 15,000 IU/week and control group was supplemented by calcium and placebo for two months. Plasma calcium concentration did not change in the vitamin D treated group while it decreased (p < 0.001) in the control group. Neither calciuria nor fractional excretion of calcium changed during the treatment period. Plasma inorganic phosphate concentration did not change in any group, but urinary inorganic phosphate excretion increased in the vitamin D treated group (p < 0.001). The starting 25-hydroxycholecalciferol plasma concentrations were almost at the deficiency range in both groups. The 25-hydroxycholecalciferol plasma concentration increased substantially (p < 0.001) in the treated group, but it remained at the starting level in control group during the treatment period. Similar plasma concentration increase (p < 0.001) was apparent also in 1.25-dihydroxycholecalciferol. Plasma intact parathormone concentration did not change in the vitamin D treated patients, while it increased (p < 0.01) in the control group. None of the vitamin D treated women suffered from hypercalcemia and mild hypercalciuria was observed in one patient. In conclusion, the study presents an evidence on the effectiveness and safety of 15,000 IU/week 25-hydroxycholecalciferol dosage schedule.

Bone Diseases, Metabolic↗
PubMed2002

Does magnesium dysbalance participate in the development of insulin resistance in early stages of renal disease?

We investigated the potential role of magnesium (Mg) dysbalance in the pathogenesis of insulin resistance (IR) in patients with mildly-to-moderately decreased renal function (creatinine: 142.8+/-11.0 mmol/l). The data were compared to those of 8 age- and sex-matched healthy controls (CTRL). The standard oral glucose tolerance test (oGTT) was performed in 61 patients. Twenty-two patients were classified as IR according to their values on fasting and after-load immunoreactive insulin concentrations. Serum and total erythrocyte Mg (tErMg) (atomic absorption spectro-photometry) and free erythrocyte Mg (fErMg) concentrations ((31) P NMR spectroscopy) were determined prior to and two hours after the glucose load. Ten out of 39 insulin-sensitive (IS) patients, but only one out of 22 insulin-resistant (IR) patients, had a low basal fErMg concentration (<162.2 micromol/l, chi2, p<0.01). IR patients had higher serum Mg, total erythrocyte Mg and bound erythrocyte Mg (bErMg) concentrations (both before and after glucose load) when compared with the IS group. Both groups responded to the glucose load with a significant decrease in serum Mg concentration (within the normal range), while the IR group also exhibited a decline in tErMg and bErMg. The mean sum of insulin needed to metabolize the same glucose load correlated positively with tErMg (r=0.545, p<0.01) and bErMg (r=0.560, p<0.01) in the IR patients. It is concluded that, at an early stage of renal dysfunction, IR is not associated with the decline in free erythrocyte Mg concentration, but the magnesium handling in red blood cells is altered.

Adult↗
PubMed2000

[Nephrologic manifestations of mitochondrial diseases].

Mitochondrial diseases, rated as rarities in paediatrics and neurology, become more and more often diagnosed in various body systems. In nephrology, mitochondrial defects play an important role in the pathogeny of tubular syndromes, interstitial nephritis, focal and segmental glomerulosclerosis, and probably also some other diseases. Review is aimed to point out such defects and to form conditions for their diagnosis and therapy.

Humans↗
PubMed1999

Acute effect of hydrochlorothiazide on renal calcium and magnesium handling in postmenopausal women.

A single 50 mg dose of hydrochlorothiazide (HCTZ) decreases the urinary excretion of calcium (U(Ca)V), clearance (C(Ca)) and fractional excretion (FE(Ca)) of calcium. This is accompanied by an increase of total calcium and ionized calcium (Ca2+) concentrations in the serum. On the other hand, HCTZ increases fractional excretion of magnesium (FE(Mg)) and decreases serum Mg2+ concentrations. Moreover, HCTZ decreases markedly clearance of phosphate (C(Pi)) and fractional excretion of phosphate (FE(Pi)) and increases serum phosphate (Pi) concentrations in healthy postmenopausal women. It is concluded that intrinsic renal cellular control promptly uncouples calcium and magnesium tubular reabsorption even without K+ depletion.

Absorption↗
PubMed1997

Dietary protein restriction in combination with angiotensin converting enzyme inhibitor improves insulin resistance in patients with chronic renal disease.

