Proton pump inhibitor use increases the risk of peritonitis in peritoneal dialysis patients.

Peritonitis is a major and the most significant complication of peritoneal dialysis (PD). Although some predictors of peritonitis in PD patients are known, the association between proton pump inhibitor (PPI) use and peritonitis has not been characterized. Here, we examined whether PPI use is a risk factor for the development of peritonitis, based on a single-center retrospective analysis of 230 consecutive Japanese PD patients at Narita Memorial Hospital. We assessed the association between PPI use and subsequent first episode of peritonitis using multivariate Cox proportional hazards models, following adjustment for clinically relevant factors. The median follow-up period was 36 months (interquartile range, 19-57 months). In total, 86 patients (37.4%) developed peritonitis. Analysis with multivariate Cox proportional hazards models revealed the following significant predictors of peritonitis: PPI use (adjusted hazard ratio [HR] = 1.72, 95% confidence interval [CI]: 1.11-2.66; P = 0.016) and low serum albumin level (per g/dl adjusted HR = 0.59, 95% CI: 0.39-0.90; P = 0.014). Thus, PPI use was independently associated with PD-related peritonitis. The results suggest that nephrology physicians should exercise caution when prescribing PPIs for PD patients.

Glomerular tip adhesions predict the progression of IgA nephropathy.

BACKGROUND: Focal segmental glomerulosclerosis-like lesions have been proposed to be predictive factors for IgA nephropathy. This single center, retrospective cohort study was designed to clarify which clinical and pathological factors are predictive of decreased estimated glomerular filtration rate (eGFR) at 5 and 10 years in IgA nephropathy patients. METHODS: Of the 229 patients with IgA nephropathy who were admitted to Aichi Medical University Hospital between 1986 and 2010, 57 were included in this study during the 5 to 10 years after renal biopsy. Clinical, laboratory, and pathological parameters were analyzed by multiple linear regression analysis with backward elimination to determine independent risk factors. After identifying such factors, we compared patients with and without each factor using the Student's t test, Wilcoxon test, or Mann-Whitney U test. RESULTS: Four variables were identified as predictive factors for progression of IgA nephropathy: initial eGFR (p = 0.0002), glomerular tip adhesion (p = 0.004), global sclerosis (p = 0.019), and diastolic blood pressure (p = 0.024). The annual decrease in eGFR of patients with (n = 9) or without glomerular tip adhesions (n = 48) was 4.13 ± 3.58 and 1.49 ± 2.89 ml/min/1.73 m2, respectively (p = 0.015). Serum total cholesterol levels were 231 ± 45 mg/dl and 196 ± 42 mg/dl, respectively (two-sided p = 0.064; one-sided p = 0.032). CONCLUSIONS: The presence of glomerular tip adhesions predicts the progression of IgA nephropathy. High levels of serum total cholesterol may affect glomerular tip adhesions.

Myeloperoxidase-antineutrophil cytoplasmic antibody-related crescentic glomerulonephritis after treatment for clinically amyopathic dermatomyositis: a coincidental combination or not?

A 60-year-old Japanese man exhibited rapidly progressive glomerulonephritis 10 years after receiving prednisolone therapy for clinically amyopathic dermatomyositis (CADM). Upon admission, there were no signs of dermatomyositis. Laboratory analyses revealed the presence of myeloperoxidase-antineutrophil cytoplasmic antibodies (MPO-ANCA) at 1,280 EU in the absence of anti-glomerular basement membrane antibody and anti-melanoma differentiation-associated gene 5 antibodies, which are typically expressed in CADM. A renal biopsy demonstrated that 14 of 29 glomeruli showed global sclerosis, and the remaining 15 glomeruli exhibited fibrotic and fibrocellular crescent formation without immunoglobulin and complement. Following treatment with 500 mg/day methylprednisolone pulse therapy for 3 days, the patient was started on 30 mg/day of prednisolone orally. On the third day of hospitalization, we began hemodialysis for uremia and anuria with three treatments of plasma exchange starting on the tenth hospital day. Unfortunately, the patient's renal function did not recover, despite decreases in CRP and MPO-ANCA levels to the normal range. This case is the first English language report of MPO-ANCA-related crescentic glomerulonephritis in a patient who had recovered from CADM.

Acute peritonitis due to Corynebacterium ulcerans in a patient receiving continuous ambulatory peritoneal dialysis: a case report and literature review.

A 55-year-old Japanese woman receiving continuous ambulatory peritoneal dialysis (CAPD) was admitted to our service with abdominal pain and cloudy peritoneal fluid. Laboratory data revealed a white blood cell count of 7.20 × 10(9 )cells/L, hemoglobin 9.8 g/dl, hematocrit 29.0%, platelet count 284 × 10(9 )cells/L, and C-reactive protein (CRP) 0.109 g/L. Peritoneal fluid white blood cell count of 2,000 cells/µl suggested acute peritonitis. An empiric trial of cefazolin and ceftazidime, subsequently switched to meropenem, vancomycin, minocycline, and amikacin, did not improve the patient's symptoms. The peritoneal fluid collected before initiation of antibiotic therapy grew Corynebacterium ulcerans. Ampicillin/sulbactam was started based on the culture and sensitivity data. On hospital day 8, the CAPD catheter was removed due to no clinical improvement and persistently increased levels of CRP to 0.0174 g/L. A 14-day course of ampicillin/sulbactam improved her clinical condition and laboratory data. Microbiological analysis revealed that C. ulcerans isolated from this patient did not produce diphtheria toxin. C. ulcerans was not isolated from her dog's oral and nasal cavities during a search for the route of her infection. We recommend that in patients with peritoneal dialysis, special attention should be paid to Corynebacterium peritonitis, especially due to C. ulcerans, which may produce diphtheria toxin, be resistant to multiple antibiotics, and frequently become recurrent.

