Tamm-Horsfall protein updated.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F Kokot.
Explore the source record for details and available documents.
In continuous ambulatory peritoneal dialysis (CAPD) patients, nutritional parameters, appetite, and transperitoneal solute movement can be modified by treatment with amino-acid-based dialysis solution (AADS). Because leptin is involved in energy expenditure and appetite regulation, we decided to examine the influence of AADS on serum and dialysate leptin concentrations. We prospectively evaluated AADS influence on leptinemia and peritoneal transport indices in CAPD patients. Nine clinically stable patients (7 males, 2 females), mean age 55.4 +/- 10.5 years, who had been treated with CAPD for 6.1 +/- 5.8 months, were studied. Examinations were conducted before treatment with 1.1% AADS (period I), after 3 months of AADS administration (period II), after 6 months of AADS administration (period III), and at 3 months after AADS discontinuation (period IV). The primary outcome measure was concentration of leptin in serum and dialysate. Secondary measures included anorexia incidence, nutrient intake, and nutritional parameters. Dialysate-to-plasma ratio (D/P), peritoneal excretion, and clearance (PCl) of leptin were calculated. After 3 months of AADS administration (period II), leptinemia was transiently lower (9.8 +/- 6.2 ng/mL vs 17.1 +/- 14.2 ng/mL, p = 0.017), while D/P (0.51 +/- 0.44 vs 0.23 +/- 0.19, p = 0.012), peritoneal excretion (72.9 +/- 85.4 micrograms/day vs 37.2 +/- 32.3 micrograms/day, p = 0.015), and PCl (4.02 +/- 3.40 mL/min vs 1.75 +/- 1.32 mL/min, p = 0.008) of leptin were higher than measurements obtained at entry. Anorexia incidence and daily protein and energy intakes showed no significant changes during the study. Total body mass, body mass index, and plasma concentrations of total protein and of albumin increased significantly during AADS treatment. A significant positive relation of leptinemia to total fat mass was observed when AADS was not used (periods I and IV). We conclude that administration of AADS in CAPD patients causes a transient decrease in leptinemia and increases in peritoneal excretion and in PCl of leptin, as well as dissociation of the physiological relationship between serum leptin level and total fat mass.
UNLABELLED: In children with celiac disease (CD) bone metabolism and mineralization are frequently disturbed. The present study aimed to assess the influence of gluten free diet (GFD) on bone mineral density (BMD) in 73 children with CD, mean age of 12.4 +/- 0.4 years and mean body mass index (BMI) 17.9 +/- 0.4 kg/m2 (mean +/- SEM). Diagnosis of CD was established according to ESPEGAN criteria. Compliance to the GFD was verified on the basis of interview and by estimation of antiendomysial antibodies (IgAEmA/IgGEmA) in blood serum. BMD was measured by dual energy X-ray absorptiometry (DEXA). Plasma calcium (Ca) and phosphorus (P) concentrations, alkaline phosphatase (AP) and its bone fraction (BAP) were estimated before BMD measurement. All children were divided into two groups. Group A consisted of 33 children where gluten free diet was strictly respected for 11.7 +/- 0.6 years. The second group (Group B) comprised 40 children without strictly respected GFD. Children who strictly followed GFD showed statistically higher BMI, AP-spine BMD and total body BMD in comparison with children without GFD (BMI 19 +/- 0.52 kg/m2 vs 17.3 +/- 0.4 kg/m2; p < 0.01, AP-spine BMD 0.951 +/- 0.04 g/cm2 vs 0.767 + 0.03 g/cm2; p < 0.005, Total Body BMD 1.013 +/- 0.02 g/cm2 vs 0.933 +/- 0.01 g/cm2; p < 0.05) respectively. No significant differences were found in plasma Ca, P, AP, BAP between both groups. A statistically significant positive correlation (p < 0.001) was found between duration of GFD and AP-spine BMD and total body BMD, respectively. A statistically significant positive correlation (p < 0.05) was also found between duration of GFD and BMI. CONCLUSION: Long-term GFD significantly improves BMD and BMI in children with CD.
