Plasma catecholamines, neuropeptide Y and leucine-enkephalin in uremic patients before and after dialysis during rest and handgrip.

UNLABELLED: We have studied the effects of handgrip on plasma levels of catecholamines, neuropeptide Y (NPY), and leu-enkephalin before and after hemodialysis of uremic patients. A cuprophan dialyzer was used. We found, that dopamine level was higher in uremia group before hemodialysis both during rest (0.38 +/- 0.39 pmol/ml) and handgrip (1.13 +/- 1.00 pmol/ml) compared to control (0.17 +/- 0.19, and 0.66 +/- 0.83 pmol/ml respectively). Hemodialysis leads to further increase of its level (0.49 +/- 0.35 pmol/ml) at rest. Epinephrine level was almost the same in uremic patients before (0.43 +/- 0.51 pmol/ml) and after dialysis (0.46 +/- 0.60) as in control subjects (0.41 +/- 0.37 pmol/ml) during the rest. Its level measured after the handgrip was the highest in uremic group after dialysis (2.10 +/- 2.00 pmol/ml), significantly lower before dialysis (1.26 +/- 0.85 pmol/ml), and the lowest in control group (0.78 +/- 0.43 pmol/ml). Norepinephrine level were very similar in uremic group before dialysis (1.54 +/- 1.05 pmol/ml), after dialysis (1.79 +/- 1.29 pmol/ml) and in control group (1.46 +/- 1.06 pmol/ml) during the rest. During the handgrip test its level was higher in uremic group after hemodialysis than before it (adequate values 8.78 +/- 4.61 and 6.70 +/- 4.74 pmol/ml). The difference between uremia group before dialysis and control group did not reach significance. The level of NPY has the tendency to increase in uremic patients. Dialysis leads to following increase of its level, but the changes did not reach the significance both in rest and handgrip. Leu-enkephalin level was higher in uremic group (9.21 +/- 7.62 pmol/ml) compared to control (5.22 +/- 1.53 pmol/ml). We observed non-significant fall of this level after dialysis (6.79 +/- 4.76 pmol/ml). We found the same tendency during the handgrip, and the changes were significant. IN CONCLUSION: uremia per se leads to increase the level of dopamine and leu-enkephaline during the rest and handgrip, but the level of epinephrine only during the handgrip; dialysis leads to further increase of dopamine during the rest, but epinephrine, norepinephrine and leu-enkephaline only during the handgrip.

[The values of selected lipid parameters and atrial pressure in persons with hyperinsulinemia and normal glucose tolerance]. / Wartosci wybranych parametrów gospodarki lipidowej i cisnienia tetniczego u osób z hiperinsulinemia i prawidlowa tolerancja weglowodanów.

In 60 healthy non-obese persons we determined fasting plasma insulin concentrations. Afterwards we performed test with oral load with 75 g glucose. We determined plasma concentration of insulin one hour and two hours after this load; we found that 14 of 60 subjects had hyperinsulinemia with normal glucose tolerance. In the group of persons with hyperinsulinaemia we have shown the increase of fasting plasma triglyceride levels and elevated diastolic blood pressure. We suggested that healthy persons with hyperinsulinemia and normal glucose tolerance have an increase risk for cardiovascular diseases.

Nifedipine reverses the abnormalities in [Ca2+]i and proliferation of B cells from dialysis patients.

