Semen quality in men with chronic kidney disease and its correlation with chronic kidney disease stages.

The aim of this study was to assess whether chronic kidney disease (CKD) has any impact on semen quality parameters in men with CKD stage 1-5. Results were collected from 66 men with different CKD stages (age 18-50 years). Age and BMI (body mass index) were recorded for each male. Higher CKD stage had a significant negative linear trend on semen volume (P < 0.05), progressive motility (P < 0.01), nonprogressive motility (P < 0.001), sperm concentration (P < 0.01), total sperm number (P < 0.01), cytoplasmic droplets (P < 0.01), teratozoospermia index (P < 0.05) and accessory gland markers, α-glucosidase activity (P < 0.05), zinc (P < 0.01) and fructose (P < 0.01). BMI per se had no significant effect on semen volume, sperm number, sperm concentration, morphology, α-glucosidase activity, fructose concentration or zinc level. A significant negative correlation between BMI and sexual-hormone-binding globulin (SHBG) (P < 0.01) was observed but not with other sex hormones. Age per se was related to a significant decrease of sperm concentration (P < 0.05), normal forms (P < 0.01) and testosterone level (P < 0.05). Our results indicate that CKD stage per se is a factor determining the number of spermatozoa available in the epididymis for ejaculation, in part independent of age-related decrease of testosterone level and BMI.

Enhanced FGFR signalling predisposes pancreatic cancer to the effect of a potent FGFR inhibitor in preclinical models.

BACKGROUND: Fibroblast growth factor receptor (FGFR) signalling has been implicated in pancreas carcinogenesis. We investigated the effect of FGFR inhibition in pancreatic cancer in complementary cancer models derived from cell lines and patient-derived primary tumour explants. METHODS: The effects of FGFR signalling inhibition in pancreatic cancer were evaluated using anti-FRS2 shRNA and dovitinib. Pancreatic cancers with varying sensitivity to dovitinib were evaluated to determine potential predictive biomarkers of efficacy. Primary pancreatic explants with opposite extreme of biomarker expression were selected from 13 tumours for in vivo dovitinib treatment. RESULTS: Treatment with anti-FRS2 shRNA induced significant in vitro cell kill in pancreatic cancer cells. Dovitinib treatment achieved similar effects and was mediated by Akt/Mcl-1 signalling in sensitive cells. Dovitinib efficacy correlated with FRS2 phosphorylation status, FGFR2 mRNA level and FGFR2 IIIb expression but not phosphorylation status of VEGFR2 and PDGFRß. Using FGFR2 mRNA level, a proof-of-concept study using primary pancreatic cancer explants correctly identified the tumours' sensitivity to dovitinib. CONCLUSION: Inhibiting FGFR signalling using shRNA and dovitinib achieved significant anti-cancer cancer effects in pancreatic cancer. The effect was more pronounced in FGFR2 IIIb overexpressing pancreatic cancer that may be dependent on aberrant stimulation by stromal-derived FGF ligands.

Increased accumulation of CD16+ monocytes at local sites of inflammation in patients with chronic kidney disease.

Patients with chronic kidney disease (CKD) display a high prevalence of cardiovascular events and acute infections. Potential effector cells are the CD16(+) monocytes, known to be increased in the peripheral circulation in CKD. The aim of this study was to assess the expression of CD16 and CX3 CR1 on peripheral and in vivo extravasated monocytes in patients with CKD (GFR < 20 ml/min × 1.73 m²) using flow cytometry. In vivo extravasated monocytes were collected from a local inflammatory site, induced by a skin blistering technique. Soluble markers were assessed by Luminex. The number of CD16(+) monocytes was significantly higher in patients with CKD compared with healthy subjects, both in the peripheral circulation (P < 0.05) and at the site of induced inflammation (P < 0.001). Patients with CKD displayed significantly higher concentration of soluble CX3 CL1 both in the peripheral circulation (P < 0.01) and in the interstitial fluid (P < 0.001). In addition, patients with CKD had a significantly higher concentration of TNF-α in the peripheral circulation (P < 0.001). On the contrary, at the inflammatory site, concentrations of both TNF-α and IL-10 were significantly lower in patients with CKD compared with healthy controls (P < 0.05 for both). In conclusion, patients with CKD have an increased percentage of CD16(+) monocytes in both circulation and at the inflammatory site, and this finding is in concurrence with simultaneous changes in CX3 CR1. Together with distorted TNF-α and IL-10 levels, this may have potential impact on the altered inflammatory response in CKD.

