In adults, membranous nephropathy (MN) is a major cause of nephrotic syndrome. However, the etiology of approximately 75% of MN cases is idiopathic. Secondary causes of MN are autoimmune diseases, infection, drugs, and malignancy. The pathogenesis of MN involves formation of immune complex in subepithelial sites, but the definite mechanism is still unknown. There are three hypotheses about the formation of immune complex, including preformed immune complex, in situ immune-complex formation, and autoantibody against podocyte membrane antigen. The formation of immune complex initiates complement activation, which subsequently leads to glomerular damage. Recently, the antiphospholipase A2 receptor antibody was found to be associated with idiopathic MN. This finding may be useful in the diagnosis and prognosis of MN. The current treatment includes best supportive care, which consists of the use of angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers, lipid-lowering agents, and optimal control of blood pressure. Immunosuppressive agents should be used for patients who suffer from refractory proteinuria or complications associated with nephrotic syndrome. Existing evidence supports the use of a combination of steroid and alkylating agents. This article reviews the epidemiology, pathogenesis, diagnosis, and the treatment of MN.

Variants of CISH are associated with susceptibility to diseases caused by diverse infectious pathogens, suggesting that negative regulators of cytokine signaling have a role in immunity against various infectious diseases. The overall risk of one of these infectious diseases was increased by at least 18% among persons carrying the variant CISH alleles.

Hepatectomy is a safe and effective treatment for hepatolithiasis, with a high stone clearance rate and fair rate of surgical complications. Recurrent stone-induced sepsis and cholangiocarcinoma are the major factors compromising long-term survival in these patients.

The viral spike (S) coat protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) engages the human angiotensin-converting enzyme2 (ACE2) cell surface receptor to infect the host cells. Thus, concerns arose regarding theoretically higher risk for Coronavirus -19 (COVID-19) in patients taking angiotensin-converting enzyme inhibitors (ACEI)/ angiotensin II type 1 receptor antagonists (ARBs). We systematically assessed case-population and cohort studies from MEDLINE (Ovid), Cochrane Database of Systematic Reviews PubMed, Embase, medRXIV, the World Health Organization data-base of COVID-19 publications and ClinicalTrials.gov through Jun 1, 2020, with planned ongoing surveillance. We rated the certainty of evidence according to Cochrane methods and the GRADE approach. After pooling the adjusted odds ratios (aOR) from the included studies, no significant increase was noted in the risk of SARS-CoV-2 infection by the use of ACEi (aOR, 0.95; 95% CI, 0.86-1.05) or ARBs (aOR, 1.05; 95% CI, 0.97-1.14). However, the random-effects meta-regression revealed that age may modify the SARS-CoV-2 infection risk in subjects with the use of ARBs (coefficient, -0.006; 95% CI, -0.016 to 0.004)-i.e.: the use of ARBs, as opposed to ACEi, specifically augmented the risk of SARS-CoV-2 infection in younger subjects (< 60 years-old). The use of ACEi might not increase the susceptibility of SARS-CoV-2 infection, severity of disease and mortality in case-population and cohort studies. Additionally, we found for the first time that the use of ARBs, as opposed to ACEi, specifically augmented the risk of SARS-CoV-2 infection in younger subjects; without obvious effects on COVID-19 outcomes.

The clinical characteristics and outcomes in patients with clinical aldosterone-producing adenomas harboring KCNJ5 mutations with or without subclinical hypercortisolism remain unclear. This prospective study is aimed at determining factors associated with subclinical hypercortisolism in patients with clinical aldosterone-producing adenomas. Totally, 82 patients were recruited from November 2016 to March 2018 and underwent unilateral laparoscopic adrenalectomy with at least a 12-month follow-up postoperatively. Standard subclinical hypercortisolism (defined as cortisol >1.8 μg/dL after 1 mg dexamethasone suppression test [DST]) was detected in 22 (26.8%) of the 82 patients. Intriguingly, a generalized additive model identified the clinical aldosterone-producing adenoma patients with 1 mg DST>1.5 μg/dL had significantly larger tumors ( P =0.02) than those with 1 mg DST<1.5 μg/dL. Multivariable logistic regression showed that the presence of KCNJ5 mutations (odds ratio, 0.22, P =0.010) and body mass index (odds ratio, 0.87, P =0.046) were negatively associated with 1 mg DST>1.5 μg/dL, whereas tumor size was positively associated with it (odds ratio, 2.85, P =0.014). Immunohistochemistry revealed a higher degree of immunoreactivity for CYP11B1 in adenomas with wild-type KCNJ5 ( P =0.018), whereas CYP11B2 was more commonly detected in adenomas with KCNJ5 mutation ( P =0.007). Patients with wild-type KCNJ5 and 1 mg DST>1.5 μg/dL exhibited the lowest complete clinical success rate (36.8%) after adrenalectomy. In conclusion, subclinical hypercortisolism is common in clinical aldosterone-producing adenoma patients without KCNJ5 mutation or with a relatively larger adrenal tumor. The presence of serum cortisol levels >1.5 μg/dL after 1 mg DST may be linked to a lower clinical complete success rate.