Unusual Pathogen in a Patient With Peritoneal Dialysis-Related Peritonitis: A Case Report.

Peritoneal dialysis (PD) is an effective modality for renal replacement therapy. A serious complication that can arise from PD is peritonitis. Over the last few decades, there have been cases of PD-related peritonitis secondary to Pasteurella multocida infections. We present the case of a 44-year-old female who presented to the emergency department with a one-day history of abdominal pain and cloudy peritoneal fluid on evaluation. Along with her physical examination findings, laboratory results of the peritoneal fluid demonstrated elevated white blood cells and neutrophils, characteristic of peritonitis. Ultimately, the culture results were positive for P. multocida. Although P. multocida is not the most common cause of peritonitis, it is a common cause in PD patients who have domesticated animals. With two out of three people being pet owners and the increased number of people on home therapies such as PD for kidney failure, it is important to educate patients about the proper precautions and techniques to prevent peritonitis and its associated complications. Additionally, proper antibiotic management should be implemented for patients with an increased risk of infection.

Effect of tumor necrosis factor alpha and vascular permeability growth factor on albuminuria in rats.

The purposes of this study were to measure the serum levels of vascular permeability growth factor (VPGF) and tumor necrosis factor alpha (TNFalpha) in minimal lesion nephrotic syndrome (MLNS) patients and to assess their effect on albuminuria in rats. Serum for VPGF and TNFalpha was obtained during relapse and remission from 18 MLNS patients. Tumor necrosis factor alpha was infused at the rate of 10 and 20 ng/h and VPGF at the rate of 20 and 40 ng/h for 5 days into the left renal artery of rats. Urinary albumin (24-h collection) was measured prior to infusion and on days 2, 4 and 5. Rats infused with 1% bovine serum albumin served as controls. Serum VPGF and TNFalpha levels in MLNS patients in relapse were not different from those seen during remission. A significant increase in albuminuria was observed on day 4 and 5 only when rats were infused with TNFalpha at the rate of 20 ng/h as compared to the excretion seen in same animals prior to the infusion of cytokine and on days 4 and 5 of normal controls. Neither VPGF nor TNFalpha seems to be the circulating pathogenic cytokine for proteinuria in MLNS. However, TNFalpha may contribute to the increased albuminuria via a paracrine effect at the glomerulus.

Proteinuria and fusion of podocyte foot processes in rats after infusion of cytokine from patients with idiopathic minimal lesion nephrotic syndrome.

BACKGROUND/AIMS: We report on the isolation of a factor secreted by peripheral blood mononuclear cells from patients with idiopathic minimal lesion nephrotic syndrome (IMLNS) in relapse and its effect on proteinuria and podocyte morphology in the rat. METHODS: Peripheral blood mononuclear cells from patients with IMLNS (in relapse and in remission) and patients with focal segmental glomerulosclerosis were cultured for 72 h. Supernatants from 20 x 10(6) cultured cells were separated by liquid chromatography into three fractions according to markers (bovine serum albumin, beta-amylase, and apoferritin). Each supernatant fraction was infused into rats for 5 days using an osmotic pump. Proteinuria, 24-hour albumin excretion or albumin/creatinine ratio in a 24-hour urine collection, was measured daily starting 3 days prior to fraction infusion. Renal tissue was obtained for electron microscopy studies. The beta-amylase fraction underwent electrophoresis using isoelectric focusing gel. RESULTS: When protein excretion was compared prior to and during supernatant fraction infusion, a significant increase in proteinuria was observed only when beta-amylase fraction from IMLNS patients in relapse was infused (p < 0.05). Protein electrophoresis of the beta-amylase fraction showed a single band at pH 6.0 only in samples from IMLNS patients in relapse. The band was composed of two proteins, beta-amylase and a 100-kDa glycoprotein. Fusion of foot processes was observed only when the beta-amylase fraction from IMLNS patients in relapse was infused. CONCLUSIONS: The infusion of the beta-amylase fraction containing a 100-kDa glycoprotein from IMLNS patients in relapse induced proteinuria and effacement of foot processes in the rat. This protein may play a role in the pathogenesis of IMLNS.

Cytokine mRNA profile in lipoid nephrosis: evidence for increased IL-8 mRNA stability.

BACKGROUND/AIMS: Proteinuria in idiopathic minimal lesion nephrotic syndrome (IMLNS) is presumed to be due to the effect of circulating factors on glomerular permeability to plasma proteins. This study examines the expression of messenger ribonucleic acid (mRNA) for cytokines thought to mediate glomerular inflammation during different stages of the nephrotic syndrome. METHODS: Messenger RNA expression and stability from peripheral blood mononuclear cells of IMLNS patients in relapse and in remission, and age matched normal controls were measured using a ribonuclease protection assay (RPA). The spontaneous and Interleukin 2 (IL-2) stimulated mRNA expression were studied. RESULTS: Spontaneous mRNA expression for Interleukin 8 (IL-8) from IMLNS patients in relapse was significantly increased when compared to IMLNS patients in remission and normal controls (p < 0.05). After 14 h of IL-2 stimulation, mRNA IL-8 levels expressed by IMLNS PBMC patients in remission were not different from those observed in normal controls. However, after 5 days of PBMC incubation, a significant increase in mRNA for IL-8 in IMLNS patients compared to controls was found (p < 0.01). Stability assay demonstrated that IL-8 mRNA transcript from the nephrotic patients remained higher than those from controls and showed a significantly prolonged life t(1/2) (p = 0.02). CONCLUSIONS: IL-8 mRNA expression is increased in IMLNS patients in relapse. Moreover, stability studies show that IL-8 mRNA life t(1/2) is prolonged due to altered post-transcriptional regulation. This finding may explain the elevated serum IL-8 levels observed in these patients during relapse and may have pathogenic significance since IL-8 has been shown to induce proteinuria in the experimental animal.