Recombinant CD40 ligand therapy has significant antitumor effects on CD40-positive ovarian tumor xenografts grown in SCID mice and demonstrates an augmented effect with cisplatin.

CD40 is a member of the tumor necrosis factor receptor family and was first identified with a monoclonal antibody raised against bladder carcinoma. Recombinant human CD40L has been shown previously to have a direct antitumor effect on an ovarian cancer cell line and ovarian carcinoma cells isolated from ascites fluid. We show here that rhuCD40L inhibits the growth of several ovarian adenocarcinomas derived from surgical specimens and grown as xenografts in severe combined immunodeficient mice. Two 14-day treatment cycles were more effective than one. This effect is apparently not mediated by natural killer cells, because blocking natural killer cell activity by antiasialo GM-1 did not diminish this effect. In addition to suppression of tumor growth, treatment with rhuCD40L resulted in an increased expression of FasL, an increase in apoptosis, and histological changes including increased fibrosis and areas of tumor destruction. Using this model, we examined the efficacy of rhuCD40L in combination with chemotherapeutic agents. The antitumor effect of rhuCD40L in combination with 4 mg/kg cisplatin (CDDP) was increased over the effect of CDDP alone. Furthermore, rhuCD40L increased the efficacy of a suboptimal dose of CDDP (2mg/kg) such that it matched that of high-dose CDDP alone. These data suggest a role for rhuCD40L therapy in combination with platinum based regimens for primary treatment of epithelial ovarian tumors.

Therapeutic and metabolic effects of sotalol.

In a single-blind, randomized study, the cardiovascular and metabolic effects of sotalol, 40 to 160 mg/day, in six patients with mild essential hypertension were compared to those of placebo at rest and during submaximal dynamic exercise. Resting blood pressure was controlled by sotalol but not the pressor response to exercise, despite reduction of tachycardia. The major metabolic finding on sotalol was an approximately 40% decrease in lipid mobilization during exercise. Alterations in muscle lactate concentrations were much like those caused by other beta-blockers. Plasma concentrations of norepinephrine and epinephrine were doubled during exercise on sotalol, epinephrine disposition more so. No effects on serum lipoproteins were observed after 6 wk on sotalol in therapeutic doses. Despite its special electrophysiologic properties, sotalol appears to induce the same cardiovascular and metabolic changes during exercise as do other beta-blockers.

A dietary fibre supplement in the treatment of mild hypertension. A randomized, double-blind, placebo-controlled trial.

OBJECTIVE: To study the effects of a dietary fibre supplement given as monotherapy upon blood pressure in mildly hypertensive patients. DESIGN: The investigation was performed as a prospective randomized, double-blind, placebo-controlled trial for 3 months. SETTING: Patients attending an outpatient hypertension clinic in a hospital. PATIENTS: Hypertensive patients with a minimum of two diastolic blood pressure (DBP) readings greater than 90 mmHg during a 2-week run-in period were included. Of the 65 patients enrolled, 63 were randomized (32 fibre, 31 placebo). Six patients did not complete the trial. INTERVENTION: Patients were treated with either fibre (7 g/day) or matching placebo. MAIN OUTCOME MEASURE: Based on previous studies, the a priori hypothesis was that dietary fibre supplementation could reduce blood pressure in hypertensive patients. RESULTS: Body weight was significantly reduced in the fibre group. Dietary fibre significantly reduced DBP and fasting serum insulin. However, no correlation between changes in body weight and systolic blood pressure or DBP was found. CONCLUSION: A dietary fibre supplement can lower DBP in mildly hypertensive patients independent of changes in body weight.

Effect of beta 1-selective and nonselective beta blockade on blood pressure relative to physical performance in men with systemic hypertension.

Eleven physically active men with systemic hypertension were studied after 5 weeks of treatment with placebo, atenolol or propranolol. A double-blind, crossover randomized design was used. Blood pressure (BP), heart rate (HR), physical performance capacity, rate of perceived exertion and blood lactate concentrations were measured during rest, exercise to exhaustion and postexercise, at 8 and 24 hours after intake of the last dose. Blood pressure at rest and during exercise was similarly decreased with both drugs (8 and 24 hours), and there was no difference between 8 and 24 hours with any of the treatments. Heart rate (8 hours) was decreased similarly by both drugs, but after 24 hours, HR at increased workloads (above 120 watts) was higher with atenolol compared with propranolol. Maximal HR was lower with propranolol than atenolol at both 8 and 24 hours. Maximal exercise loads (8 and 24 hours) were 231 and 232 watts with placebo, 211 and 212 with propranolol and 228 and 227 with atenolol. That is, maximal workload was decreased with propranolol compared with placebo and atenolol at both 8 and 24 hours. No difference was found between placebo and atenolol at either 8 or 24 hours. The rate of perceived exertion values were higher with propranolol than atenolol. Blood lactate concentrations did not differ according to treatments. The results indicate that atenolol, when given in a dose that decreases resting and exercise BP to the same extent as propranolol, limits physical performance less than propranolol.

