Kidney disease affects millions of people worldwide and is a financial burden on the healthcare system. Protein phosphatase 2A (PP2A), which is involved in renal development and the function of ion-transport proteins, aquaporin-2 and podocytes, is likely to serve an important role in renal processes. PP2A is associated with the pathogenesis of a variety of different kidney diseases including podocyte injury, inflammation, tumors and chronic kidney disease. The current review aimed to discuss the structure and function of PP2A subunits in the context of kidney diseases. How dysregulation of PP2A in the kidneys causes podocyte death and the inactivation of PP2A in renal carcinoma tissues is discussed. Inhibition of PP2A activity prevents epithelial-mesenchymal transition and attenuates renal fibrosis, creating a favorable inflammatory microenvironment and promoting the initiation and progression of tumor pathogenesis. The current review also indicates that PP2A serves an important role in protection against renal inflammation. Understanding the detailed mechanisms of PP2A provides information that can be utilized in the design and application of novel therapeutics for the treatment and prevention of renal diseases.

Urinary podocalyxin and nephrin are urine markers of podocyte dysfunction that may reflect the integrity of kidney\'s filtration barrier. Studies on their respective roles in glomerular diseases are still underway. However, the isolated and unsystematic manner in which they are being studied does not permit proper identification of their roles in each glomerular disease. As such, there is little or no appreciation of what research has already achieved and what remains to be achieved as the research direction is not clearly defined. We explored the recent studies and outlined the major findings regarding the value of both biomarkers in each of the three glomerular disease entities. Our review covered diabetic nephropathy, membranous nephropathy and IgA nephropathy.

Identification of genes, associated mutations and genotype-phenotype correlations in steroid-resistant nephrotic syndrome (SRNS) is being translated to clinical practice through genetic testing. This review provides an update on the genes and mutations associated with SRNS along with a suggested approach for genetic testing in patients with SRNS.
CONCLUSIONS: The number of indentified genes associated with SRNS is increasing along with our understanding of their impact on treatment response and risk of recurrence. A systematic approach to genetic testing in patients with SRNS might aid the physician in selecting appropriate treatment.

BACKGROUND: Collapsing glomerulopathy may occur in an idiopathic (primary) form and in association with a wide spectrum of infectious and inflammatory conditions and medications. The association of collapsing glomerulopathy with human immunodeficiency virus (HIV)-1 infection is well established; less certain is the association with other viral infections.
METHODS: We searched PubMed for articles in all languages that addressed glomerulopathies associated with parvovirus B19, cytomegalovirus (CMV), Epstein-Barr virus (EBV), hepatitis C virus (HCV) and simian virus 40 (SV40).
RESULTS: Case reports and small-case series link infection with these common viruses and glomerular injury. The evidence for a pathogenic role is generally stronger for glomerulonephritis than for collapsing glomerulopathy.
CONCLUSIONS: The evidence linking collapsing glomerulopathy with CMV is relatively strong but not yet conclusive, while the evidence for a pathogenic role for EBV and parvovirus B19 is weaker.