Explore the source record for details and available documents.
The sugar moiety of Tamm-Horsfall protein (THP) is altered by pathological conditions. The aim of this study was to investigate the composition of THP glycans in urinary diseases. THP was isolated from the urine of patients with urinary tract infection (group A), glomerulonephritis or interstitial nephritis (group B), and Bartter's syndrome (BS) (group C). Monosaccharides, N-glycan profile, THP reactivity with specific lectins and some other proteins were analyzed. THP of patients from groups A, B, and C showed lower amounts of N-acetylgalactosamine (P<0.05, P<0.005, and P<0.05, respectively) than controls; this was reflected in lower reactivity with Phaseolus vulgaris lectin (P<0.005, P<0.05, and P<0.005). Reduced amounts of N-acetylglucosamine were noticed in groups A (P<0. 05) and B (P<0.05). In group A lower amounts of galactose and alpha2, 6-linked sialic acid, as determined by reactivity with Datura stramonium lectin (P<0.005) and Sambucus nigra lectin (P<0.005), were observed. In patients with BS there was a shift from tetrasialylated glycans towards less-sialylated chains. We found also that THP of all patients binds more strongly to IgG(1) (P<0.005, for all patient groups). Our results indicate that the urinary diseases examined affect the THP sugar moiety and the binding of THP to IgG(1).
Insulin stimulates the production of endothelin-1 (ET-1) and nitric oxide (NO) by isolated endothelial cells. Additionally, insulin-dependent glucose transport and insulin-mediated NO production partially share common elements in signal transduction. There are discordant data on plasma ET-1 levels during acute euglycemic systemic hyperinsulinemia in normotensive men and men with essential hypertension (EH) (known to be insulin-resistant), as well as on the relations between insulin sensitivity and vascular function. Our aim was to assess the response of approximate measures of whole-body generation of NO and ET-1 to acute euglycemic hyperinsulinemia in EH patients and controls. We studied 17 newly diagnosed untreated men with uncomplicated EH and 10 normotensive controls. Plasma ET-1 and urinary excretion of nitrite plus nitrate, stable NO metabolites (Uno(x)), were measured before and during a 3-hour hyperinsulinemic-euglycemic clamp. Both in hypertensives and normotensives, plasma ET-1 levels were reduced after 2 hours of the clamp (EH: baseline, 3.1+/-1.9 pg/mL; 2 hours, 1.9+/-1.2 pg/mL, P = .04 v baseline; controls: baseline, 4.2+/-2.6 pg/mL; 2 hours, 2.8+/-1.4 pg/mL, P = .04 v baseline). No significant changes in Uno(x) during the clamp were observed. Changes in Uno(x) during the clamp (deltaUno(x)) and differences in plasma ET-1 measured before the end and before the beginning of the clamp (deltaET-1) were correlated in the controls (r = .75, P = .01) but not in EH (r = -.01, P = .97). No parameter of glucose metabolism correlated with basal Uno(x), basal plasma ET-1, deltaUno(x), and deltaET-1, whether absolute or percent values, in either group. Thus, acute euglycemic hyperinsulinemia produces a decrease in plasma ET-1 in both EH patients and controls. The lack of correlation between deltaUno(x) and deltaET-1 under these conditions in EH may suggest an impairment of systems governing interactions between the NO-dependent pathway and ET-1. In addition, insulin actions on glucose metabolism and on the endothelial mediators appear dissociated.