Typing of coagulase-negative staphylococci from peritonitis in CAPD-patients by the PhP-CS system and REA.

Coagulase-negative staphylococci (CNS) were the most common bacteria causing peritonitis in patients treated with continuous ambulatory peritoneal dialysis (CAPD). In order to investigate if the same clone was responsible for the peritonitis in the different patients and if the exit site was the source of infection we followed 68 patients on CAPD for 2 years. During this period 9 patients had 12 episodes of peritonitis caused by CNS. Cultures were taken from exit site and peritoneal fluid in all patients at peritonitis and during the first study year at monthly intervals. In each culture up to 10 isolates of CNS were randomly collected and frozen. All 437 CNS isolates from the patients with CNS peritonitis were typed using a biochemical typing method and 41 isolates identical by this method were further discriminated by a DNA fingerprinting method. Identical strains were in no case isolated from different patients, indicating that no virulent strain was spread between the patients. The isolates causing the peritonitis were never found at the exist sites before the first day of the peritonitis in any patient. In only two patients was the same strain found at the exit site and in the peritoneal fluid on the first day of peritonitis. It thus seems that no virulent clone of CNS was infecting the patients and we found no evidence of CNS at the exit site causing the peritonitis.

Prognostic factors and treatment of severe ethylene glycol intoxication.

OBJECTIVE: Analysis of prognostic factors and treatment of a large epidemic of ethylene glycol intoxication. DESIGN: Retrospective case review comparing 16 survivors with 6 patients who died. SETTING: Cooperative study between county hospitals, a university hospital, and a poison information centre. PATIENTS AND PARTICIPANTS: Survival review of 36 serious cases and chart review of 17 cases. INTERVENTION: Time to initial treatment with intravenous fluids, sodium, bicarbonate, ethanol, and dialysis. MEASUREMENTS: Clinical data at admission and blood chemistry at 0, 24, 48, and 72 h. RESULTS: 6 of 36 patients (17%) died; 11 of 17 patients whose charts were reviewed survived and 3 had chronic renal failure. All but 2 patients had acute renal failure. Neither delay to admission, intravenous dialysis, HCO3 or alcohol was related to outcome. At admission more patients who subsequently died had seizures, were comatose, were more acidotic, and had lower base excess and higher potassium levels than those who survived. Urine contained oxalate crystals in 10 of 14 cases. At 24 h the potassium level was higher and the base excess lower in those who died. Blood ethylene glycol levels for the patients who died and survived were no different. All survivors were dialyzed, but 2 patients who died had no dialysis. No survivor needed chronic dialysis and none had organic brain lesions. CONCLUSION: In patients with severe ethylene glycol intoxication, severe acidosis, hyperkalemia, seizures, and coma at admission carry a dismal prognosis. We believe very large amounts of intravenous HCO3 should be used immediately for rapid correction of the metabolic acidosis. Intravenous ethanol and hemodialysis should be started early and continued until acidosis is corrected.

The distribution and localization of hsp110 in brain.

Hsp110 is one of the few, major heat shock proteins of mammalian cells and was one of the earliest heat shock proteins described. However, it has only recently been cloned and studied at the molecular level. It has been noted that of all tissues examined, brain expresses the highest level of hsp110, with expression levels in unstressed brain being similar to the levels seen in heat shocked cells. The present report describes a combined Northern and Western blot analysis of hsp110 expression in various regions of mouse and human brain. These observations are further expanded by an immunohistochemical characterization of hsp110 cellular localization in mouse brain. It is seen that although hsp110 is an abundant protein in most regions of the brain, its expression is heterogeneous, with little being detectable in the cerebellum. Within the cerebral hemispheres, hsp110 is present in neurons in all regions including the cerebral cortex, the hippocampus, the thalamus and the hypothalamus. In contrast, in the cerebellum, the Purkinje cells are the major hsp110 containing cells while the more abundant granule cells show little if any hsp110 labeling. Since hsp110 has been shown to protect cells and proteins from thermal damage, this differential pattern of expression may have ramifications in the pathophysiology of brain, specifically involving cerebellar sequelae.

