Successful treatment of streptococcal toxic shock syndrome complicated by primary peritonitis and bilateral empyema in a healthy young woman: Identification of uncommon clone emm103 and novel sequence type 1363.

Streptococcal toxic shock syndrome (STSS) has a dramatic clinical course and high mortality rate. Here, we report a case of STSS complicated by primary peritonitis and bilateral empyema. A previously healthy young woman was diagnosed with STSS complicated by primary peritonitis and bilateral empyema. Blood culture results on admission were negative. Sever shock, respiratory failure, systemic inflammation, thrombocytopenia, renal failure, ascites, and pleural effusion occurred, mimicking thrombocytopenia, anasarca, fever, reticulin fibrosis/renal failure and organomegaly (TAFRO) syndrome. Retesting blood cultures identified Streptococcus pyogenes. Gram staining of ascites and pleural fluid indicated gram-positive cocci in chains. Antibiotics, immunoglobulins, and surgical intervention led to recovery without complications. Ex-post genotypic analyses showed uncommon emm103.0 (cluster E3) of emm long sequence (784 base) and novel sequence type 1363. STSS diagnosis can be difficult as it mimics other systemic inflammatory diseases. Therefore, it is crucial for clinicians to perform microbiological examinations from infection foci, even if the initial culture is negative.

Nivolumab-associated glomerular endothelial injury in a patient with gastric cancer.

A 68-year-old male with gastric cancer was treated with tegafur/gimeracil/oteracil and oxaliplatin for 6 months. Thereafter, he was treated with paclitaxel and ramucirumab for 3 months. However, neither regimen had much effect. Thus, he was treated with nivolumab for 2 months, but he developed proteinuria, microhematuria, and an acute kidney injury. A kidney biopsy revealed occasional swollen endothelial cells and proliferating mesangial cells. Few abnormal findings were seen in the tubules or interstitial tissue. Immunofluorescent staining showed segmental immunoglobulin A and complement component 3 deposition, in the mesangial area. Electron microscopy showed a small amount of electron-dense deposits in the paramesangial area and swollen endothelial cells. Mesangial interposition, the loss of endothelial cell fenestration, and subendothelial edema were also observed. Furthermore, foot process effacement and villous transformation of epithelial cells were noted. After the discontinuation of nivolumab, the patient's renal function gradually improved, and his proteinuria disappeared. Nivolumab treatment was restarted at that time because of cancer progression; however, it was ineffective. No occult blood was detected from 7 months after the administration of the last dose of nivolumab. This is a unique case, in which a kidney biopsy revealed evidence of nivolumab-associated glomerular endothelial injury.

Successful Sodium Level Correction with a 3% Saline Bolus before Intermittent Hemodialysis for a Patient with Severe Hyponatremia Accompanied by Acute Kidney Injury.

A 60-year-old man presented to the emergency department with lightheadedness. He had severe hyponatremia (109 mEq/L) complicated by acute kidney injury (AKI) (serum creatinine: 9.08 mg/dL). Because he was somnolescent, his hyponatremia was initially treated by administering a 130-mL bolus of 3% saline 2 to 5 times per day for 5 days. He subsequently underwent intermittent hemodialysis without any neurological problems. Previous reports have described patients with hyponatremia and AKI being treated with continuous renal replacement therapy. However, our strategy might be a feasible, low-cost treatment strategy of treating patients with hyponatremia and AKI who do not require immediate hemodialysis.

Idiopathic immune complex-mediated tubulointerstitial nephritis with hypocomplementemia and neutrophil-rich interstitial infiltrates
.

A 69-year-old man presented with acute kidney injury, hypocomplementemia, antinuclear antibody, and anti-dsDNA antibody. He had no signs of systemic lupus erythematosus or Sjögren syndrome. He had not begun taking any new drugs in the preceding 6 months. Kidney biopsy revealed 13 glomeruli, 3 with global sclerosis. The remaining glomeruli showed slight mesangial proliferation. The interstitial inflammation was extensive, comprising mainly mature lymphocytes and plasma cells, neutrophils, and a few eosinophils. Remarkable granular and diffuse deposition of IgG and C1q was observed along the tubular basement membranes. Electron microscopy showed electron-dense deposits in the tubular basement membrane. Immunohistochemistry showed only 1 - 4 IgG4-positive plasma cells per high-power field and an IgG4/CD138 ratio of ~ 10%. He was treated with oral prednisolone 35 mg/day, and his kidney function gradually improved. This is a unique case that is not consistent with any known disease entities with immune complex-mediated tubulointerstitial nephritis.
.