This paper is a summary of results obtained in our studies on leptinemia in patients with chronic renal failure treated with recombinant human erythropoietin (rHuEPO), in kidney transplant patients, in patients with essential hypertension, and in pregnant women with preeclampsia. In this study, we found that rHuEPO treatment has a suppressive effect on leptinemia in patients with endstage renal failure. These results suggest that the appetite stimulating effect of rHuEPO may be mediated by a reduction of leptin synthesis and release. At the early stage of successful kidney transplantation, a significant decline of leptinemia was noticed, which was not related either to the excretory function of the graft or the kind and dose of immunosuppressants. In kidney transplant patients with grafts functioning well for 2.5 years, significantly elevated leptinemia was found. From these results, we may conclude that factors other than the excretory function of the graft and the kind and dosage of immunosuppressants may be involved in the pathogenesis of abnormal leptinemia in these patients. Both in normotensive subjects and patients with essential hypertension, a positive correlation was found between leptinemia and mean blood pressure, suggesting that leptin may be involved in the regulation of blood pressure. Both healthy and preeclamptic pregnant women show higher leptinemia than nonpregnant women. In preeclamptic women, leptin levels in maternal vein blood, umbilical cord blood, and amniotic fluid were significantly higher than respective values found in healthy pregnant women. In contrast to healthy pregnant and nonpregnant women, in women with preeclampsia, no correlation was found between the body mass index (BMI) and leptinemia. In preeclamptic women the abnormally elevated leptinemia was not related to blood pressure. Finally, no correlation was found between leptinemia in maternal and umbilical cord blood. From these studies, it follows that the elucidation of abnormal leptin secretion in the pathogenesis of preeclampsia needs further study.
Our aim was to investigate systemic nitric oxide (NO) production and its potential determinants such as insulin resistance, dyslipidemia, and circulating methylated analogs of L-arginine in uncomplicated essential hypertension (EH). Nineteen newly diagnosed, untreated male subjects with mild pure uncomplicated EH and 11 normotensive controls were studied at rest after an overnight fast. The groups had comparable age, body mass index, creatinine clearance, cholesterol, fasting glucose, and insulin. In hypertensives, the urinary excretion rate of nitrite plus nitrate (Unox), an index of endogenous NO production, was depressed (56+/-17 vs. 77+/-23 micromol/mmol creatinine; p < 0.05), whereas plasma levels of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthesis, were increased (2.4+/-1.1 vs. 1.1+/-0.7 microM; p < 0.005). Circulating concentrations of symmetric dimethylarginine were similar in both groups (1.4+/-1.3 vs. 1.5+/-1.1 microM; p = NS). The L-arginine-to-ADMA ratio was reduced in hypertension (3.3+/-0.5 vs. 4.5+/-0.8; p < 0.001 for In-transformed data). There was no correlation between Unox and either the magnitude of insulin resistance or dyslipidemia in EH. Thus in male subjects with EH, endogenous systemic NO formation appears depressed, which is unrelated to accompanying insulin resistance or dyslipidemia. Circulating ADMA levels are increased in uncomplicated EH, which may be of potential relevance.
UNLABELLED: Leptin and neuropeptide Y (NPY) seem to play an important role in food intake and energy expenditure. Leptin is secreted by adipose tissue in proportion fo fat stores and is presumed to be an important anorectic hormone. NPY is produced by the hypothalamus, and in contrast to leptin, is one of the most potent appetite stimulants yet demonstrated. On the other hand, in most patients increased appetite is present after successful kidney transplantation. Finally, a stimulatory effect of glucocorticoids on leptin secretion was reported. The present study aimed to assess the relationship between plasma leptin and NPY levels and body mass index (BMI) in haemodialyzed patients (HDP) with chronic renal failure and in kidney transplant patients (KTP). In both groups, BMI was of the same magnitude as in healthy controls. Despite the presence of a normal BMI, leptin levels in KTP (25.2 +/- 3.6 ng/ml) and in HDP with chronic renal failure (25.3 +/- 4.2 ng/ml) were higher than in controls (11.7 +/- 1.8 ng/ml). The mean plasma NPY level in KTP (168.0 +/- 10.3 pg/ml) was significantly higher (p < 0. 01) than in controls (70.7 +/- 5.9 pg/ml) and in HDP (77.0 +/- 5.7 pg/ml). In all examined groups, a significant positive correlation was found between leptinaemia and BMI. CONCLUSIONS: (1) KTP are characterized by significantly elevated leptinaemia in spite of a normal BMI. In KTP this increased leptinaemia does not seem to be dependent only upon the fat mass and the kind and dosis of immunosuppressive therapy. (2) Similarly to healthy subjects, female KTP and HDP show markedly higher leptinaemia than males. (3) In contrast to healthy subjects and HDP, KTP are characterized by significantly elevated plasma NPY levels.