Insulin resistance (IR) and secondary hyperinsulinaemia are major risk factors of atherosclerosis and probably also of related glomerulosclerosis. Angiotensin converting enzyme inhibitors (ACEI), while improving IR in essential hypertension, do not improve it in patients with chronic renal disease. Thus, the combination of ACEI and low protein diet was evaluated. Thirty-eight patients with various kidney diseases and mild to moderate impairment of kidney function were included in the study. Thirteen of them suffered from IR. Their dietary protein intake was decreased from > or = 1.0 g/kg/d to 0.6-0.7 g/kg/d. Moreover, they were treated by ACEI enalapril at dosages of 2-10 mg/d depending on the absence/presence and severity of hypertension. The patients were followed for 8 months. No clinically relevant kidney disease progression (KDP) was found. IR patients improved remarkably. IR was examined by the oral glucose tolerance test and glucose, insulin and C-peptide determinations. Their increased plasma triglyceride, VLDL concentrations and proteinuria decreased, HDL concentration increased. Acid-base balance and anaemia did not change. It is concluded that protein restriction in combination with ACEI treatment improve IR and the associated dyslipoproteinaemia and proteinuria.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

[Insulin resistance in kidney diseases].

Insulin resistance (IR) is found in different kidney diseases in almost half the patients with mild to medium severe disorders of renal functions; in advanced renal failure it is almost constant. In addition to pathogenetic mechanisms known in other diseases of Reaven's syndrome it has some specific features: Already in the early stages calcitriol production is impaired, and if the calcium intake is not increased and calcitriol is not substituted, secondary hyperparathyroidism with osteodystrophy develops. The intracellular concentration of free Ca increases and the intracellular concentration of free Mg declines. Activation of the renin angiotensin system (RAS) stimulates Ca release from intracellular reserves and potentiates thus the cumulation of free Ca in the cytoplasm. Magnesium plays a special part as it influences glucose utilization by several mechanisms. Diagnosis, prevention and therapy of IR are an essential part of comprehensive prevention of progressing nephropathies with a predicted decline of patients requiring dialysis by cca 30% by the year 2000. This calls, however, for concentrated efforts of all health professionals.

Humans↗
PubMed1994

[Insulin resistance: its clinical importance and trends in modern research].

Insulin resistance is the major pathogenetic link of atherosclerosis development and progression. The clinical diagnosis is made on the basis of analysis of glycemic and insulinemic response during the oral glucose tolerance test. Insulin resistance prevalence is constant in NIDDM and advanced renal failure, and almost 50% in early stages of essential hypertension and kidney diseases. Its prevention and therapy are effective. The increase of free Ca and decrease of free Mg concentrations participate both in insulin resistance and hemodynamic changes in diseases of the Reaven's syndrome. The intracellular mineral dysbalance is caused by the alteration of Na+,H(+)-antiporter. (Fig. 1, Tab. 4, Ref. 51.).

Humans↗
PubMed1993

The prevalence of insulin resistance in essential hypertension.

The prevalence of insulin resistance and/or glucose intolerance (IR/GI) was evaluated in 98 patients with essential hypertension of various stages: a) Almost 35% of them had an abnormal or diabetic glucose tolerance test and 47% of the total number suffered from either/both IR/GI. b) The prevalence was high from stage I essential hypertension, which pointed to an early development of IR/GI, and no further increase during the development of hypertension was found if no antihypertensive drugs influencing IR/GI were taken by the patients. c) Obesity doubled the prevalence of IR/GI. d) No changes in total and HDL cholesterol or triglycerides were found in patients with IR/GI or stage-dependent. e) The presented criteria could be used for the diagnosis of IR/GI in clinical practice.

Female↗
PubMed1992

Metabolic effects of enalapril in the treatment of essential hypertension.

In an open two-month study with an initial placebo period, the effect of enalapril on glucose tolerance, insulin (IRI) sensitivity and lipid profile was evaluated in 20 patients with mild to moderate essential hypertension. The following results were obtained: 1. Enalapril produced a favourable effect of blood pressure both in monotherapy and if combined with a diuretic. 2. Therapy did not lead to significant differences in blood glucose, IRI or IRI/glucose increase at 1 or 2 hours of oral glucose tolerance test either in patients with monotherapy or combination therapy, and with normal or disturbed glucose tolerance, respectively. 3. Serum lipids (total and HDL-cholesterol and triglycerides) did not change significantly in any group of patients.

Adult↗
PubMed1992

[Enalapril in the treatment of nephrogenic hypertension].

In a half-year open clinical study the authors investigated the antihypertensive action of enalapril--an inhibitor of the angiotensin converting enzyme--and its action on renal functions in a group of 11 patients with nephrogenic hypertension. In seven patients monotherapy, using a mean dose of 12 mg, was sufficiently effective. In the remaining four patients treatment was combined with diuretics. It was revealed: that: 1. a significant drop of systolic and diastolic pressure occurred with a concurrent decline of the total peripheral vascular resistance, 2. a slight (statistically not significant) reduction of the glomerular filtration as well as quantitative proteinuria with a decline of glomerular hypertension. 3. In this group of patients without left ventricular hypertrophy no signs of regression of its mass were present. 4. Even in patients with nephrogenic disease no negative effect on the lipid, carbohydrate and purine metabolism was observed. The subjective tolerance of the preparation was very satisfactory.

