Superior mesenteric artery syndrome complicating dialysis patients with peritoneal failure--report of 3 cases.

We report 3 cases of superior mesenteric artery syndrome in patients previously on maintenance peritoneal dialysis converted to hemodialysis after peritoneal failure. All 3 patients presented with repeated vomiting and severe malnutrition. It is postulated that complications arising from peritoneal dialysis such as peritoneal sclerosis, adhesions and collections after CAPD peritonitis may be important contributing factors for the SMA syndrome in these 3 patients. All of them succumbed within six months of diagnosis. The first 2 patients received gastrointestinal bypass surgery and died post-operatively due to impaired wound healing and nosocomial sepsis. The 3rd patient was treated conservatively with nasoduodenal feeding but succumbed to aspiration pneumonia. It is postulated that complications arising from peritoneal dialysis including peritoneal sclerosis, adhesions and collections after CAPD peritonitis may contribute to the SMA syndrome in these patients. Our experience suggests that SMA syndrome in end-stage renal disease patients is associated with high surgical morbidity and mortality possibly related to their poor pre-morbid condition and pre-existing malnutrition. Aggressive parenteral nutrition should be considered to build up the general status before proceeding to surgical intervention.

Low-dose corticosteroid and mycophenolate for primary treatment of minimal change disease.

BACKGROUND: Mycophenolate has been shown to be effective in glomerular disease. However, the role of mycophenolate in the first-line treatment of adult-onset idiopathic minimal change disease (MCD) has not been systematically studied in a randomized fashion. AIM: To evaluate the therapeutic efficacy of enteric-coated mycophenolate sodium combined with low-dose corticosteroid as first-line treatment for MCNS. DESIGN: A prospective, open-label, randomized clinical trial. METHODS: Twenty adult patients with biopsy proven MCD were recruited and randomly assigned to receive either enteric-coated Mycophenolate Sodium (EC-MPS) plus low-dose prednisolone (Group 1: Prednisolone 0.25 mg/kg/day, n = 10) or standard-dose prednisolone (Group 2: Prednisolone 1 mg/kg/day, n = 10). RESULTS: After 24 weeks of therapy, eight patients in Group 1 vs. seven of patients in Group 2 achieved complete remission (P = 0.606). Both groups showed a significant reduction of urine protein excretion (P < 0.05) and increased serum albumin (P < 0.001) vs. baseline levels. However, no significant between-group differences were demonstrated. The relapse rate was also similar in both groups. Both treatment regimens were well tolerated but there were more patient reported adverse effects in the standard-dose prednisolone group. CONCLUSION: EC-MPS plus low-dose prednisolone is non-inferior to standard-dose prednisolone therapy in inducing clinical remission and preventing relapse in adult-onset idiopathic MCD and is associated with better tolerability and less adverse effects. This trial is registered with the ClinicalTrials.gov number NCT01185197.

Non-viral Smad7 gene delivery and attenuation of postoperative peritoneal adhesion in an experimental model.

BACKGROUND: Postoperative intra-abdominal adhesion is associated with high morbidity and mortality. Smad7, a protein that occupies a strategic position in fibrogenesis, inhibits the transforming growth factor (TGF) beta/Smad signalling pathway. In this study the therapeutic potential of exogenous Smad7 in preventing fibrogenesis in postoperative intra-abdominal adhesion was investigated. METHODS: Intra-abdominal adhesion was induced in a rodent model by peritoneal abrasion. Smad7 was delivered into the peritoneal cavity by a non-viral ultrasound-microbubble-mediated naked gene transfection system. The effect of Smad7 transgene on adhesion formation was studied by measuring changes in TGF-beta, fibrogenic factors, alpha-SMA and Smad2/3 activation in the anterior abdominal wall. RESULTS: Four weeks after surgical abrasion, all rats developed significant peritoneal adhesion with enhanced TGF-beta expression, increased levels of extracellular matrix components and activated myofibroblasts, accompanied by decreased Smad7 expression and increased Smad2/3 activation. In rats treated with the Smad7 transgene, the incidence and severity of peritoneal adhesion were significantly reduced, with biochemical downregulation of fibrogenic factors and inhibition of Smad2/3 activation. Serial quantitation using magnetic resonance imaging revealed a significant reduction in adhesion areas from day 14 onwards. CONCLUSION: Ultrasound-microbubble-mediated gene transfection provides timely targeted gene delivery for the treatment of postoperative peritoneal adhesions.

