BackgroundWhile the majority of adult-onset minimal change nephrotic syndrome (MCNS) is a primary or an idiopathic form of disease, it can also occur as a secondary form. Reports on the spontaneous remission of MCNS are rare since the condition is typically treated with corticosteroids. We herein describe the spontaneous remission of adult-onset MCNS in a patient who developed nephrotic syndrome after type B influenza infection.Case presentationA 50-year-old woman experienced fever, cough, malaise, and low back pain, which had persisted for 6 days before she presented to our hospital, and edema of the face and limbs, which had persisted for 5 days before her presentation. She was diagnosed with type B influenza infection and later exhibited an exacerbation of facial edema, decreased urine output, and a high level of proteinuria. She was referred to our department after the diagnosis of nephrotic syndrome. On admission, her proteinuria level was 20.88 g/gCr and her selectivity index value was 0.13. The examination of a kidney biopsy specimen obtained on the fourth day of hospitalization under a light microscope revealed minor abnormalities. An immunofluorescence showed only nonspecific granular IgM deposits in the mesangium. Electron microscopy showed extensive foot process effacement without any immune complex deposits. Based on these findings, the patient was diagnosed with MCNS. After admission, the proteinuria decreased to 0.06 g/gCr with rest and sodium restriction (6 g/day) alone; a complete remission from nephrotic syndrome was observed at approximately 2 weeks after the onset of symptoms. There have been no signs of recurrence of nephrotic syndrome in the one years since.ConclusionWe experienced a rare case in which spontaneous remission of MCNS occurred within a short period of 2 weeks after influenza B infection. When patients present with nephrotic syndrome after an infection, it is necessary to consider MCNS in the differential diagnosis, which also includes post-infectious glomerulonephritis and the acute exacerbation of IgA nephropathy.

Rationale:Pulmonary tumor thrombotic microangiopathy (PTTM) is a rare but lethal complication of carcinoma, defined as non-occlusive pulmonary tumor embolism complicated by fibrocellular intimal proliferation of the small pulmonary arteries, with eventual occlusion of the pulmonary arteries. Hemodynamic deterioration caused by this condition leads to high mortality.Patient concerns:A 46-year-old woman who had undergone radiation therapy for anaplastic oligoastrocytoma and who was taking temozolomide presented with cough and palpitations.Diagnoses:A 12-lead electrocardiogram showed sinus tachycardia and SIQIII TIII, with negative T in V1–3. Ultrasound cardiography showed a distended right ventricle. Enhanced chest computed tomography showed no significant thrombus in the major pulmonary artery. The patient's condition deteriorated the next morning, with her blood pressure decreasing to 40 mmHg and her SpO2 unmeasurable. She suffered cardiac arrest.Interventions:We initiated venoarterial extracorporeal membranous oxygenation (VA-ECMO) and her blood pressure increased to 80 mmHg. Her hemodynamic status stabilized and she was weaned off VA-ECMO on intensive care unit (ICU) day 3.Outcomes:Gastroesophageal endoscopy on ICU day 4 revealed gastric cancer (Borrman type IV), and she arrested again and died on ICU day 5. Autopsy confirmed gastric cancer and PTTM.Lessons:VA-ECMO rapidly stabilized the hemodynamic status of this patient with PTTM, and may thus be a possible bridging therapy for deterioration of PTTM prior to initiating imatinib.

The influence on the Cl(-) assay of the addition of Br(-) varied significantly between different ion electrode machines. Clinical nephrologists therefore need to be able to recognize the characteristics of the specific machines used in their hospitals.

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