[Diabetic nephropathy and prevention of diabetic nephropathy caused chronic renal insufficiency]. / Dijabeticka nefropatija i prevencija kronicnog bubreznog zatajenja uzrokovanog dijabetickom nefropatijom.

There is an ongoing trend of a rapid increment in the frequency of diabetes mellitus, expecially the non-insulin dependent form. By the end of the 2nd millenium 150 million cases were recorded worldwide, while the estimations predicted doubling the number by the year 2030. Numerous chronic complications accompany the disease, among them micro-, as well as macrovascular prevail, affecting small and large blood vessels. This paper provides a literature review on the topic of diabetic nephropathy, the main microvascular complication of diabetic disease. Microalbuminuria is the earliest sign of the diabetic renal involvement, with more than 30 mg and less than 300 mg of albumins in 24 h urine sample. The reduction of renal function begins with albuminuria leaving microalbuminuria level and entering the pathologic proteinuria range. Renal failure advances through the 5 stages, the final fifth occurring fortunately only in a minor proportion of the patients. The final stage ensues in 232 of 100 000 diabetic patients, according to the US data. However, in many developed countries there are 30-40% of new patients entering chronic dialysis treatment for diabetic nephropathy. Pathogenesis of diabetic nephropathy is based on hyperglycemia and distinct hemodynamic changes, glomerular hyperfiltration and high intraglomerular pressure. The important role have oxidative stress, advanced glycation end products, some cytokines, growth factors and sorbitol pathway. Nevertheless, genetic influence is considered by far the most important risk factor for diabetic nephropathy. Heritage determines the susceptibility in one and the protection in another diabetic patient. At the moment of pathologic proteinuria occurrence, glomerular filtration rate begins to decline for 1.2 ml/min/monthly in some patients, making the annual reduction of 7-14 ml/min/1.73 m2 of body surface area. Improving glycemia, blood pressure control, renal anemia correction with rHu-Epo, dyslipidemia control, reduction in protein intake, i.e. management of the nongenetic factors, could slower the renal function loss in some of the patients. Hence, these measures could reduce the proportion of the patients reaching end-stage renal disease, having in mind that morphological and functional changes are reversible only within certain limits. Therefore, the success of kidney protection is better if commenced earlier.

[The impact of glucose absorbed from dialysis solution on body weight gain in peritoneal dialysis treated patients]. / Utjecaj glukoze apsorbirane iz dijalizata na tjelesnu tezinu peritonejskom dijali lijecenih bolesnika.

A proportion of peritoneal dialysis (PD) patients experience substantial body weight (BW) gain with time. It is caused by fat tissue accumulation or fluid retention. It is believed that fat tissue accumulates due to caloric contribution of glucose absorbed from dialysis solution or to the mitochondrial fat regulatory uncoupling protein (UCP) gene polymorphism. This study examined BW fluctuations in 40 patients (24 females, 16 males), treated by PD at least 36 months (initial mean age 54.50+/-9.00 years, mean BW 68.00+/-8.50 kg and mean height 164.00+/-8.50 cm), relation of the BW fluctuation and caloric contribution of glucose absorbed from dialysis solution and characteristics of the patients with BW gain. Initial BW increased after 6, 12, 24 and 36 months by 5.90+/-3.50 kg, 7.90+/-4.90 kg, 9.50+/-5.00 and 11.00+/-5.00 kg, or for 8.68, 11.62, 13.97 and 16.18% of the initial value, respectively. After the first 6 and 12 months 38 patients gained weight, 39 after 24 and all 40 patients after 36 months. There was not significant correlation between BW gain and caloric contribution of glucose absorbed from dialysis solution. Female patients had initially lower BW, but for the first 12 months period significantly increased BW more than males, and not for the other observed periods. High transporters (patients with higher transport, higher transmission of glucose from peritoneal solution into the blood, and urea and creatinine in the opposite direction, with rapid decrement of osmolality gradient between dialysate and blood that is necessary for excessive fluid elimination), had lower initial BW and, although without statistical significance, only within the first period increased BW more than low transporters. In conclusion, with time BW gain was found in all the PD dialysis patients, it was not related to caloric contribution of glucose absorbed from dialysis solution, and women and high transporters increased BW weight more than men and low transporters in the first year of treatment. The BW gain is at least in part caused by fluid retention.