Downregulation of renal tubular Wnt/ß-catenin signaling by Dickkopf-3 induces tubular cell death in proteinuric nephropathy.

Studies on the role of Wnt/ß-catenin signaling in different forms of kidney disease have yielded discrepant results. Here, we report the biphasic change of renal ß-catenin expression in mice with overload proteinuria in which ß-catenin was upregulated at the early stage (4 weeks after disease induction) but abrogated at the late phase (8 weeks). Acute albuminuria was observed at 1 week after bovine serum albumin injection, followed by partial remission at 4 weeks that coincided with overexpression of renal tubular ß-catenin. Interestingly, a rebound in albuminuria at 8 weeks was accompanied by downregulated tubular ß-catenin expression and heightened tubular apoptosis. In addition, there was an inverse relationship between Dickkopf-3 (Dkk-3) and renal tubular ß-catenin expression at these time points. In vitro, a similar trend in ß-catenin expression was observed in human kidney-2 (HK-2) cells with acute (upregulation) and prolonged (downregulation) exposure to albumin. Induction of a proapoptotic phenotype by albumin was significantly enhanced by silencing ß-catenin in HK-2 cells. Finally, Dkk-3 expression and secretion was increased after prolonged exposure to albumin, leading to the suppression of intracellular ß-catenin signaling pathway. The effect of Dkk-3 on ß-catenin signaling was confirmed by incubation with exogenous Dkk-3 in HK-2 cells. Taken together, these data suggest that downregulation of tubular ß-catenin signaling induced by Dkk-3 has a detrimental role in chronic proteinuria, partially through the increase in apoptosis.

Identification and characterization of human serum alpha2-HS glycoprotein as a jacalin-bound protein.

We recently adopted immobilized jacalin as an affinity adsorbent to purify human serum IgA for laboratory study. In the course of our investigation, we detected a serum protein that co-eluted with IgA from jacalin-agarose affinity column. It constituted in significant quantity (24.0 +/- 0.9%, n = 30) of total jacalin-bound protein (JBP) and the yield was equivalent to 0.4 +/- 0.1 mg per ml serum. The molecular mass of this protein was 55 kDa with electromobility in the alpha 2 region as demonstrated by SDS-PAGE and immunoelectrophoresis. N-terminal microsequencing of this 55 kDa protein revealed that it is human alpha 2-HS glycoprotein (alpha 2HSG). The molecular interaction of alpha 2HSG with jacalin was characterized by competitive ELISA: human serum IgA, human colostrum secretory IgA (sIgA), and monosaccharides including D-galactose and melibiose exhibited strong inhibitory effect on its binding to jacalin. Accordingly, we propose that human alpha 2HSG binds in a similar manner as that of the bovine fetuin to jacalin. In addition, alpha 2HSG displays similar binding property to jacalin from different geographic area (India and Malaysia) and from different laboratory preparations (Sigma, Pierce and 'homemade' jacalin).

Mycophenolate mofetil in the treatment of steroid-resistant primary focal segmental glomerulosclerosis.

We report our experience in using mycophenolate mofetil (MMF) for the treatment of steroid-resistant focal segmental glomerulosclerosis (FSGS) in two patients. Patient 1, who was treated on disease presentation, responded well with sustained complete remission. Patient 2, who had unsuccessful steroid treatment 4 yrs before and was re-treated with MMF, showed transient retardation in renal disease progression but eventually progressed to end-stage renal failure. Our observation illustrates that MMF could be useful in treating steroid-resistant FSGS if administered at an early phase of the disease, well before histologic damage becomes irreversible. Its efficacy requires validation in randomized, controlled trials. The current armamentaria for the treatment of this condition are also discussed.

