Age-Related Differences of Organism-Specific Peritonitis Rates: A Single-Center Experience.

Peritonitis remains an important cause of morbidity and mortality in peritoneal dialysis (PD) patients, but its incidence and the distribution of causative organisms vary widely between institutions and age groups. This study was performed to investigate the recent status and risk factors of PD-related peritonitis and to clarify differences between age groups. We retrospectively reviewed the medical records of 119 PD patients treated at our department between January 2002 and January 2013. We calculated both overall and organism-specific peritonitis rates and also analyzed risk factors. Sixty-three episodes of peritonitis occurred during 261.5 patient-years for an incident rate of 0.24 episodes/patient-year. Multivariate analysis showed that older age (≥65 years) and hypoalbuminemia (<3.0 g/dL) were associated with an increased risk of peritonitis (P = 0.035 and P = 0.029, respectively). In elderly patients (≥65 years old), the rate of peritonitis due to Gram-positive and Gram-negative bacteria was 0.17 and 0.08 episodes/patient-year, respectively, and Gram-positive peritonitis was markedly more frequent than in younger patients (<65 years old). In particular, there was a high frequency of Staphylococcus aureus peritonitis in elderly patients (0.09 episodes/patient-year) and it had a poor outcome. At our department, the risk of peritonitis was increased in older patients and patients with hypoalbuminemia. The distribution of causative organisms was markedly different between age groups and analysis of organism-specific peritonitis rates helped to identify current problems with our PD program.

Dialysis Amyloid Deposition in the Aortic Valve and Its Association with Aortic Stenosis.

BACKGROUND: The relationship between dialysis amyloid (DA) deposition in the aortic valve (AV) and aortic stenosis (AS) is unknown. METHODS: This was a cross-sectional study. AV specimens of dialysis patients (median vintage: 8.8 years) consecutively collected from cardiac surgeries (n = 56) or autopsies (n = 13) were examined by a board-certified pathologist blinded to clinical data. DAs were considered to be present if deposits were stained both by Congo red with apple-green birefringence under polarized light and by anti-ß2-microblobulin antibody. Degree of deposition was graded as follows: Amyloid (-), no deposit; Amyloid (1+), occasional small deposits; Amyloid (2+), multiple small to large deposits or a single large deposit. Calcification was defined as a calcified deposit with a diameter >1 mm in the specimen. Severe AS (sAS) was defined as a mean gradient >50 mm Hg by echocardiogram. We examined the proportion of DAs and the association between DAs and the sAS. RESULTS: DAs were present in 71% (n = 49) of specimens and primarily co-localized with calcification. Non-dialysis related amyloid was found in one specimen. After excluding this specimen, sAS was associated with 'Amyloid (1+) and Calcification >1 mm' and 'Amyloid (2+) and Calcification >1 mm' (vs. 'Amyloid (-) and Calcification ≤1 mm', odds ratios (ORs): 13.5 and 34.2, respectively). Furthermore, after adjustment for covariates, sAS was found to be associated with 'Amyloid (2+) and Calcification >1 mm' (OR: 24.3). CONCLUSIONS: DA deposition in the AV was prevalent among dialysis patients. DA deposition with accompanying calcification might contribute to the severity of AS.

AA amyloid nephropathy with predominant vascular deposition in Crohn's disease.

A 44-year-old man with a 17-year history of Crohn's disease (CD) was referred to our nephrology department on suspicion of drug-induced nephrotoxicity. Over the preceding 18 months, he had slowly progressive renal insufficiency with slight urinary abnormalities. His disease activity had been well controlled up to that point with 5-aminosalicylic acid and azathiopurine. Laboratory examination revealed slight proteinuria without hematuria and an elevated serum creatinine level of 1.4 mg/dl. Pathological examination revealed amyloid A (AA) deposition in the kidney, predominantly in the arterial and arteriolar walls with little to none in the glomerular capillaries. AA amyloidosis is typically accompanied by glomerular amyloid deposition and massive proteinuria. In the present case, however, vascular amyloid deposition was predominant, and the renal function was deteriorated with slight urinary abnormalities. The present case confirmed the importance of conducting a definitive pathological diagnosis of renal insufficiency in CD patients.

[Case of mesangial proliferative glomerulonephritis complicated with multicentric Castleman's disease].

We report a case of a 47-year-old man with multicentric Castleman's disease (MCD) and progressive renal dysfunction due to mesangial proliferative glomerulonephritis, possibly from IgA nephropathy. At age 36 years, he was referred to a hematologist due to hypergammaglobulinemia. Because of systemic lymph node swelling, he underwent right cervical lymph node biopsy at age 41 years and MCD (plasma cell type)was diagnosed. During this period, microscopic hematuria and persistent proteinuria occurred and his renal function deteriorated (serum creatinine (Cr) rising from 0.7 mg/dL to 1.4 mg/dL). Treatment with intravenous methylprednisolone at the dose of 1 g daily for 3 days followed by oral prednisolone at 20 mg daily reduced his lymphadenopathy and improved the renal function. However, his renal function deteriorated again, from Cr 0.8 mg/dL to 1.8 mg/dL over 6 years in line with gradual prednisolone tapering to 6 mg daily. At age 47 years, he was referred to our nephrology department and underwent a renal biopsy. The microscopic examination showed IgA nephropathy with crescent formation, accompanied by mild lymphoplasmacytic tubulointerstitial nephritis. Treatment with the same dose of intravenous methylprednisolone therapy followed by oral prednisolone at 40 mg daily, improved his proteinuria, hematuria and renal dysfunction. The coexistence of MCD and IgA nephropathy is a rare phenomenon. In addition, IL-6, overproduced by MCD might have influenced the mesangial cell proliferation and the activity of IgA nephropathy in the present case.