Regardless of the underlying etiology, tubulointerstitial fibrosis is a common mechanism in the progression of chronic kidney disease (CKD) to end-stage renal disease. Epithelial-mesenchymal transition (EMT) of renal tubular cells plays an important role in tubulointerstitial fibrosis. Transforming growth factor-?1/Sma and Mad protein (TGF-?1/Smad) is thought to be a main signaling pathway for EMT of renal tubular cells. Progressive renal disease is also characterized histologically by an interstitial infiltrate of mononuclear cells. The chemokines secreted from renal tubular cells can trigger integrin-dependent adhesion of circulating mononuclear cells that leads to infiltration at tubulointerstitial space. The direct interaction of integrin lymphocyte function-associated antigen 1(LFA-1: ?L?2 integrin) on mononuclear cells and its ligand, intracellular adhesion molecule-1(ICAM-1) on renal tubular epithelial cells, contributes to a part of the EMT of renal tubular cells.

Peritoneal fibrosis (PF) is a common morphological change in peritoneal dialysis (PD) patients. With the progression of PF, peritoneal membrane function is impaired, which leads to ultrafiltration failure. Furthermore, PF is an essential precursor condition for the development of encapsulating peritoneal sclerosis (EPS), which is the most serious complication of PD. Epithelial-mesenchymal transition (EMT) of peritoneal mesothelial cells (PMCs) plays a crucial role in PF. Transforming growth factor-?1 (TGF-?1) was thought to be the main regulator of EMT in PMCs. High glucose, hypertonicity, low pH, glucose degradation products and advanced glycation end-products in PD solution were suggested to induce TGF-?1 production. In addition, chronic inflammation mediated by infiltration of immune cells and peritoneal angiogenesis also play pivotal roles for the progression of PF.

Renal involvement associated with various viruses has been identified, with each associated with a different disease type. Accumulated studies have revealed the pathogenesis and optimal therapies of nephritis associated with viral infections. This review focuses on the nephritis associated with viral infections.

Malnutrition is a very common condition in patients with chronic kidney disease (CKD), especially after the 3rd stage (GFR 30-59 mL/min/1.73 m2). It affects virtually every organ and the function of the entire organism as well and therefore influences the survival. Moreover, the supplementation of amino acids could correct the negative nitrogen balance of those patients improving their survival rates, while little is known regarding any possible negative effect of this supplementation of amino acids on the acid-base balance. We investigated the impact of parenteral infusion of two different kinds of amino acid solutions (specific for CKD patients and nonspecific) in 25 patients (12F, 13M), suffered from chronic renal failure in stages 3 and 4 (GFR 16 to 45.1 mL/min/1.73 m2). The specific for uremic CKD patients solution A was administrated for 5 days, and after an interval of one week, we treated the same patients for another 5 days with the second non-specific solution B, with usual composition), in order to investigate their influence on patients’ acid-base balance. Comparing the results of the first and the last infusion of solution A, neither pH nor blood gases analysis presented significant differences, while solution B induced statistically significant changes in both pH and blood gases, (p=0.0001). Acidosis was resulted in by the reduction of serum levels of HCO3 - whereas not any significant change observed in serum lactate levels after the infusion of each solution. These results suggest that for patients with chronic kidney disease in stages 3 and 4 who require the administration of a supplementary amino acid solution, the CKD-specific solution A may be preferred, since it prevents the worsen of the metabolic acidosis, which is commonly present in these patients.