Pacemaker infection with propionibacterium and a nephritic sediment.

Like any other implanted foreign body, the different parts of pacemakers (pulse generator pocket, epicardial or transvenous leads) can become infected. Staphylococcus aureus and coagulase-negative staphylococci are the causative organisms in most of the cases (65 â 75%), propionibacterium is described to be involved in only 1% of cases. This report describes a case of nephritic sediment in a young female patient with a pacemaker implantation 9 years ago because of a third degree atrioventricular block, in which a battery exchange was necessary 2.5 years ago. This young patient was referred from a nephrologist for renal biopsy because of a nephritic sediment and diffuse complaints including low-grade fever with a suspected underlying autoimmune disease. The laboratory examinations were all negative with the exception of a diminished C3 complement level. Blood cultures were positive for propionibacterium, but the microbiologists were considering it as a contamination. 11 more blood cultures collected thereafter were all positive and a transesophageal ultrasound revealed a small vegetation at 1 of the transvenous electrodes of the pacemaker. Because of a penicillin allergy she was treated with clindamycin, and the blood cultures were negative after a few days. After a full course (7 weeks) of antibiotic treatment the C3 complement level normalized and a series of 10 blood cultures remained negative 10 â 15 days after discontinuation of antibiotic therapy. Discussing all the differential diagnoses of a nephritic sediment combined with hypocomplementemia, positive blood cultures and a vegetation on a pacemaker electrode in the transesophageal ultrasound, the diagnosis of an immune complex glomerulonephritis due to a propionibacterium pacemaker infection needs no confirmation by renal biopsy.

New facts about encapsulating peritoneal sclerosis as a sequel of long-term peritoneal dialysis - what can we do?

A long lasting peritoneal dialysis (PD) leads to a special disease, so-called encapsulating peritoneal sclerosis (EPS). The hallmarks of the latter stages of the disease are intestinal obstructions and, as a consequence, malnourishment. For the precise diagnosis radiology and pathology are essential. (Triad ''typical clinical picture- typical radiology- typical pathology''.) In the middle of the pathological process of EPS is proliferative fibrosis and sclerosis of the peritoneum that subsequently leads to the assembly of the typical ''cocoon'' and obstruction. In EPS we found in the peritoneum increased amounts of vascular endothelial growth factor (VEGF) fitting the hallmark of increased neoangiogenesis and blood exudates with fibrinous matrix on the peritoneum as a feeding ground for proliferation of fibroblasts. Additionally, the number of mast cells in EPS is decreased and therefore the chymase and other fibrinolytic enzymes. The ''plasma-leak'' hypothesis focuses on fibrin and our findings help to explain most of the pathophysiology. Since the mortality of EPS is still high, emphasis should be laid on preventive treatment. Since glucose and advanced glycation endproducts (AGEs), including glucose degradation products (GDPs), are responsible for fibrosis and sclerosis of the peritoneum, biocompatible peritoneal dialysis solutions with reduced amounts of AGEs and GDPs are recommended. Additionally, a careful monitoring of patients, especially after 5-8 years of PD is very important. In case of the first signs of EPS, cessation of the modality is necessary. Thanks to this approach, most end-stage EPS pictures can be avoided.

Hepatic expression of galectin-3 and receptor for advanced glycation end products in patients with liver disease.

BACKGROUND: Advanced glycation end products (AGEs) are a heterogeneous group of glycosylated proteins (of which carboxymethyl-lysine (CML) is the most common) which accumulate during ageing processes and play an important role in the pathogenesis of a variety of chronic diseases. Impaired hepatic function might result in elevated levels of AGEs, as the liver represents the major site of AGE metabolism. The actions of AGEs are mediated by various receptors, among which the AGE-receptor complex (including galectin-3 as an essential part) is thought to have a cytoprotective effect, and receptor for advanced glycation end product (RAGE) a cytotoxic effect. AIM: To assess the relationship between CML and expression of galectin-3 and RAGE in different histological structures in biopsy specimens from patients with varying degrees of liver impairment. METHOD: Immunohistochemical staining of 164 biopsies from patients with varying degrees of liver impairment was performed to determine the levels of CML, galectin-3 and RAGE in hepatocytes, Kupffer cells and bile ducts by a semiquantative score. RESULTS: Independent of diagnosis, CML and RAGEs were detected in hepatocytes, whereas galectin-3 was present only in hepatocytes of cirrhotics. By contrast, CML and galectin-3 were highly expressed in Kupffer cells (well correlating levels, highest scores in cholestasis) whereas expression of RAGEs was not significant. All three assessed biochemical markers showed their highest levels of expression/detection in bile ducts. CONCLUSION: These findings indicate an increased susceptibility of hepatocytes to the detrimental effects of AGEs and underline the protective function of Kupffer cells. Furthermore, the biliary system seems to play an important role in the disposition of AGEs.