Both animals and patients with chronic renal failure have impaired B cell function due, in part, to elevated levels of cytosolic calcium ([Ca2+]i). Treatment of HD patients with nifedipine has normalized [Ca2+]i of their polymorphonuclear leukocytes (PMNL) and caused marked improvement in the phagocytic property of the PMNL. This observation may have important clinical implications if this drug exerts a similar effect on other cells such as B cells. We examined [Ca2+]i, proliferation of B cells in response to mitogen, the magnitude of the PTH-induced inhibition of B cell proliferation, and the ATP content of mononuclear cells in 11 hemodialysis patients treated with nifedipine, 12 patients without nifedipine therapy and 11 normal subjects. Serum levels of IgG was also measured in the two groups of patients. There were no significant differences in the age, duration of hemodialysis, blood levels of calcium, phosphorus or PTH (571 +/- 193 vs. 484 +/- 127 pg/ml) among the two groups of patients. The hemodialysis patients without nifedipine therapy compared to those without nifedipine treatment have significantly (P < 0.01) higher levels of [Ca2+]i (120 +/- 1.9 nM vs. 94 +/- 2.2 nM), lower ATP content of mononuclear cells (0.45 +/- 0.06 nmol/10(6) cells vs. 0.68 +/- 0.04 nmoles/10(6) cells), impaired proliferation (5.8 +/- 0.31 x 10(3) cpm vs. 9.8 +/- 0.38 x 10(3) cpm) and smaller inhibition of B cell proliferation by PTH compared to those treated with nifedipine. The values in the patients treated with nifedipine were still modestly but significantly different than in normal subjects. The serum IgG levels of the patients without nifedipine therapy (1210 +/- 71 mg/dl) were significantly lower than those of the patients treated with nifedipine (1594 +/- 81 mg/dl). Thus, the treatment of hemodialysis patients with nifedipine produced marked and significant improvement in the metabolic and functional parameters of B cells despite no changes in blood levels of PTH. These data indicate that the calcium channel blocker, nifedipine, interferes with PTH-induced rise in [Ca2+]i of B cells of hemodialysis patients and consequently improves their metabolism and function. These observations if confirmed in other human cells may provide for a rational therapeutic approach to ameliorate the signs and symptoms of uremia.

Pharmacokinetics of theophylline in obesity.

Pharmacokinetic analysis of theophylline was performed in 16 obese women before and after 3-week weight-reducing treatment. Decrease of clearance, increase of t1/2, AUC, and MRT were observed. There were no differences between the volume of distribution before and after weight-reducing treatment. Our results suggest that ideal body weight should be used to calculate a loading dose of theophylline for obese patients; weight-reducing treatment may be connected with changes in biotransformation and elimination of theophylline more than with its distribution.

Abnormalities in hepatic lipase in chronic renal failure: role of excess parathyroid hormone.

Post-heparin hepatic lipase activity is reduced in chronic renal failure (CRF). This could be due to reduced synthesis, decreased activity, and/or impaired secretion of the enzyme. Further, the factor(s) responsible for such derangements are not elucidated. We examined hepatic lipase metabolism in normal, 6-wk-old CRF rats, CRF-PTX (parathyroidectomized) rats, and CRF and normal rats treated with verapamil (CRF-V, normal-V) using liver homogenate, hepatic cell culture for 8 h, and in vitro liver perfusion. The Vmax of hepatic lipase in liver homogenate was significantly (P < 0.01) reduced and the Km was significantly (P < 0.01) increased in CRF rats, but the values were normal in CRF-PTX, CRF-V, and normal-V rats. Culture of hepatic cells for 8 h was associated with an increase in hepatic lipase activity but the increment in CRF rats was significantly (P < 0.01) lower than that of normal, CRF-PTX, CRF-V, and normal-V rats. Both parathyroid hormone (PTH)-(1-84) and 1-34 inhibited the production of hepatic lipase in cultured cells from normal, CRF-PTX, CRF-V, and normal-V rats. The expression of the mRNA of the hepatic lipase was significantly reduced in CRF animals with the ratio between it and that of house keeping gene G3DPH being 15 +/-3% compared to 40 +/- 1.3% in normal, 44+/-2.9% CRF-PTX, 44 +/- 5.4% in CRF-V, and 39 +/- 3.9% in normal-V rats. Infusion of heparin to the in vitro hepatic perfusion system increased the activity of hepatic lipase in the effluent in all groups of rat except in CRF animals. Infusion of PTH-(1-34) in dose of 10(-6) M into the liver perfusion system inhibited the increase in post-heparin hepatic lipase activity. The data show that in CRF (a) the mRNA of hepatic lipase is downregulated, and hepatic lipase production, activity and release are impaired, (b) that this is due to the state of secondary hyperparathyroidism of CRF since both acute and chronic excess of PTH were associated with these abnormalities, (c) and that prevention of excess PTH by PTX of CRF rats or blocking the effect of PTH by treatment with verapamil corrected the derangement in hepatic lipase metabolism.

Effects of parathyroid hormone on hepatocyte pHi and Na(+)-H+ exchanger activity.