Hemofiltration in digoxin overdose.

We used hemofiltration to treat a patient with digoxin overdose complicated by refractory hyperkalemia, congestive heart failure, chronic renal failure, and complete atrioventricular heart block. Hemofiltration was associated with a progressive fall in plasma digoxin level and potassium level. This was accompanied by resolution of the heart failure and complete heart block. Hemofiltration appears to provide a therapeutic alternative in digoxin overdose.

Pathologic hip fractures secondary to amyloidoma. Case report and review of the literature.

Amyloidoma primarily involving bone and lymph node is described in a 60-year-old male patient. The patient had pathologic fractures of both hips through a deposit of amyloid in the neck of the femur. The prolonged insidious course of the disease was uncomplicated by hypercalcemia, hematologic abnormalities, or renal failure so characteristic of untreated myeloma. The bone marrow contained less than 10 percent plasma cells in different stages of maturity. Radionuclide bone scanning demonstrated other osseous amyloid lesions that were not detected by routine radiologic examination. This is the first reported case of pathologic fractures of both hips secondary to amyloidoma.

Primary glomerulonephritis with detectable glomerular hepatitis B virus antigens.

The glomerular pathology and hepatitis B virus (HBV) antigens in renal biopsies were investigated in 100 consecutive patients with both primary glomerulonephritis and positive serology for hepatitis B surface antigen (HBsAg). Glomerular HBV antigens including HBsAg, hepatitis B core antigen (HBcAg), and hepatitis B e antigen (HBeAg) were examined in frozen tissue using both polyclonal and monoclonal antibodies. HBV serology and glomerular antigens were correlated. Using monoclonal antibodies, at least one of the three HBV antigens was detectable in glomeruli in 39% of the cases. These findings correspond mainly to detectable glomerular HBsAg and HBeAg in 22.3 and 28.4% of cases, respectively. A good correlation was found between glomerular and serum HBeAg but not observed for HBsAg. Serum HBcAg was not examined and not correlated with glomerular staining. When the diagnosis of HBV-related glomerulonephritis was based strictly on detectable glomerular antigens, three distinctive morphologies were identified: membranous nephropathy, mesangiocapillary glomerulonephritis, and mesangial proliferative glomerulonephritis with immunoglobulin A (IgA) deposits (IgA nephropathy). Each of these lesions may be seen in pure form or occasionally in overlapping form leading to double glomerulopathies. Glomerular HBeAg and HBsAg were associated with subepithelial and mesangial immune complexes, respectively. Rare overlap between membranous nephropathy and IgA nephropathy further emphasized the distinctive pathology of HBV-related glomerulonephritis and the independent etiological role of HBeAg and HBsAg. In other glomerulonephritis, which rarely demonstrated glomerular HBV antigens, the pathogenetic role of chronic HBV infection remains to be proven.

Gene expression and synthesis of natriuretic peptides by cultured human glomerular cells.

