The registry data focused new light on the epidemiology of kidney diseases in Poland. These data should be used in future follow-up and prospective studies.

Diabetic nephropathy (DN) is the most common cause of end-stage renal disease (ESRD), both in the USA and in Europe; moreover, its incidence is rising worldwide. The main laboratory markers of DN progression are albuminuria and a reduction in glomerular filtration rates, although progression of the disease has been observed even in the absence of these biomarkers. Renal impairment, associated with diabetes, results from damage to the glomerular filtration barrier, at the level of highly differentiated glomerular epithelial cells: podocytes. These cells regulate glomerular filtration and many immunological processes occurring at this level. The earliest possible diagnosis of diabetic kidney disease (DKD) and implementation of intensive treatment offers the possibility of preventing or substantially delaying the onset of ESRD. In this article, we review various urinary biomarkers linked with glomerular podocyte cytophysiology as potentially sensitive diagnostic tools for the early detection of DKD. These biomarkers have predictive potential for assessing the progression toward end-stage nephropathy.

Since kidney transplant recipients are at enhanced risk for developing severe upper gastrointestinal disease and Helicobacter pylori (Hp) is an important pathogen in active gastritis and peptic ulcer, we performed gastroduodenoscopic examination, coupled with assessment of Hp colonization in 29 renal allograft recipients complaining of recurrent dyspepsia. Results were compared with those of 25 chronically hemodialyzed patients and 16 subjects free from renal disease, also suffering from upper gastrointestinal symptoms of similar severity. We found that while transplant recipients have had a high prevalence of Hp infection (62 vs. 34.6% in dialysis and 43.6% in control dyspeptic patients), active gastritis was clearly less frequently seen in these patients than in control subjects (transplant group: 6.9%, dialysis 3.8%, control 31.3%) and peptic ulceration was totally absent. Prevalence of Hp colonization was even higher in renal graft recipients on triple posttransplant immunosuppression (82%). In dyspeptic transplant and dialysis patients, colonization with Hp did not account for development of active inflammatory lesions, an association frequently seen in subjects free from renal disease and immunosuppressive therapy.

Previous studies in this laboratory have documented tumor necrosis factor alpha (TNF) release by macrophage laden glomeruli in the accelerated autologous form of nephrotoxic serum nephritis (AA-NTSN). We now report that the administration of anti-TNF antiserum to rats with the AA-NTSN reduces albuminuria in a dose related manner (day 8 postinduction) and limits glomerular necrosis (P less than 0.05) without affecting the endogenous creatinine clearance (CCr). Protease inhibitors block cytolytic activity of TNF in vitro and reduce glomerular necrosis in experimental nephritis in vivo. The combined administration of anti-TNF antiserum and an amidine-type protease inhibitor (BABIM) to rats with the AA-NTSN caused a greater diminution of albuminuria and histopathology than observed in rats treated with either agent alone, and also prevented the fall in CCr otherwise observed in this model system. Since, in our studies, BABIM did not inhibit cytolytic TNF activity in vitro, we conclude that the effects of combined administration of these two agents are mediated by independent mechanisms. Our results highlight the pathogenic significance of local TNF release in immune renal disease accompanied by prominent glomerular macrophage accumulation.