Parathyroid hormone (PTH) induces a rise in cytosolic calcium--[Ca2+]i--in many cells. A rise in [Ca2+]i activates the Na(+)-H+ antiport, but PTH inhibits the Na(+)-H+ exchanger in kidney cells. Since PTH induces a rise in [Ca2+]i of hepatocytes, we examined the effect of PTH on their Na(+)-H+ antiport and intracellular pH(pHi). PTH caused an initial activation of Na(+)-H+ exchanger, and this stimulation is amiloride sensitive. The activation of the Na(+)-H+ exchanger was followed by progressive inhibition. This inhibitory effect was dose dependent and occurred over a wide range of external sodium concentrations. PTH also caused a progressive rise in hepatocyte pHi which became apparent after the initial activation of the Na(+)-H+ antiport. This alkalinization of hepatocytes occurred when the cells were placed in sodium or potassium media. These actions of PTH were mimicked by dibutyryl cyclic AMP and 12-o-tetradecanoylphorbol-13-acetate(TPA) and were abolished by H-89 (an inhibitor of protein kinase A), staurosporine (an inhibitor of protein kinase C), and the calcium channel blockers verapamil or nifedipine. The data are consistent with the formulation that PTH, through the activation of the cAMP-protein kinase A pathway, protein kinase C, and calcium channels inhibitable by verapamil or nifedipine, induces a rise in [Ca2+]i of hepatocytes. The latter event causes an initial activation of Na(+)-H+ antiport which is followed by a rise in pHi. Also, PTH may facilitate a Ca2+/2H+ exchange across the hepatocyte membrane and causes an initial and persistent rise in pHi, since the rise in pHi occurred under conditions where Na(+)-H+ antiport is inactive (potassium media). In addition, PTH either directly or through activation of second messenger(s) leads to an increased ammonia content of hepatocytes which could maintain a high pHi. Consequently, the Na(+)-H+ antiport is inhibited in an effort to restore the pHi back to normal.

Polymorphonuclear leukocytes in non-insulin-dependent diabetes mellitus: abnormalities in metabolism and function.

OBJECTIVE: To determine basal levels of cytosolic calcium ([Ca2+]i) and phagocytic activity in polymorphonuclear leukocytes (PMNLs) from patients with non-insulin-dependent diabetes (NIDDM). DESIGN: Prospective cohort study. SETTING: A university-county hospital. MEASUREMENTS: Cytosolic calcium levels, adenosine triphosphate (ATP) content, and phagocytosis of PMNLs from patients with NIDDM and from controls. INTERVENTION: In patients with NIDDM, we evaluated the effect of treatment with an oral hypoglycemic agent (glyburide) on [Ca2+]i levels, ATP content, and the phagocytosis of PMNLs. PATIENTS: 22 controls and 34 patients with NIDDM were examined. Fifteen patients were studied before and after 3 months of treatment with glyburide. RESULTS: Polymorphonuclear leukocytes from patients with NIDDM showed significantly elevated basal levels of [Ca2+]i (68 +/- 9.6 compared with 43 +/- 4.9 nmol/L; P < 0.01); reduced ATP content (1.30 +/- 0.58 compared with 2.35 +/- 0.45 nmol/10(6) PMNLs; P < 0.01); and impaired phagocytosis (117 +/- 21.0 compared with 145 +/- 17.4 micrograms oil/10(7) PMNLs per minute; P < 0.01) compared with controls. There was a direct and significant correlation (P < 0.01, r = 0.80) between [Ca2+]i levels in PMNLs and serum glucose levels and an inverse correlation between phagocytic ability and [Ca2+]i levels (P < 0.01; r = 0.62) as well as between phagocytic activity and fasting serum glucose levels (P < 0.01, r = 0.54) in patients with NIDDM. Glyburide therapy resulted in significant reduction in fasting serum glucose levels; in PMNLs, this treatment resulted in a significant reduction in [Ca2+]i levels, a significant increase in ATP content, and a significant improvement of phagocytosis. CONCLUSIONS: Patients with NIDDM have elevated [Ca2+]i levels in PMNLs. This abnormality is probably induced by hyperglycemia and is primarily responsible for the imparied phagocytosis seen in these patients.

Impaired agonist-induced calcium signaling in hepatocytes from chronic renal failure rats.

