In September 2009, a 79-year-old man developed pyrexia, malaise, and anorexia. A local clinic diagnosed active inflammation and renal failure (Cr, 2.3mg/dL). Since the symptoms were not relieved by an oral antibiotic and renal function deteriorated (Cr, 14.9mg/dL), he was referred to our hospital for further evaluation after 1 week. Daily hemodialysis was required because of anuria. Chest X-ray films showed pneumonia affecting the right lower lung field. Continuous fever and marked inflammation despite broad-spectrum antibiotic therapy suggested an autoimmune disease. Autoantibodies containing anti-neutrophil cytoplasmic antibody (ANCA) and anti-glomerular basement membrane (GBM) antibody were all within normal limits. A contrast-enhanced CT scan demonstrated irregular constriction of renal artery branches and low enhancement of the bilateral kidneys. Partial wall thickening of the jejunum and constriction of a jejunal artery branch were also seen. A renal biopsy demonstrated severe acute tubular necrosis without angiitis in small vessels and glomeruli. These findings suggested marked renal ischemia due to inflammation of medium-size renal arteries caused by classical polyarteritis nodosa (PN). Steroid pulse therapy followed by oral prednisolone (40mg daily) was administered, and his symptoms improved markedly. The prednisolone dose was gradually decreased to 10mg daily, and there have been no signs of recurrence for 1 year. Rapidly progressive renal insufficiency is rare in patients with classical PN. Early diagnosis and therapy are vital for successful treatment.

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Hypercalcemic crisis is a serious and potentially life-threatening complication of markedly increased serum calcium concentrations most commonly due to primary hyperparathyroidism. We report a case of an 80-year-old man with diabetes mellitus and chronic renal failure, who presented to the emergency department with somnolence, dysarthria and severe hypercalcemia (16.3mg/dL). Despite intensive treatment including elcatonin, alendronate, and intermittent hemodialysis with low calcium dialysate, serum calcium still reached high levels between hemodialysis treatments. The patient was then treated with 4mg of intravenous zoledronate. This treatment greatly reduced the serum calcium level and improved clinical symptoms without major adverse effects. The patient was diagnosed as having primary hyperparathyroidism and was treated by parathyroidectomy. Administration of zoledronate seems to be an effective modality for hypercalcemic crisis in patients with end-stage renal disease.

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A 34-year-old male with end-stage renal failure due to type1 diabetes started peritoneal dialysis (PD) via a double-cuffed Tenckhoff catheter in April 2008. He was using a double-bag system with manual connectology and underwent nocturnal intermittent PD. In January 2009, he developed his first episode of peritonitis, presenting with slight fever, abdominal pain, diarrhea, vomiting and cloudy dialysate. Physical examination demonstrated abdominal rebound tenderness. Drained dialysate was cloudy with an elevated cell count of 2,500/μL (96% polymorphonuclear leukocytes). He was admitted to the hospital and successfully treated with 8 days of intraperitoneal or intravenous cefazolin and ceftazidime, followed by oral cefotiam for 6 days. There was no recurrence of peritonitis thereafter. Neisseria subflava was isolated from the dialysate and was identified as the pathogen causing peritonitis. Neisseria subflava is commensal in the upper respiratory tract, but may rarely cause infections, such as endocarditis and meningitis. A few cases of Neisseria peritonitis have been reported in PD patients, even in those without concomitant diseases. In the present case, contamination by a droplet from the mouth was considered the most probable cause of peritonitis, because the patient did not wear a mask during bag exchanges. The importance of wearing a mask for infection control during PD bag exchanges was reconfirmed.

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This report describes an 85-year-old man with chronic kidney disease and chronic heart failure with a history of repeated hospitalization due to volume overload. Hemodialysis (HD) was initiated in October 2009. He took warfarin because of chronic atrial fibrillation (Af). To prepare for the establishment of an arterio-venous fistula, we switched warfarin to heparin. Post operatively, warfarin was administered again. On the 11th postoperative day, he complained of abdominal pain after supper. At that time, clinical and laboratory findings were unremarkable. He than received pain-relieving medicine, which masked the symptom and allowed him to sleep during the night. The next morning, abdominal pain was worsening and rebound tenderness was noted. Enhanced computed tomography demonstrated superior mesenteric artery (SMA) occlusion. Since 13 hours had passed from the first symptom, we considered that interventional radiology (IVR) was inadequate and recommended surgery to resect the intestine. The patient and his family rejected surgery and the patient died 42 hours after the abdominal pain had initially occurred. It is still difficult to manage SMA occlusion even though diagnostic imaging and treatment have recently been developed. Even now, the outcome of SMA occlusion is extremely poor. One of the reasons is the difficulty to diagnose the disease soon after the abdominal pain initially occurs as in our case. Although Af is the most frequent cause of SMA occlusion, the indications for warfarin administration in HD patients with Af have not been established, which makes this case more complicated. A strategy for warfarin use in HD patients with atrial fibrillation needs to be investigated.

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