A case of chronic kidney disease with thrombotic microangiopathy in a hematopoietic stem cell transplant recipient.

A 23-year-old Japanese man who had undergone hematopoietic stem cell transplantation for acute lymphocytic leukemia from an HLA-identical sibling 6 years earlier developed proteinuria and impaired kidney function. Kidney biopsy revealed thrombotic microangiopathy with a moderate increase in mesangial matrices and glomerular microaneurysm featuring retention of red blood cells. The patient's kidney function gradually deteriorated, requiring the institution of treatment with angiotensin II receptor blockers and angiotensin-converting enzyme inhibitors, and progressing to continuous ambulatory peritoneal dialysis 4 years after the initial kidney biopsy. Eventually, kidney transplantation was performed with his mother as the donor. His kidney function is stable on immunosuppressive drugs at 2 years after transplantation. This report reflects the growing number of patients with chronic kidney disease with thrombotic microangiopathy all over the world.

Effects of combination therapy with angiotensin II type I receptor blockers and calcium channel blockers on renal function in hypertensive patients/a retrospective, "real-world" comparative study.

BACKGROUND: Combination therapies with angiotensin II type I receptor blockers (ARBs) and calcium channel blockers (CCBs) are frequently administered to hypertensive patients, because these regimens have renoprotective and antihypertensive effects. However, few studies have focused on the renoprotective effects of individual CCBs when combined with ARBs for hypertension. METHODS: Two hundred eighty-six outpatients prescribed three different CCBs (benidipine [CAS 91599-74-5], amlodipine [CAS 111470-99-6] and controlled release nifedipine (nifedipine CR) [CAS 21829-25-4]) for hypertension in combination with ARBs during a 4-year period were registered in a retrospective comparative study. The factors that influenced the appearance of renal events defined as doubling of serum creatinine were investigated. RESULTS: The renal event rate was significantly lower in the benidipine than in the amlodipine (p < 0.05) and nifedipine CR (p < 0.01) groups. Multivariate analysis revealed hazard ratios for renal events to be significantly higher with chronic kidney disease (CKD) and lower with benidipine. Moreover, among patients with CKD, the benidipine group showed a significantly lower renal event rate than the amlodipine (p < 0.05) and nifedipine groups (p < 0.05). CONCLUSION: In hypertensive patients treated with ARB and CCB, benidipine exhibits a better renoprotective effect than other drugs of this class (amlodipine and nifedipine CR).

An IgA1-lambda-type monoclonal immunoglobulin deposition disease associated with membranous features in a patient with chronic hepatitis C viral infection and rectal cancer.

A 61-year-old man infected with hepatitis C virus developed urinary protein. Two-dimensional electrophoresis and immunoblotting of sera revealed no monoclonal proteins. Light microscopy and immunofluorescence of a kidney biopsy specimen demonstrated bubbling appearance and formation of spikes, associated with predominantly IgA1-lambda deposition, but not IgG, along glomerular capillary walls. Electron microscopy showed electron-dense deposits without any fibrillary structure located in the glomerular basement membrane. Seven months after the kidney biopsy, the patient had a surgical operation for rectal cancer. One year later, the urinary protein was still present. The present case is the first report of an IgA1-lambda-type monoclonal immunoglobulin deposition disease associated with membranous features.

Copper(II) complexes of a series of polypyridine ligands possessing a 1,2-bis(2-pyridyl)ethane common moiety: incorporation and hydrolysis of phosphate esters.

Two tetradentate ligands 1,2-bis[2-((dimethylamino)methyl)-6-pyridyl]ethane (L1) and 1,2-bis[2-(N-piperidinomethyl)-6-pyridyl]ethane (L2) and a hexadentate ligand 1,2-bis(2-((methyl(pyridylmethyl)amino)methyl)-6-pyridyl)ethane (L3) were prepared as part of a series of new polypyridine ligands possessing a 1,2-bis(2-pyridyl)ethane common moiety. L1 and L2 form mononuclear Cu(II) complexes [Cu(L)(Cl)](ClO4) [L = L1 (1) and L2 (2)], respectively. L3 forms a dinuclear Cu(II) complex [Cu2(L3)((PhO)2PO2)2](ClO4)2 (3) or a hexanuclear Cu(II) complex [Cu6(L3)3((PhO)PO3)4](ClO4)4 (4) in the presence of (PhO)2PO2- monoanion or (PhO)PO3(2-) dianion, respectively. The structures of 1-4 were determined by X-ray analysis. The structures in solution were investigated by means of FAB and CSI MS spectrometers. The structural flexibility of the common 1,2-bis(2-pyridyl)ethane moiety and of the pendant groups allows complexes 1-4 to adapt to the various structures. Each Cu ion in 1 and 2 adopts a square pyramidal geometry with one Cl ion and two pendant groups (L1 and L2) binding in a bis-bidentate chelate mode. There is no steric repulsion between the pendant groups, so that the ligands specifically stabilize the mononuclear structures. L3 binds two Cu(II) ions with two pendant groups in tridentate chelate modes and, with the incorporation of phosphate esters, various dinuclear units are formed in 3 and 4. In 4, a dinuclear unit of [Cu2(L3)]4+ links two dinuclear units of [Cu2(L3)(PhOPO3)2] with four (mu3)-1,3-PhOPO3(2-) bridges. The hydrolytic activity of 2 and a dicopper(II) complex of L3 was examined with tris(p-nitrophenyl) phosphate (TNP) as a substrate.