Some hormones exert their action by inducing a rise in cytosolic calcium [Ca2+]i (calcium signal), and therefore, a blunting in hormone-induced calcium signal would engender resistance to the action of the hormone. Chronic renal failure (CRF) is associated with resistance to the action of a variety of hormones, a rise in [Ca2+]i and decrease in the amount of mRNA of one hormone receptor, the PTH-PTHrP receptor. We examined the calcium-signal induced by PTH, angiotensin II, vasopressin and glucagon in hepatocytes from CRF animals, evaluated the effect of the basal level [Ca2+]i on the calcium signal and explored the effect of [Ca2+]i on the mRNA of the receptors of these agonists. Hepatocytes from CRF rats have elevated basal levels of [Ca2+]i and display significantly reduced calcium signals induced by all these hormones, while the calcium signals were normal in PTX-CRF animals and those treated with verapamil both of which have normal levels of [Ca2+]i despite CRF. The calcium signals induced by dibutyryl cyclic AMP and G protein activator (GTP gamma S) were normal in hepatocytes from CRF animals despite the high levels of [Ca2+]i. Northern blotting experiments revealed that the levels of the mRNA of the receptors of PTH-PTHrP, angiotensin II and vasopressin were significantly reduced in hepatocytes from CRF animals but PTX-CRF rats and those treated with verapamil had either significantly greater or even normal amounts of the mRNA of these receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic renal failure increases cytosolic Ca2+ of hepatocytes.

Chronic renal failure (CRF) is associated with increased Ca2+ content of liver and reduced hepatic lipase activity. This has been attributed to a rise in cytosolic Ca2+ ([Ca2+]i) of the hepatocytes, but data on this issue are lacking. We examined the [Ca2+]i and ATP content of hepatocytes as well as the activity of Na(+)-K(+)-adenosinetriphosphatase (Na(+)-K(+)-ATPase), Ca(2+)-ATPase, and Na+/Ca2+ exchanger of hepatic membrane vesicles from normal rats, animals with 6 wk of CRF, CRF normocalcemic parathyroidectomized (CRF-PTX) rats, and CRF and normal animals treated with verapamil (CRF-V, normal-V). [Ca2+]i in hepatocytes of CRF rats was higher (281 +/- 7.4 nM) and ATP lower (6.4 +/- 1.8 nmol/mg protein) than in normal (209 +/- 5.3 nM; 12.5 +/- 0.89 nmol/mg protein), CRF-PTX (212 +/- 1.0 nM; 13.7 +/- 0.79 nmol/mg protein), normal-V (215 +/- 2.3 nM; 14.2 +/- 0.77 nmol/mg protein), and CRF-V rats (209 +/- 7.4 nM; 14.8 +/- 0.72 nmol/10(6) cells). The Na(+)-K(+)-ATPase, the maximal velocity of Ca(2+)-ATPase, and the activity of the Na+/Ca2+ exchanger were reduced, whereas the Michaelis constant of Ca(2+)-ATPase was increase in CRF rats compared with the other four groups of rats. The values in the latter groups were not different.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of treatment of hemodialysis patients with nifedipine on metabolism and function of polymorphonuclear leukocytes.

Both animals and patients with chronic renal failure have impaired phagocytosis, which is most likely due to elevated basal levels of cytosolic calcium ([Ca2+]i) and reduced adenosine triphosphate (ATP) content of their polymorphonuclear leukocytes (PMNLs). In animals with chronic renal failure, these derangements are prevented or reversed by their treatment with a calcium channel blocker. This observation may have important clinical implications if these drugs exert a similar effect in humans with chronic renal failure. We examined the basal levels [Ca2+]i, ATP content, and phagocytosis in PMNLs from 11 normal subjects, 18 hemodialysis patients (seven of whom had diabetes mellitus), and 18 hemodialysis patients treated with nifedipine (eight of whom had diabetes mellitus). The basal levels of the [Ca2+]i content of the PMNLs in hemodialysis patients without nifedipine therapy were significantly (P < 0.01) elevated (nondiabetic patients, 77 +/- 3.2 nmol/L; diabetic patients, 75 +/- 1.9 nmol/L) compared with normal values (42 +/- 0.9 nmol/L). Treatment with nifedipine was associated with the return of [Ca2+]i toward normal values in both the nondiabetic (51 +/- 4.5 nmol/L) and diabetic (54 +/- 2.5 nmol/L) hemodialysis patients. The ATP content of PMNLs from hemodialysis patient was significantly (P < 0.01) reduced compared with normal, and nifedipine therapy restored the ATP content to normal values. Phagocytosis was significantly (P < 0.01) impaired in hemodialysis patients (nondiabetic patients, 78 +/- 4.0 micrograms oil/10(7) PMNLs/min; diabetic patients, 77 +/- 4.8 micrograms oil/10(7) PMNLs/min). Nifedipine therapy returned the impaired phagocytosis toward normal (nondiabetic patients, 133 +/- 2.5 micrograms oil/10(7) PMNLs/min; diabetic patients, 129 +/- 6.4 micrograms oil/10(7) PMNLs/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of captopril and thiorphan on the proliferation of human neoplastic cell lines and their influence on cytostatic activity of interferon alpha or cytotoxic activity of doxorubicin.