[Disturbances in volume and electrolytes with intestinal and kidney diseases]. / Volumen- und Elektrolytstörungen bei Darm- und Nierenerkrankungen.

The intestines and kidney are the most important excretion organs. Both organ systems are key players in keeping the homeostatic balance regarding hydration and electrolytes. Disturbances of function can lead to enormous and sometimes life-threatening complications. Intestinal diseases lead often to diarrhoea, which can be associated with fluid loss of up to 20 l per day. The accompanying electrolyte disturbances can be hypo- or hypernatremia in combination with hypokalemia. The therapy is substitution guided by knowledge of the pathophysiology. Kidney diseases lead to excessive volume and electrolyte balances, depending on the underlying molecular or pathological defect, but deficiencies can also be found. In case of kidney impairment with 30-50% total loss of function, calcium and phosphate metabolism is impaired.

[Untreated homocystinuria in adulthood]. / Unbehandelte Homocystinurie im Erwachsenenalter.

HISTORY: Pronounced osteoporosis was discovered in a 44-year-old man presenting with an herniated intervertebral disk. He reported severe myopia, incomplete dislocation of the lenses and retinal detachment. He did not know of any thrombembolic events in the past. On physical examination Marfan-like appearance and a funnel chest were noted. Because of these findings Marfan syndrome was suspected. INVESTIGATIONS: Considering the findings of the x-rays, homocystinuria was suspected as a cause of osteoporosis, despite apparently normal cognitive functions. This diagnosis was confirmed by greatly increased values of serum homocysteine and a positive test for urinary homocystine. Since methionine and homocystine were both elevated, the diagnosis of cystathionin-beta-synthase deficiency was established. DIAGNOSIS, TREATMENT AND COURSE: After taking folate and vitamin B6, the homocysteine level decreased moderately. Betaine and subsequently vitamin B12 were added. Homocysteine values declined markedly on this therapeutic regimen. Two years later the patient was admitted again because of atypical angina. Coronary heart disease could be excluded by coronary angiography. CONCLUSION: Diagnosis of premature osteoporosis should prompt consideration of homocystinuria even in adults. Premature arteriosclerosis, thrombembolic diseases, dislocation of the lens and retinal detachment may give further clues.

Sustaining continuous ambulatory peritoneal dialysis after herniotomy.

Controversy still exists as to whether peritoneal dialysis (PD) treatment can be safely continued after herniotomy. Many nephrologists withhold PD treatment for several weeks after herniotomy for fear of dialysate leakage and hernia recurrence. Here, we report on 9 patients (2 women, 7 men) in whom herniotomy was performed for umbilical (n = 3), inguinal (n = 5), or cicatricial hernia (n = 2), or for open processus vaginalis (n = 2). Surgery was performed according to the Lichtenstein method with insertion of a polypropylene mesh and ligation of the hernia sac. In all patients, PD treatment was paused for the day of surgery and for 1-3 days postoperatively, depending on residual renal function. Over the next several days, low-volume (1.0-1.5 L), high-frequency (6 per day) exchanges were started. The patient's original PD regimen was gradually reinstated over the next 2-4 weeks. All patients recovered rapidly, with no uremia or dialysis-related complications. Particularly, no leakage and no hernia recurrence could be observed 3 months thereafter. None of the patients had to be hemodialyzed intercurrently. In conclusion, continuing a modified regimen of CAPD treatment after herniotomy seems to be safe, with excellent patient comfort.

Containers for waste causing peritonitis in CAPD patients.