Intralipid removal from plasma of uraemic and intensive care patients.

The removal rates from plasma of Intralipid and (125)I-albumin, simultaneously injected i.v., were analyzed in 10 chronic renal failure (CRF) patients. The results were compared with 9 intensive care unit (ICU) patients and five healthy subjects as controls. The fractional removal rates of Intralipid (k2) were significantly lower for the CRF patients compared to both ICU patients and healthy subjects. The initial plasma concentration of Intralipid, calculated by extrapolation of the elimination curve back to zero-time (y0), showed significantly higher values for CRF patients and healthy subjects compared to ICU patients. Removal curves expressed as ratios between Intralipid and (125)I-albumin paralleled the elimination curves for Intralipid, which suggests that the slope of the curves depends on Intralipid removal and not on leakage of macromolecules from the circulation. The very low initial plasma concentration of Intralipid in the ICU patients cannot be explained by a hyperdynamic circulation, but may be attributed to a rapid first passage disappearance of Intralipid from plasma into tissues such as the pulmonary vasculature.

Lipolytic and circulatory responses to noradrenaline infusion in hypothyroid subjects before and during thyroxine substitution.

The hypothyroid state in humans is associated with a diminished lipolytic response to noradrenaline in adipose tissue in vitro. In the present study we have investigated the situation in vivo in order to see if such a change in receptor response could be demonstrated in adipose tissue and in the circulatory system. The change in glycerol production rate, induced by an infusion of noradrenaline, was used as an index of adipose tissue adrenergic responsiveness. The results showed that the lipolytic response was decreased by about 50% in the hypothyroid state and that it was normalized when the substitution dose had been increased to 0.10-0.15 mg/day thyroxine. The circulatory response was monitored by measurements of blood pressure and pulse rate. The resting diastolic pressure was transiently lowered by substitution. Similarly the rise in systolic blood pressure induced by l-noradrenaline was transiently increased by substitution. Thus no clear-cut change in receptor response with substitution could be demonstrated by measuring BP and pulse rate only. This result could be due to the fact that the system is more complex than the adipose tissue. The finding of a reduced adrenergic receptor response in vivo in the adipose tissue is in accordance and extends earlier findings in vitro.

Taste acuity in patients with chronic renal failure.

Taste acuity for the four primary tastes has previously been shown to be impaired in patients with chronic renal failure (CRF) and maintenance dialysis treatment, although data on CAPD (continuous ambulatory peritoneal dialysis) patients are insufficient. In a test group of 57 CRF patients and 57 healthy controls, matched for age, sex and body mass index (BMI, kg/m2) taste acuity for the four primary tastes was determined. Fourteen patients were on CAPD treatment and 12 patients on hemodialysis (HD). No patients or controls were diabetic, on antibiotic treatment or had a malignant disease. Taste tests were standardized and performed on dialysis-free days for HD-patients. Taste acuity for bitter and salt was significantly lower for preuremic patients compared to their controls. In CAPD-patients taste detection of bitter was impaired and in HD-patients detection of salty taste was impaired. In conclusion taste acuity is impaired in uremic patients and dialysis patients including CAPD. The mechanism for taste alterations remain to be explained.

Granulocyte stimulating factor in patients on peritoneal dialysis and LPS stimulated peripheral blood mononuclear cells.

Dialysate and serum levels of granulocyte-colony stimulating factor (G-CSF), granulocyte macrophage colony stimulating factor (GM-CSF) and leukemia inhibitory factor (LIF) were analyzed in patients with continuous ambulatory peritoneal dialysis (CAPD). Samples from the peritoneal effluent and from serum were obtained during the first months of dialysis and during peritonitis from the first three dialysate bags drained on the day of admittance and form nightbags on days three and ten. Serum samples were drawn on days one and ten. On the first day of infection G-CSF was detected in twelve out of fifteen samples in the dialysate and reached its peak median level, 443 pg/ml, in the first drained bag and thereafter decreased significantly. Also in serum a peak, 190 pg/ml, was observed on the first day. LIF was found in six of ten analyzed dialysate samples, with a peak median level of 77 pg/ml on day one, while only four of ten patients had detectable GM-CSF. Peripheral blood mononuclear cells from non-infected CAPD patients were stimulated with lipopolysaccharide and G-CSF levels in the supernatants increased significantly (P < 0.05) after 6 h stimulation. We conclude that G-CSF is produced locally in the dialysate during the acute stage of peritonitis and to a lesser extent also systemically. These findings are in line with G-CSF production after LPS stimulation of peripheral blood mononuclear cells.

