Uncharted Territory: Frequent Relapsing, Steroid Sensitive Secondary Minimal Change Nephrotic Syndrome Cause by Solid Tumor of the Gastro-Esophageal Junction —(Case Presentation and Review of the Literature)

We reported a biopsy proved case of minimal change nephrotic syndrome in a 72-year-old patient. The minimal change nephrotic syndrome has been steroid sensitive, but the patient had 7 relapses over a span of 5 years. Each time the dose of steroid is tapered, a relapse of the nephrotic syndrome occurred. Eventually, the patient was complaining of dysphagia and difficulty swallowing. Hospital work-up with barium swallow, endoscopy, and CT of the chest, abdomen and pelvis, revealed a focal stenotic lesion with mild to moderate esophageal dysmotility 7/15/2022. A diagnosis of an ulcerating lesion with biopsy confirmed a neuro-endocrine carcinoma of the gastro-esophageal junction was entertained. The CT of the chest/abdomen/pelvis, 7/19/2022, has shown, an esophageal mass of 5.1 × 5.6 × 7 cm of the gastro-esophageal junction with ulceration. No evidence of spread beyond the esophagus and stomach. The histology revealed a poorly differentiated neuroendocrine tumor of the gastro-esophageal junction. The patient underwent several rounds of chemotherapy, radiation, and surgery culminating in tumor control. His nephrotic syndrome was resolved after the tumor has been controlled by surgery and chemotherapy.

Pathogenesis of childhood idiopathic nephrotic syndrome:a paradigm shift from T-cells to podocytes

Background:Nephrotic syndrome is the most common cause of kidney disease in children,but its pathogenesis remains unclear.This article reviews the novel aspects of the mechanisms underlying massive proteinuria in minimal-change disease,which is the most common form of childhood nephrotic syndrome.Data sources:This article integrates the findings of a PubMed database search for English language articles published in the past 40 years(from September 1974 to February 2014)using the key words"pathogenesis","minimal change nephrotic syndrome"or"idiopathic ne phrotic syndrome".Results:Unknown humoral factors associated with T-cell dysfunction have been thought to play an important role in the pathogenesis of minimal-change disease.However,recent findings are changing this paradigm,i.e,visceral glomerular epithelial cells(podocytes)may be involved via expression of molecules such as CD80 and angiopoietin-like 4.Conclusions:Recent evidence suggests that minimal-change disease results from interactions between humoral factors and dysfunctional podocytes.In addition to immunosuppressant drugs that target lymphocytes,a biological agent such as an antibody against the abnormal molecule(S)expressed by podocytes may provide novel drug treatment for minimal-change disease.