Fungal infection is a rare cause of peritonitis in patients on chronic peritoneal dialysis. In this population, fungi are found in less than 2 percent of all cases of primary episodes of peritonitis (1). More often, a primary bacterial peritonitis treated with antibiotic therapy leads to secondary fungal infection (2). Candida species cause 74.5% of the episodes of fungal peritonitis (2). The fungi invade the peritoneal cavity from the skin peri- or intraluminally through the catheter (3). Filamentous fungi are rare (4,5). Treatment of fungal peritonitis commonly consists of removal of catheter and antifungal drugs (3). Here we describe two cases of fungal peritonitis caused by mycelial fungi, where the source of the microorganism could be special containers used for biological waste, which are popular in Germany

Stimulated IFNgamma and IL-10 secretion of blood mononuclear cells in patients on renal replacement therapies show different secretion patterns.

Infection is still a leading cause of morbidity and mortality in patients on renal replacement therapy (RRT). Although the role of the immune system is of great importance, little is known about the influence of the mode of RRT to the preferential excretions of regulator cytokines of mononuclear cells. Therefore, we investigated the stimulated IFNgamma (Th1) and IL-10 (Th2) secretions of mononuclear cells from patients on RRT. Blood was drawn from 10 controls, 15 patients on hemodialysis (HD), 15 on peritoneal dialysis (PD), and 10 after kidney transplantation (Tx). The cells were separated, and phytohemagglutinine (PHA) was added for stimulation. After 0, 6, and 24 h, IFNgamma and IL-10 (pg/ml) were measured by enzyme-linked immunosorbent assay. IFNgamma secretion was significantly enhanced 6 (p < 0.001) and 24 h (p = 0.002) after stimulation in all groups (in mean +/- SEM). The analysis of the subgroups 6 h after adding PHA showed significant differences (p = 0.0239) with the lowest IFNgamma in Tx (16 +/- 5) and the highest in PD (79 +/- 30). For IL-10, secretion was enhanced in all groups 6 h after stimulation (p < 0.0116). The lowest secretions were seen in HD (18 +/- 8) and controls (27 +/- 9); the highest secretions were in Tx (98 +/- 20) and PD (57 +/- 12). The differences between HD and Tx (p < 0.01) and HD versus PD (p = 0.05) were significant. The stimulated cytokine secretion of blood mononuclear cells is preserved with RRT. The modes of RRT could influence the pattern of cytokine secretion. Surprisingly, the cells from patients on PD showed enhanced IL-10 secretion compared to HD. Presumably, this is due to the chronic contact of peritoneal dialysis fluids with monocytes and the lymphatic system in PD.

A new lactate-based, plasticizer-free, neutral peritoneal dialysis fluid provided in a two-compartment system: effect on peripheral leukocyte function.

BACKGROUND: A new neutral peritoneal dialysis fluid (PDF; Balance) provided in a two-compartment bag (pH 7.4, no plasticizers, minimal glucose degradation products - GDP) was investigated in comparison with a neutral control (Hanks' balanced salt solution with gelatin 0.1%) and other PDFs with standard properties and plasticizers (Andy plus, pH 5.2, GDP), plasticizer free (stay safe, pH 5.2, GDP), and in addition plasticizer free after sterile filtration instead of heat sterilization (pH 5.2) regarding the function of peripheral blood leukocytes. METHODS: Blood was drawn from 12 volunteers, and blood monocytes (MN) and polymorphonuclear leukocytes (PMNL) were collected. The cells were incubated for 30 min in control medium and the PDFs: glucose 1.5% (83 mmol/l) and 4.25% (238 mmol/l). Respiratory burst of cells was evaluated by chemiluminescence and superoxide (SO) generation after stimulation with phorbol myristate acetate. RESULTS: In comparison with the control medium, incubation of MN in the two-compartment PDF showed preservation of respiratory burst. In contrast, the incubation of MN in standard PDF and plasticizer-free PDF showed impaired functions. The same was found for PMNL. SO anion measurement in MN and PMNL after incubation in the new two-compartment PDF also showed preservation of cell function in comparison with the control medium. The incubation of PMNL in standard PDF and plasticizer-free PDF with a high glucose content showed depressed SO anion generation. CONCLUSIONS: These in vitro data demonstrate a better preservation of in vitro phagocyte function with adaptation of pH and reduction of glucose, GDP, and plasticizers in PDFs. The best results are achieved with the two-compartment, lactate-based neutral PDF.

Influence of plasticizer-free CAPD bags and tubings on serum, urine, and dialysate levels of phthalic acid esters in CAPD patients.