BACKGROUND: Atrial natriuretic peptide, brain natriuretic peptide and C-type natriuretic peptide belong to a family of hormones that have natriuretic and vasodepressor activity and may play a pathophysiologic role in hypertension, heart failure and renal failure. Whereas immunoreactive human forms of these three natriuretic peptides are found in renal tubules, it is not clear whether they are derived from the systemic circulation or from local production. OBJECTIVE: To examine the gene expression of natriuretic peptides in cultured human glomerular cells. MATERIALS AND METHODS: We sought to determine the presence of messenger RNA encoding for these natriuretic peptides using polymerase chain reaction following reverse transcription. The polymerase chain reaction products were confirmed by direct sequencing. Atrial natriuretic peptide, brain natriuretic peptide and C-type natriuretic peptide in cell-culture supernatants were measured by radioimmunoassays (with detection limits of 2.1, 2.1 and 0.21 pmol/l, respectively). RESULTS: Atrial natriuretic peptide messenger RNA was not found in mesangial or glomerular epithelial cells (despite stimulation with tumor necrosis factor-alpha) except when the cells were cultured with a high concentration of fetal bovine serum (> 10%). Similarly, this peptide was not detected in supernatant unless the cells were cultured with fetal bovine serum at concentrations of > 10%. Brain natriuretic peptide messenger RNA was readily detected in cultured mesangial and glomerular epithelial cells with a lower concentration in the former. Brain natriuretic peptide was not found in the supernatant of resting mesangial cells but became detectable when incubated with tumor necrosis factor-alpha or fetal bovine serum. C-type natriuretic peptide messenger RNA was detected in mesangial and glomerular epithelial cells with a higher concentration in the latter. C-type natriuretic peptide was detected in the supernatant of resting glomerular epithelial cells and levels rose when incubated with increasing concentrations of tumor necrosis factor-alpha or fetal bovine serum. However, C-type natriuretic peptide was not detected in the supernatant of resting mesangial cells and remained undetectable following incubation with tumor necrosis factor-alpha or fetal bovine serum. CONCLUSION: Our results suggest differences in the synthesis of natriuretic peptides between glomerular mesangial and epithelial cells.

Gene expression of the renin-angiotensin system in human kidney.

BACKGROUND: Immunocytochemical studies have revealed that all components of the renin-angiotensin system are widely distributed in human tissues yet the information on the gene expression of the renin-angiotensin system in various types of cell remains scarce. OBJECTIVE: We explored the presence of a local renin-angiotensin system in human kidney. METHODS: We sought to determine the presence of messenger RNA (mRNA) encoding for renin, angiotensinogen, and angiotensin converting enzyme (ACE) in cultured human glomerular cells and human umbilical vein endothelial cells using a two-step polymerase chain reaction. The gene expression of the renin-angiotensin system in normal human kidney and in diseased kidney was studied by in-situ hybridization using synthetic oligonucleotides. RESULTS: By using a two-step polymerase chain reaction, renin, angiotensinogen, and ACE mRNA were found in cultured mesangial and epithelial cells but only ACE mRNA was present in human umbilical vein endothelial cells. Renin mRNA was detected in juxtaglomerular granular cells and also in glomerular and tubular epithelia in normal kidney by in-situ hybridization. A similar tubular, but not mesangial, distribution was found with angiotensinogen and ACE mRNA. In contrast, stronger signals for renin, angiotensinogen and ACE mRNA were detected in mesangial and epithelial cells of kidney tissues from hypertensive patients and from patients with renal pathology characterized by mesangial proliferation (immunoglobulin A nephropathy, diabetes mellitus, or lupus nephritis). CONCLUSIONS: That gene expression of the renin-angiotensin system occurs in resident glomerular cells supports the hypothesis that there is a local renin-angiotensin system in human kidney. Our findings support the previous speculation that the renin-angiotensin system could be a local factor involved in the progression of chronic renal failure and consequent development of hypertension.

Coexistence of Kaposi's sarcoma and tuberculosis in a renal transplant recipient.

BACKGROUND: We describe a case of Kaposi's sarcoma that developed in a renal transplant recipient as early as 5 months after the transplant. METHOD: The Kaposi's sarcoma evolved in an aggressive manner, involving the oral mucosa, the cervical and mediastinal lymph nodes, the gastrointestinal tract, and possibly the lung. Histological features of tuberculosis were also detected incidentally on an excisional biopsy of the lymph node. The patient was given 12 months of antituberculous chemotherapy. At the same time, immunosuppression was gradually tapered over a 2- to 3-week period. RESULTS: Despite the aggressive nature of the disease, the Kaposi's sarcoma regressed completely without the institution of chemotherapy. The patient remained disease-free after a follow-up period of 30 months. The kidney allograft, however, was rejected and the patient required dialysis again. CONCLUSION: Although lymphadenopathy is a well-recognized feature in organ transplant recipients who develop Kaposi's sarcoma, one has to watch out for other coexisting diseases, such as tuberculosis, lymphoma, and cytomegalovirus infection.