BACKGROUND: Leptin is produced and released by adipocytes in proportion to fat stores. Leptin as an anorectic hormone plays an important role in the regulation of food intake, energy expenditure, and insulin secretion. In contrast, neuropeptide Y, insulin, cortisol, and growth hormone are presumed to be appetite modulators. Leptin and neuropeptide Y are both involved in the activation of sympathetic tone. Increased body fat stores in obese patients are involved in the pathogenesis of some metabolic disorders (e.g., hyperinsulinaemia, glucose intolerance) and arterial hypertension. METHODS AND RESULTS: Based on this pathophysiological background, we tried to assess the relationship between plasma leptin and blood pressure in 41 patients with essential hypertension (EHP; 20 females, 21 males, mean age 38.7+/-1.9 years, mean body mass index - BMI - 25.8+/-0.5 kg/m2) and in an appropriately sex- and BMI-matched control group of 27 normotensive healthy subjects (NHS; 11 females, 16 males, mean age 39.7+/-2.5 years, mean BMI 24.8+/-0.6 kg/m2). The plasma leptin concentration did not differ significantly between EHP and NHS (13.0+/-1.9 vs. 8.1+/-1.0 ng/ml, respectively). In both groups a significant positive correlation was found between BMI and plasma leptin concentration (p<0.0001). A significant positive correlation (p<0.02) was found between leptinaemia and mean (MAP), systolic and diastolic blood pressures, if data were analyzed for all examined subjects or separately only for women. Such a correlation could not be confirmed for male NHS and EHP subjects. The plasma neuropeptide Y concentration was higher in EHP than in NHS (77.1+/-23.0 vs. 63.6+/-9.8pg/ml, p = 0.05). In contrast to neuropeptide Y plasma insulin, cortisol, and growth hormone concentrations were similar in EHP and in NHS. CONCLUSION: Both EHP and NHS are characterized by a positive correlation between BMI and leptinaemia. Leptin may be indirectly involved in blood pressure regulation, especially in women of both NHS and EHP.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In this paper a female patient with severe acute intermittent porphyria is presented in whom routine pharmacological treatment was unsuccessful. After five haemodialysis sessions a dramatic improvement of the clinical status was observed in spite of markedly elevated urinary excretion of porphyrin metabolites. Further studies are mandatory in order to evaluate the effectiveness of acute intermittent porphyria treatment.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
UNLABELLED: Leptin (LP) and neuropeptide Y (NPY) are involved in the regulation of appetite and energy expenditure. As was shown in our previous studies healthy non pregnant and pregnant women are characterized by a significant positive correlation between maternal body mass index (BMI) and plasma leptin concentration. On the other side participation of both leptin and obesity in the pathogenesis of essential hypertension is presumed. The present study aimed to answer the following question: to what extend LP and NPY are involved in the pathogenesis of arterial hypertension in pregnant women with EPH gestosis. One to 2 days before delivery plasma LP and NPY concentration were estimated in 43 healthy pregnant women, in 18 pregnant women with EPH gestosis and in 26 healthy non pregnant women. In pregnant women with EPH gestosis, mean arterial blood pressure (MAP) (114.6 +/- 1.3 mm Hg) and mean leptinaemia (21.9 +/- 8.5 ng/ml) were significantly higher than in healthy pregnant women (89.1 +/- 0.9 mm Hg and 15.0 +/- 1.3 ng/ml respectively) and in non pregnant women (MAP--91.56 +/- 1.4 mm HG i LP--10.9 +/- 1.7 ng/ml). In healthy pregnant women, in women with EPH gestosis and in healthy nonpregnant women plasma NPY concentrations were of similar magnitude (42.3 +/- 4.1 vs 43.7 +/- 8.5 vs 50.7 +/- 6.1 pg/ml respectively). In pregnant women with EPH gestosis a significant positive correlation was found between diastolic blood pressure or MAP and plasma NPY concentration. Leptinaemia was significantly correlated with systolic, diastolic and MAP respectively only when results obtained in both groups of pregnant women were analyzed together. CONCLUSIONS: 1) leptin seems to be involved in the regulation of blood pressure both in healthy and preeclamptic pregnant women, 2) participation of NPY in the pathogenesis of hypertension in preeclamptic women is likely.