Increased levels of transforming growth factor beta 1 and basic fibroblast growth factor in patients on CAPD: a study during non-infected steady state and peritonitis.

Long-term influence of continuous ambulatory peritoneal dialysis (CAPD) on concentrations of transforming growth factor beta1 (TGF-beta1) and basic fibroblast growth factor (bFGF) in the peritoneal effluent, and the effect of peritonitis on these cytokines were investigated. TGF-beta1 and bFGF were assayed in effluent samples from dialysate bags collected during the initial week of treatment with CAPD and at 5 months. To determine the effect of peritonitis, dialysate bags were collected on admission to the hospital and on days 3 and 10 and also during non-infected steady state. Serum was drawn prior to infection and on days 1 and 10. TGF-beta1 increased more than threefold during the longitudinal follow-up period, median concentrations of 35 pg/ml to 106 pg/ml (P<0.05). No change in bFGF was seen during this initial 5 months. TGF-beta1 was increased on the first day of peritonitis (median concentration 169 pg/ml) and reached its maximum on day 3 of infection, (median concentration 216 pg/ml) (P<0.05 vs non-infected state, median concentration 39 pg/ml). Basic FGF reached a maximum on day three of infection (median concentration 7.7 pg/ml; P=0.01 vs non-infected state) and then slowly declined. In conclusion, TGF-beta1 is influenced by CAPD treatment per se, and together with bFGF is increased during peritonitis, indicating its importance in the peritoneum and its potential involvement in the development of tissue fibrosis and eventually ultrafiltration failure.

Increased expression of CD25 and HLA-DR on lymphocytes recruited into the peritoneal cavity in non-infected CAPD patients.

The impact of uremia per se, peritoneal dialysis (PD) and hemodialysis (HD) treatment was evaluated on characteristics of lymphocytes. CD4, CD8, CD25 and HLA-DR were analyzed, with flow cytometry, in lymphocytes prepared from peripheral blood of uremic (n = 10) and hemodialysis patients (n = 10). Peritoneal dialysate was also obtained from patients on CAPD (n = 12). A decreased relative and absolute lymphocyte count was observed in peripheral blood from uremic, HD and CAPD patients compared to healthy controls (p < 0.03, p < 0.03 and p < 0.02, respectively). On the other hand, the relative distribution of lymphocytes was significantly higher in peritoneal dialysate compared to peripheral blood of CAPD patients (p < 0.02). Likewise, the absolute CD4 positive lymphocyte count was lower in the peripheral blood from uremic. HD and CAPD patients as compared to healthy controls (p < 0.001, respectively). In CAPD patients the relative distribution of CD4 positive cells (p < 0.001) was lower, while quantitative CD25 level (p < 0.01) and the relative count of HLA-DR (p < 0.0001) was increased in the peritoneal dialysate compared to blood. Taken together a selective activation of lymphocytes in peritoneal dialysate as compared to peripheral blood from uremic, HD and CAPD patients was observed. The altered biological function of the inflammatory cells may therefore explain the increased susceptibility to infectious diseases.

Difference in the blood monocyte phenotype between uremic patients and healthy controls: its relation to monocyte differentiation into macrophages in the peritoneal cavity.

The phenotypic alterations between blood monocytes from 11 patients with end-stage renal disease, who had been on peritoneal dialysis for less than one week, and blood monocytes from 10 healthy controls, were analyzed. In addition, peritoneal macrophages in the dialysate effluent were enclosed. Analysis of functional receptor density was performed using immunostaining and flow cytometry. The phenotypic characterization was selected to represent various biological functions such as adhesion, phagocytosis (CD11b/CD18, CD11c/CD18, CD16), antigen-presentation (HLA-DR, ICAM-1), differentiation (transferrin receptor, CD71), receptor for LPS (CD14) and initiation of the coagulation cascade (Tissue factor, CD142). The proportion of CD16-positive blood monocytes and the quantitative level of ICAM-1 were higher in the patient group, compared to healthy controls. A significant increase in the quantitative level of CD11b/CD18, CD11c/CD18, HLA-DR and ICAM-1, transferrin receptor, CD14 and CD16, was found on peritoneal macrophages, compared to monocytes, harvested both from the corresponding patients, as well as from healthy donors. In contrast, we did not find any significant differences in the expression of tissue factor between monocytes and peritoneal macrophages. In conclusion, phenotypic differences exist between monocyte populations in the blood circulation of CAPD patients, and healthy individuals. We also show that transmigration of monocytes into the peritoneal cavity implies a selective up-regulation of functional receptors, preferentially related to adhesion, and antigen-presentation in a steady-state situation in non-infected CAPD patients.