OBJECTIVES: To evaluate the impact of a plasticizer-free device on exposure to di-(2-ethylhexyl) phthalate (DEHP) and its major metabolites in patients on continuous ambulatory peritoneal dialysis (CAPD). DEHP is the most commonly used plasticizer in polyvinyl chloride (PVC) products; it is added to CAPD bags in order to improve the flexibility of the material. Since DEHP leaches out of the plastic matrix, patients on CAPD are exposed to considerable amounts of DEHP and its metabolites. DESIGN: A prospective cross-over study. SETTING: Department of nephrology in a teaching hospital. PARTICIPANTS: Six patients (4 female, 2 male) stable on peritoneal dialysis (PD) for at least 6 months. INTERVENTIONS: Patients were switched from a plasticizer-containing PVC CAPD system (A.N.D.Y. Plus, Fresenius Medical Care, Bad Homburg, Germany) to a polyolefine-made plasticizer-free system (stay-safe, Fresenius). MAIN OUTCOME MEASURES: Prior to and 42 days after the switch, 24-hour effluent dialysate and urine collections were performed and 10 mL blood was drawn. Concentrations of DEHP, mono-(2-ethylhexyl) phthalate (MEHP), phthalic acid (PA), and 2-ethylhexanol (2-EH) in urine, dialysate, and serum were determined using gas chromatography/mass spectrometry. RESULTS: Complete data were obtained from 5 patients. Serum levels of PA decreased significantly during the study period (0.137 +/- 0.078 mg/L vs 0.124 +/- 0.049 mg/L, p = 0.04), and the respective levels of DEHP decreased insignificantly (0.097 +/- 0.076 mg/L vs 0.069 +/- 0.046 mg/L, p = 0.07), whereas the concentrations of MEHP and 2-EH remained unchanged. Urine concentrations of PA were high (0.81 +/- 0.69 mg/L) but did not change substantially (0.70 +/- 0.50 mg/L). Effluent dialysate concentrations of MEHP and PA decreased significantly (0.0176 +/- 0.004 mg/L vs 0.0040 +/- 0.0007 mg/L, p = 0.043 and 0.158 +/- 0.056 mg/L vs 0.111 +/- 0.051 mg/L, p = 0.043, respectively). CONCLUSIONS: Although PD patients seem to be exposed to other sources of phthalates in addition to dialysis, use of plasticizer-free devices may help to reduce potentially immunosuppressive exposure to phthalate esters.

Phthalic acid is the main metabolite of the plasticizer di(2-ethylhexyl) phthalate in peritoneal dialysis patients.

Di(2-ethylhexyl) phthalate (DEHP) is the most commonly used plasticizer in polyvinyl chloride (PVC) plastics, and is therefore a major constituent of continuous ambulatory peritoneal dialysis (CAPD) bags. Because DEHP is not chemically bound, it leaches out of the plastic matrix. Recently, we found that leukocyte function in vitro is impaired by a mixture of metabolites of DEHP. In the present study, we investigated the metabolism of DEHP in patients on CAPD. The study group consisted of 10 stable patients, on CAPD for at least 6 months, using a plasticizer-containing PVC PD system [ANDY Plus (Fresenius Medical Care, Bad Homburg, Germany)]. Effluent dialysate and urine samples were collected over 24 hours, and a 10 mL blood sample was drawn. Concentrations of DEHP and its metabolites mono(2-ethylhexyl) phthalate (MEHP), phthalic acid (PA), and 2-ethylhexanol (2-EH) were determined in urine, dialysate, and serum using gas chromatography/mass spectrometry. Additionally, the degree of glucuronidation of the phthalic acid esters in urine were determined. In serum, dialysate, and urine, PA was the predominant metabolite of DEHP (0.205 +/- 0.067 mg/L, 0.284 +/- 0.180 mg/L, and 1.34 +/- 1.00 mg/L, respectively), but concentrations of MEHP were low (0.0100 +/- 0.0056 mg/L, 0.022 +/- 0.008 mg/L, 0.011 +/- 0.0064 mg/L, respectively). Urinary MEHP was glucuronidated to approximately 15%. PA was 35% eliminated as a glucuronide. Unlike healthy subjects, PD patients do not eliminate DEHP mainly in the form of MEHP or MEHP metabolites. They further break these compounds down to PA. The fact that concentrations of PA in urine exceed by far the respective serum concentrations indicates that PA is secreted by the kidney. Further research on the toxicological aspects of plasticizers in uremic patients should take these findings into account.