UNLABELLED: Ultrafiltration during haemodialysis (HD) may be the cause of blood pressure (BP) decline due to reduction of blood volume. In some patients, however, BP does not decrease or even rises during HD. The aim of the study was to answer the question: do uraemic hypertensive patients, showing a decline of mean blood pressure (MAP) during HD session (group A) differ from those showing a stable MAP during HD session (group B) with respect to hormonal profile of aldosterone (ALD), vasopressin (AVP), atrial natriuretic peptide (ANP), endothelin-1,2 (ET-1,2), blood nitric oxide (NO) and plasma renin activity (PRA). A total of 39 haemodialysed, hypertensive patients (17 female, 22 men) were studied. 24 patients (group A) showed a MAP decline of 10 mm Hg or more, while 15 patients (group B) showed MAP changes of less than +/- 10 mm Hg during HD session. PRA, ALD, AVP, ANP, ET-1,2, NO concentration were assessed in blood samples withdrawn from the arterial blood line before HD and after 60, 120, 180 and 240 minutes of HD session. Plasma ET-1,2 and blood NO concentration were also assessed after 30 minutes of HD. BV was continuously monitored with a Crit-Line equipment, BP was measured before and every 30 minutes on HD. Before HD session both examined groups showed similar baseline plasma levels of ALD, AVP, ANP, ET-1,2, NO, PRA and MAP. A 4-hours HD induced a significant increase in plasma ALD and AVP concentrations and a significant decline in ANP level in both groups of patients. In group A, PRA and blood NO concentration increased significantly, while plasma ET-1,2, level did not change during HD. In group B, no significant changes in PRA and blood NO level were noticed, while plasma ET-1,2 rose markedly. In addition in group B, a significant positive correlation was found between MAP and plasma ET-1,2 level changes, but a significant negative correlation between MAP and blood NO level changes. CONCLUSION: Patients with a decline of MAP over 10 mm Hg during HD differ from those with a stable MAP by a different response of plasma ET and blood NO to HD induced volume changes.
Anemia is a common complication of chronic renal failure (CRF). With the availability of recombinant human erythropoietin (rhEPO) over the last decade, much progress has been made in the management of anemia in patients with end-stage renal disease (ESRD) [Eschbach 1995, Gimenez and Scheel 1994, Muirhead et al. 1995, Winearls 1995]. The clearest benefit of rhEPO in ESRD is a substantial reduction in transfusion dependency, which reduces the need for hospital admission and the risk of viral transmission. Improvements in hemostasis and a decrease in human leucocyte antigen (HLA) antibodies have also been reported. Beneficial effects of rhEPO on the cardiovascular system in ESRD include regression of left ventricular hypertrophy (LVH), improvement of angina, and a modest increase in aerobic work capacity. Treatment of anemia with rhEPO has also been shown to improve cognitive function, socialization and quality of life in dialysis patients, although this has not led to better vocational rehabilitation or employment status. It has also been reported that a lower hemoglobin (Hb) content is an independent risk factor for increased mortality in hemodialysis patients [Harnett et al. 1995]. Clearly, therefore, treatment of anemia associated with ESRD is required and beneficial. The optimum treatment of anemia prior to dialysis, however, is still a matter for debate.