Abnormalities of thyroid function are common in patients with nephrotic syndrome (NS). However, a limited number of studies have reported on the association between clinicopathologic features and thyroid dysfunction in patients with NS. We retrospectively studied 317 patients who had been definitively diagnosed with NS. The NS patients with thyroid dysfunction showed higher urine protein, creatinine and lipid levels and lower albumin and hemoglobin than those with normal thyroid function, with no significant differences of pathological types. After dividing thyroid dysfunction groups into five subgroups, interestingly, membranous nephropathy was the most common pathologic type, both in normal thyroid group and in subclinical hypothyroidism group (40.4% and 46.7%, respectively), followed by minimal change disease (28.1% and 21.7%, respectively); while in the hypothyroid, low T3, and low T3T4 groups minimal change disease is now the leading type (48.8%, 33.3% and 38.6%, respectively). High levels of urinary protein, creatinine, cholesterol, and platelets were independent risk factors predicting thyroid dysfunction, while higher albumin and hemoglobin were protective factors. We demonstrated that the type of renal pathology was different among NS patients in different thyroid dysfunction subgroups. Interpretation of the interactions between thyroid and renal function is a challenge for clinicians involved in the treatment of patients with NS.

Objective: In kidney diseases, uncontrolled blood pressure, inflammation, oxidative stress, imbalanced immunity response, and metabolic dysfunction were associated with the progressive deterioration of renal function. Short-chain fatty acids (SCFAs), as a group of metabolites fermented by gut microbiota exerted regulatory effects on kidney diseases through their activation of trans-membrane G protein-coupled receptors and their inhibition of histone acetylation. In this review article, we updated recent research advances that provided an opportunity to explore our understanding in physiology and function of SCFAs in kidney disease. Data sources: We performed a comprehensive search in both PubMed and Embase using “short-chain fatty acids” and “kidney” with no restrictions on publication date. Study selection: After reading through the title and abstract for early screening, the full text of relevant studies was identified and reviewed to summarize the roles of SCFAs in kidney diseases. Results: Though controversial, growing evidence suggested SCFAs appeared to have a complex but yet poorly understood communications with cellular and molecular processes that affected kidney function and responses to injury. From recent studies, SCFAs influenced multiple aspects of renal physiology including inflammation and immunity, fibrosis, blood pressure, and energy metabolism. Conclusions: The roles of intestinal SCFAs in kidney diseases were exciting regions in recent years; however, clinical trials and animal experiments in kidney diseases were still lacked. Thus, more research would be needed to obtain better understanding of SCFAs’ potential effects in kidney diseases.

No abstract