The cardiovascular response at rest and during exercise in hypothyroid subjects to thyroxine substitution.

Rapid and intense thyroxine substitution can lead to heart failure and myocardial infarction in hypothyroid patients. We have analyzed the normalization of the circulatory system in hypothyroid subjects on a gradual thyroxine substitution. Fourteen hypothyroid patients were studied repeatedly with an orthostatic test and a standardized symptom-limited exercise test during substitution. ST and T abnormalities were observed in 51 and 33%, respectively, before substitution. Many of these changes were normalized upon substitution at a dose level of 0.15 mg/d thyroxine. The pulse reaction to standing was enhanced early during substitution. The capacity to perform work, on the other hand, responded more slowly to thyroxine substitution, and was significantly increased only after six months of full substitution. This difference in the time course of recovery may be of clinical importance when substituting patients with hypothyroidism and ischemic heart disease.

Interleukin-10, interferon gamma, interleukin-2, and soluble interleukin-2 receptor alpha detected during peritonitis in the dialysate and serum of patients on continuous ambulatory peritoneal dialysis.

OBJECTIVE: To analyze interleukin (IL)-10, interferon gamma (IFN-gamma), IL-2, and soluble IL-2 receptor alpha (sIL-2R alpha) in the dialysate and serum of patients on continuous ambulatory peritoneal dialysis (CAPD). DESIGN AND PATIENTS: Samples from dialysate bags were collected during the initial month of dialysis. During peritonitis, samples were collected from the first three bags on the day of admittance to the hospital and from the night bags on days 3 and 10. Serum samples were drawn on days 1 and 10. RESULTS: IL-10 was detected in all dialysate samples except one on the first day of infection, with a peak median level of 50 pg/mL and a slow decrease thereafter. In serum the median levels never exceeded detectable levels. Patients infected with Escherichia coli or Staphylococcus aureus had higher IL-10 levels in dialysate on day 3 as compared to the remaining patients (p < 0.05). If the catheter had to be drawn, because of persistent cloudy dialysate, the IL-10 levels remained elevated for a longer time (p < 0.05). IFN-gamma and IL-2 were detected only in the dialysate of patients infected with either S. aureus or S. epidermidis. Only one serum sample showed increased IFN-gamma. SIL-2R alpha was found in all the serum and dialysis samples from the first day of infection. Contrary to the analyzed cytokines, the receptor showed severalfold higher levels in serum as compared to the dialysate. During the infection the receptor levels in the dialysate increased, while they remained stationary in the serum, indicating a local production. CONCLUSION: This is the first time IL-10 has been demonstrated in the dialysate during peritonitis in CAPD patients. In view of its role as a suppressor of the immune and inflammatory responses, it is a potentially important observation, which might have clinical implications in the future.

Phenotypic alterations of recruited eosinophils in peritoneal fluid eosinophilia.

OBJECTIVE: To characterize eosinophils and soluble factors in effluent from continuous ambulatory peritoneal dialysis (CAPD) patients and connect these findings to related conditions with eosinophilic accumulation. PATIENTS: Three newly started CAPD patients, two with peritoneal fluid eosinophilia (PFE) and one with bacteria-induced peritonitis. One patient with PFE was followed up for 10 visits during a 7-month period. METHODS: Leukocytes were analyzed in dialysate and peripheral blood from the patients, by flow cytometry, and soluble mediators by ELISA or CAP technique. RESULTS: We found an increased number of neutrophils in the effluent from the patient with bacteria-induced peritonitis; accumulation of eosinophils in combination with negative cultures was noted in the patients with PFE. Increased levels of interleukin (IL)-5 and eosinophil cationic protein, but equal levels of eotaxin, were found in effluent from the PFE patients compared to the patient with neutrophilia. Peritoneal fluid eosinophils were activated by means of EG2, CD11b, CD9, and CD69 expression. Compared to blood eosinophils, the cytokine receptors for IL-5 and granulocyte-macrophage colony-stimulating factor, but not IL-3, were down regulated. CONCLUSION: The finding of activated eosinophils in combination with IL-5 and eotaxin in PFE indicates existing similarities between PFE and conditions found during recruitment of eosinophils in allergic inflammatory responses.