Effect of fluvastatin on lipoprotein profiles in treating renal transplant recipients with dyslipoproteinemia.

A single, blinded placebo-drug trial was conducted to study the efficacy and safety of fluvastatin, a new 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, in treating dyslipoproteinemia in 16 renal transplant recipients who had been on an immunosuppressive regimen that included cyclosporine (CsA). They were studied for 32 consecutive weeks, with 4 weeks of baseline treatment, 4 weeks of placebo, 12 weeks of treatment with fluvastatin 20 mg daily, and 12 weeks of fluvastatin 40 mg daily. Blood samples were obtained every 4 weeks for measurement of the lipoprotein profiles, which included total cholesterol (TC), triglyceride, low density lipoprotein (LDL)-, high density lipoprotein (HDL)-, HDL2-, HDL3- and very low density lipoprotein-cholesterol (C), apolipoprotein (Apo) A-1, Apo B, and lipoprotein(a). Fifteen patients completed the trial. After 12 weeks of treatment, fluvastatin 20 mg significantly reduced TC by 13.4% (from 6.7 +/- 0.5 [mean +/- SEM] to 5.8 +/- 0.2 mmol/L), LDL-C by 22% (from 4.1 +/- 0.3 to 3.2 +/- 0.2 mmol/L), and Apo B by 13.2% (from 159.6 +/- 8.8 to 138.6 +/- 9.2 mg/dl) (P < 0.005). The subsequent 12-week treatment of fluvastatin 40 mg significantly reduced TC by 16.4% to 5.6 +/- 0.3 mmol/L, LDL-C by 29.3% to 2.9 +/- 0.2 mmol/L, and Apo B by 18.2% to 130.6 +/- 5.5 mg/dl (P < 0.00005). There was no significant change in levels of other lipoproteins, including lipoprotein (a). There were no significant changes in the whole blood trough CsA concentrations, renal and liver function tests, and serum creatine phosphokinase level during treatment when compared with baseline and placebo. No patient complained of myalgia or failed to complete the study due to side effects of the drug. Fluvastatin appears to be safe and effective in treating dyslipoproteinemia in renal transplant recipients who are maintained on CsA.

Nosocomial outbreak of parvovirus B19 infection in a renal transplant unit.

BACKGROUND: Parvovirus B19 (B19) infection is known to cause chronic infection leading to anemia in immunocompromised patients. Although nosocomial B19 infections in immunocompetent patients have been documented, no outbreaks in immunocompromised patients have been previously reported. Whether transmission can occur from a patient with chronic infection is also unknown. METHODS: An outbreak of B19 infection in a renal transplant unit was investigated by molecular analysis of the virus strains and a case-control study. RESULTS: Three patients had genetically identical virus strains suggesting the occurrence of nosocomial transmission. The index case transmitted infection many weeks after the onset of her clinical symptoms. Other patients at risk of acquiring infection were those most intensively immunosuppressed. Viral load in the serum correlated with the hematological response. A rebound in the viral load was associated with clinical relapse and the failure of i.v. immunoglobulin therapy. CONCLUSION: Nosocomial transmission of B19 can occur from immunocompromised patients even when they are in the chronic stage of the infection. The clinical and virological response to i.v. immunoglobulin therapy is variable and depends on the overall level of immunosuppression of the patient.

Measured-to-predicted creatinine generation ratio increases with time and decline in residual renal function in continuous ambulatory peritoneal dialysis.