We have assessed the effect of thiorphan or captopril on proliferation of two human tumor cell lines, A549 and HL60 including their influence on the cytostatic activity of interferon alpha or doxorubicin. The results showed that captopril inhibits the proliferation of both A549 and HL60 cells lines but thiorphan has antiproliferative effect only on A549 cells in a dose-dependent manner. However, neither captopril nor thiorphan administered in combination with interferon alpha or doxorubicin enhanced cytotoxic potential of doxorubicin and cytostatic activity of interferon alpha.

[The effect of short-term erythropoietin therapy on selected parameters of cell mediated and humoral immunity in hemodialyzed uremic patients]. / Wplyw krótkotrwalego leczenia erytropoetyna na zachowanie sie wybranych parametrów odpornosci komórkowozaleznej i humoralnej u hemodializowanych chorych na mocznice.

This study aimed to assess the influence of short-term therapy with recombinant human erythropoietin (rhEPO) on selected parameters of humoral and cell mediated immunity in haemodialyzed uraemic patients (HDP). In 12 HDP before, and after 1 and 3 months of rhEPO therapy the following parameters were assessed: nitroblue tetrazolium (NBT) test, NBT test after latex stimulation, number of B, T and CD4 and CD4- and CD8-positive T lymphocytes, serum concentrations of IgG, IgA and IgM. The number of granulocytes with a positive NBT test was significantly higher after 3 months of rhEPO therapy. The number of granulocytes with a positive NBT test after latex stimulation increase both after 1 and 3 months of rhEPO therapy but significantly only after 3 months of treatment. The number of CD4-positive T lymphocytes increased significantly after 3 months of rhEPO therapy, while the number of CD8-positive lymphocytes decreased significantly after 1 month of therapy. The CD4/CD8 ratio increased significantly after 3 months of rhEPO therapy. Serum IgA concentration increased significantly after 1 and 3 months, while serum IgG level only after 3 months of rhEPO therapy. From the results obtained in this study it follows that rhEPO therapy exerts a positive effect on function of both T and B lymphocytes in haemodialyzed uraemic patients.

Leucine enkephalin level in rat hypothalamus, striatum, hippocampus and adrenal glands in experimental rat uremia.

The aim of the study was to analyze the effect of experimental uremia elicited in Wistar rats by 5/6 kidney resection on the leu-enkephalin level in hypothalamus, striatum, hippocampus and adrenal glands. We found, that in uremic rats leu-enkephalin levels decreased in striatum and in adrenal glands. The level of leu-enkephalin in adrenal glands was directly related to plasma creatinine. The weight of uremic rats was significantly lower than that of control rats.

Mechanisms of PTH-induced rise in cytosolic calcium in adult rat hepatocytes.