Adult↗
PubMed1991

[The effect of dipyridamole on hippurate excretion in healthy volunteers and in patients with renal insufficiency].

Organic anions retained in patients with renal failure participate in a substantial way in the metabolic acidosis and thus also the catabolism in renal failure. The basic disorder is the reduced capacity of the transport system of organic ions. Therefore drugs are sought to enhance its activity. Acute investigation of healthy volunteers revealed that 150 mg dipyridamol increased the urinary hippurate excretion, while the serum hippurate concentration declined. In patients with renal failure there is the same tendency, though less marked, and due to the variability of functions of individual patients this trend is insignificant. It is assumed that this hitherto not described action of dipyridamol may be of therapeutic importance when administered to patients with impaired renal function.

Dipyridamole↗
PubMed1991

[The effect of a single administration of magnesium sulfate on glucose tolerance and insulinemia in healthy volunteers].

The effect of 2.0 g magnesium sulfate on glucose tolerance and immunoreactive insulin (IRI) response to glucose application was studied in 10 healthy normomagnesemic volunteers: a) Serum magnesium concentration (Mg) increased markedly and remained on the increased values during the study. Total erythrocyte Mg concentration did not change. b) The infusion application of 40 g glucose increased glykemia which returned promptly to fasting levels after the infusion termination. Mg did not influence the glycemic response. c) IRI concentration increased even more than glucose to the glucose load. Mg decreased the IRI response and even IRI/glucose ratio significantly. In conclusion, Mg increased insulin sensitivity even in healthy normomagnesemic subjects.

Adult↗
PubMed1991

[A decrease in magnesium in the serum and blood lymphocytes after intravenous infusion of glucose].

The authors assessed in a group of 10 healthy volunteers the Mg content of serum, in erythrocytes (Er) and lymphocytes (Ly) before infusion and during three hours after infusion of 400 ml 10% glucose without added Mg and with addition of 10 ml 20% MgSO4 (magnesium sulphate, Spofa). It was revealed that glucose infusion without Mg reduces significantly serum magnesium as well as Mg in lymphocytes and the reduced values persist for at east three hours after termination of the infusion. In 3 of 10 volunteers the values dropped beneath the lower range of reference values; two of these three volunteers developed also clinical manifestations of Mg deficiency. Mg in Er was not affected by the glucose infusion. The glucose infusion with Mg raised significantly the serum Mg and Mg in Ly; Mg in Er did not change. Based on the submitted results the authors recommend prevention of Mg deficiency induced by glucose infusion by Mg supplementation, in particular in patients with cardiovascular diseases.

Adult↗
PubMed1991

Serum hippurate and its excretion in conservatively treated and dialysed patients with chronic renal failure.

54 healthy volunteers or patients with normal kidney and liver function, 17 patients with decreased kidney function and 12 dialysed patients were evaluated for their serum hippurate accumulation and kidney excretion. It was found that there was an inverse relationship between serum hippurate and the clearance of endogenous creatinine (CCr) and a free relationship between fractional excretion of hippurate and CCr. The excretory capacity in residual nephrons was increased. This was caused by the greater glomerular filtration load which increased up to 25 times and tubular secretion which increased 7 times in dialysed patients. The relative contribution of glomerular filtration to hippurate excretion rose from about 20% in controls to almost 50% in dialysed patients. True kidney adaptation was localized in the organic anion transport system of proximal tubules.

Hippurates↗
PubMed1991

[Angiotensin-converting enzyme inhibitors in the diagnosis and treatment of kidney diseases].

The authors describe in a review the use of inhibitors of the angiotensin converting enzyme, in particular enalapril, in the treatment of nephrogenic hypertension, glomerulopathies without hypertension, renovascular hypertension with unilateral or bilateral stenosis of the renal artery and diabetic nephropathy. They draw attention to specific traits in the treatment of different disorders, risk of treatment and the ensuing tactics of indication, dosage and monitoring.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Magnesium deficiency impairs rat soleus muscle glucose utilization and insulin sensitivity.

Insulin resistance (IR), probably a common pathway of atherosclerosis development in various diseases, was suggested to be related to magnesium (Mg) deficiency. The in vivo observations required an in vitro extension. The study was performed on isolated rat soleus muscle incubated in Ringer bicarbonate with/without Mg. Mg deficiency inhibited basal, insulin- and tolbutamide-stimulated glucose utilization. Insulin-stimulated glucose utilization was inhibited even in the case that insulin was given to rats before sacrifice. Similar inhibition of glucose utilization was found in Ca deficiency and the simultaneous lack of Mg had no additive effect. It is concluded that Mg deficiency inhibits glucose utilization at the level of Ca mediation of glucose transport regulation.

Animals↗