The expression of measured-to-predicted creatinine generation ratio (M/P) has been proposed as an index of compliance in continuous ambulatory peritoneal dialysis (CAPD) patients. Although M/P may not be sensitive enough for cross-sectional study, serial monitoring has been suggested to identify noncompliance. We attempted to evaluate serial changes of M/P from a nonselected group of CAPD patients. Sixty-three patients, all followed up for 2 years, were reviewed retrospectively. Their M/P ratios at years 0 and 2 were computed and compared. Baseline M/P had a normal distribution with a mean of 0.96 +/- 0.26. There was significant correlation between baseline M/P and residual glomerular filtration rate (GFR; r = -0.81; P < 0.0001). There were weak correlations between M/P and duration of dialysis (r = 0.52; P < 0.0001), body weight (r = -0.52; P < 0.0001), Kt/V (r = 0.31; P < 0.02), weekly creatinine clearance normalized to body surface area (r = 0.53; P < 0.0001), and serum albumin level (r = -0. 28; P < 0.05). After 2 years, M/P increased in 56 of 63 patients (88. 9%). Average M/P increased from 0.96 +/- 0.26 to 1.31 +/- 0.27 (P < 0.0001). Multivariant analysis showed M/P at year 0, which was largely determined by residual GFR, was the only independent factor affecting increase in M/P from year 0 to year 2. The general trend of increasing M/P was still present when only anuric patients were analyzed, although that was not statistically significant (1.21 +/- 0.14 to 1.32 +/- 0.24; P = 0.12). The finding of increasing M/P with time in CAPD patients, particularly those with significant residual renal function, suggests M/P may not be a reliable indicator of noncompliance, even for serial follow-up of the same patient. Better methods for assessment of compliance in CAPD patients are required.

Acute renal failure after immersion in seawater polluted by diesel oil.

Acute renal failure after exposure to toxic doses of hydrocarbon has been uniformly associated with multiorgan failure. We report a case of isolated acute renal failure in a patient after immersion in seawater polluted by diesel oil. The sites of absorption were likely to be skin, gastrointestinal tract, and lung. Investigations showed renal impairment as the only consequence from the exposure. The patient recovered uneventfully and did not require dialysis. This case highlighted the unusual consequence of isolated renal involvement resulting from hydrocarbon toxicity.

Majocchi's granuloma and posttransplant lymphoproliferative disease in a renal transplant recipient.

Renal transplant recipients are predisposed to infection and malignancy because of underlying long-term immunosuppressive therapy. In this case report, a renal transplant patient with coexisting Trichophyton rubrum granuloma (Majocchi's granuloma) and posttransplant lymphoproliferative disease (PTLD) is presented, showing the undesirable effects of heavy immunosuppression. Majocchi's granuloma was probably associated with PTLD as a reflection of overimmunosuppression.

Tuberculosis infection in Chinese patients undergoing continuous ambulatory peritoneal dialysis.

A retrospective study of the prevalence and pattern of tuberculosis in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) was performed. Thirty-eight cases of tuberculosis were diagnosed among 790 patients (18 men, 20 women; mean age, 58 +/- 12.6 years) between July 1994 and June 2000. The interval between the initiation of CAPD and onset of tuberculosis ranged from 1 to 168 months (median, 22 months). There were 18 cases of pulmonary tuberculosis, 14 cases of tuberculous peritonitis, 5 cases of tuberculous lymphadenitis, and 1 case of tuberculous synovitis. Patients with pulmonary tuberculosis usually presented with fever, constitutional symptoms, and pleural effusion or pulmonary infiltrates on chest radiograph. Abdominal pain and turbid dialysate were the main presenting symptoms in patients with tuberculous peritonitis. Diagnosis was established by positive culture in 20 patients, typical histological characteristics on a tissue biopsy specimen in 10 patients, and response to empirical antituberculous treatment in 8 patients. The duration of symptoms before the diagnosis of tuberculosis and initiation of antituberculous treatment ranged from 7 to 57 days (median, 30 days). Antituberculous treatment consisted of isoniazid, rifampicin, pyrazinamide, and ofloxacin for 9 to 15 months. Antituberculous treatment generally was well tolerated. Twenty-seven patients (71%) completed antituberculous treatment. No recurrence of tuberculosis was observed after a mean follow-up of 19.8 months. Eleven patients (29%) died while on antituberculous treatment; none of the deaths appeared to be directly caused by tuberculosis. We conclude that: (1) tuberculosis is prevalent among CAPD patients in our locality; (2) extrapulmonary tuberculosis, particularly tuberculous peritonitis, is common; and (3) a high index of suspicion for tuberculosis among CAPD patients is warranted to ensure early diagnosis and prompt initiation of treatment.