Available data indicate that the liver is a target organ for parathyroid hormone (PTH) and that this effect is most likely mediated by PTH-induced calcium entry into hepatocytes. The present study examined the effects of both PTH-(1-84) and its amino-terminal fragment [PTH-(1-34)] on cytosolic calcium concentration ([Ca2+]i) of hepatocytes and explored the cellular pathways that mediate this potential action of PTH. Both moieties of PTH produced a dose-dependent rise in [Ca2+]i, but the effect of PTH-(1-84) was greater (P < 0.01) than an equimolar amount of PTH-(1-34). This effect required calcium in the medium and was totally [PTH-(1-34)] or partially [PTH-(1-84)] blocked by PTH antagonist ([Nle8,18,Tyr34]bPTH-(7-34)-NH2] and by verapamil or nifedipine. Sodium or chloride channel blockers did not modify this effect. 12-O-tetradecanoylphorbol 13-acetate (TPA), an activator of protein kinase C, dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), and G protein activator also produced a dose-dependent rise in [Ca2+]i. Staurosporine abolished the effect of TPA, and both staurosporine and calphostin C partially inhibited the effect of PTH. Staurosporine and verapamil together produced greater inhibition of PTH action than each alone. Rp-cAMP, a competitive inhibitor of cAMP binding to the R subunit of protein kinase A, and N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89), a protein kinase A inhibitor, blocked the effect of both DBcAMP and PTH, but the effect of these agents was greater (P < 0.01) on DBcAMP action. G protein inhibitor and pertussis toxin partially blocked the action of PTH. The data indicate that 1) PTH increases [Ca2+]i of hepatocytes; 2) this action of the hormone is receptor mediated; 3) the predominant pathway for this PTH action is the stimulation of a G protein-adenylate cyclase-cAMP system, which then leads to stimulation of a calcium transport system inhibitable by verapamil or nifedipine or activation of L-type calcium channels; 4) activation of protein kinase C is also involved; and 5) the PTH-induced rise in [Ca2+]i is due, in major parts, to movement of extracellular calcium into the cell.

[Natural history of allergic reactions to Hymenoptera insect bites]. / Historia naturalna odczynów alergicznych wywolywanych uzadleniami owadów blonkoskrzydlych.

In 30 patients suffering from systemic allergic reactions following Hymenoptera insect bites risk factors have been evaluated. Life-style, place of living, patients' age, sex and the presence of atopy have been considered. Moreover, the clinical course and value of the intracutaneous quantitative tests have been analysed and their value in both the diagnosis and prognosis of the said reactions have been assessed. Significant correlation between the results of quantitative diagnostic tests and severity of the hypersensitivity to insect poison has been found. A phenomena of the spontaneous diminished skin reactions has been noted. It has been found that only an individual analysis of the natural history might be a base for the choice of appropriate therapy.

[Correlation between symptoms and results of rhinomanometric measurements of nasal patency in patients with seasonal allergic rhinitis]. / Zwiazek miedzy samopoczuciem a wynikami rinomanometrycznych pomiarów droznosci nosa u chorych na sezonowy niezyt nosa.

The aim of presented study were to assess the usefulness of rhinomanometry in monitoring course of disease and effectivity of treatment in seasonal allergic rhinitis (SAR) through answering the question whether and eventually which relationship exists between patient's general feeling and results of rhinomanometric measurements of nasal patency (NP). The study involved 114 subjects with SAR divided into 3 groups dependent on phase of disease and severity of complaints and 30 healthy volunteers. For results see table I. Nasal flow and resistance measured at differential pressure 75 Pa in groups I, III and IV did not differ significantly. In group II nasal flow values were lower (alpha < 0.001) and resistance values higher (alpha < 0.001) as compared with remaining groups. Thus, the beginning of symptoms is related to lowering of NP as compared with symptom-free phase of SAR. In the symptom-free period NP do not differ from healthy population. The results of rhinomanometric measurements of NP are useful in monitoring of course of SAR in assessment of effectivity of treatment.

[Testing the efficacy of fluconazole in treatment of oral and throat candidiasis in patients after kidney transplantation]. / Badania skutecznosci flukonazolu w leczeniu kandydozy blon sluzowych jamy ustnej i gardla u chorych po przeszczepieniu nerki.

Eleven kidney transplant recipients with the oral or/and throat candidiasis which occurred during the first 3 months after transplantation were studied. Fluconazole was administered orally in the dose of 50 mg each 24, 48, 72 h, according to creatinine clearance. No clinical symptoms of candidiasis on the third day of the treatment were observed. In all patients, negative mucosal cultures were noted at the 8th day after first fluconazole dose. During fluconazole was with in normal range. Furthermore, no changes in serum bilirubin alanine transaminase, lactate dehydrogenase and alkaline phosphatase activities were observed. Serum creatinine decreased during this follow-up. In the 30th day after fluconazole administration cessation the mycological evidence of Candida p. reinfection were noted in 25% of patients. Fluconazole is highly efficient and safe agent to manage the oral and throat candidiasis in renal transplant recipients.