Changes of cytokine profiles during peritonitis in patients on continuous ambulatory peritoneal dialysis.

Continuous ambulatory peritoneal dialysis (CAPD) has emerged as an important dialysis treatment modality worldwide. One of the major complications is bacterial peritonitis, which may result in subsequent technique failure because of loss of peritoneal clearance or peritoneal fibrosis. Bacterial peritonitis leads to the release of proinflammatory cytokines from resident and infiltrating cells in the peritoneal cavity. We studied 35 patients undergoing CAPD with acute bacterial peritonitis. All patients treated with antibiotics for 2 weeks after the clinical diagnosis of peritonitis had a good recovery. Peritoneal dialysate effluent (PDE) was collected on days 1, 3, 5, 10, 21, and 42 after the start of treatment. Cell populations were monitored by flow cytometry. PDE levels of interleukin-1beta (IL-1), IL-6, transforming growth factor-beta (TGF-beta), and basic fibroblast growth factor (FGF) were measured by enzyme-linked immunosorbent assay. Gene transcription of TGF-beta in macrophages from PDE was measured by quantitative polymerase chain reaction. Bacterial peritonitis was associated with a sharp increase in total cell and neutrophil counts (400-fold) in PDE up to 3 weeks after peritonitis despite clinical remission (P < 0.0001). There was an increased absolute number of macrophages during the first 3 weeks despite the reduced percentage of macrophages among total cells in PDE compared with noninfective PDE. There was a progressive increase in the percentage of mesothelial cells or dead cells in the total cell population in PDE over the entire 6-week period. PDE levels of IL-1, IL-6, TGF-beta, and FGF increased markedly on day 1 before their levels decreased gradually. PDE levels of these cytokines or growth factors were significantly greater than those in noninfective PDE (n = 76) throughout the study period (P < 0.01). Similarly, TGF-beta complementary DNA (cDNA) molecules per macrophage were significantly greater than those of macrophages in noninfective PDE throughout this period (P < 0.01). There was no significant correlation between PDE levels of TGF-beta and TGF-beta cDNA molecules per macrophage, suggesting that peritoneal macrophages are not the only source of TGF-beta in PDE. We conclude there is an active release of proinflammatory cytokines and sclerogenic growth factors through at least 6 weeks despite apparent clinical remission of peritonitis. The peritoneal cytokine networks after peritonitis may potentially affect the physiological properties of the peritoneal membrane.

Factors predicting outcome of fungal peritonitis in peritoneal dialysis: analysis of a 9-year experience of fungal peritonitis in a single center.

Fungal peritonitis causes significant morbidity and mortality for patients undergoing continuous ambulatory peritoneal dialysis (CAPD). We retrospectively reviewed 70 episodes of fungal peritonitis in a single center over the last 9 years in 896 CAPD patients. Seventy percent of the episodes of fungal peritonitis were caused by Candida species, among which 50% were Candida parapsilosis. As a result of fungal peritonitis, 44% of the patients died, whereas further peritoneal dialysis failed in 14%, requiring a change to long-term hemodialysis. Only 37% managed to continue CAPD. The remaining 5% either underwent transplantation or were lost to follow-up. We identified the factors associated with poor outcome, namely mortality and technique failure. The presence of abdominal pain, bowel obstruction, and a catheter remaining in situ were significantly associated with greater mortality. Abdominal pain, antibiotic use within 3 months before fungal peritonitis, and complication by bowel obstruction were associated with greater technique failure. In choosing antifungal agents with catheter removal, oral fluconazole alone appears equally as effective as combined oral fluconazole with 5-flucytosine for peritonitis caused by Candida species. For peritonitis caused by species other than Candida, the choice of antifungal therapy needs to be individualized, based on fungal species and sensitivities.