Risk factors in diabetic nephropathy progression at present.

Diabetic nephropathy is becoming an increasingly important cause of morbidity and mortality worldwide as a consequence of increasing prevalence of type 2 diabetes and obesity. The glomeruli of patients with diabetes are characterized by glomerular hypertrophy, widening of the glomerular basement membrane, mesangial expansion, podocytopenia leading to nodular (Kimmelstiel-Wilson) glomerulosclerosis. Many studies have reported the initiation and progression of incipient nephropathy in type 1 diabetes patients, but only limited data are available in type 2 diabetes patients. The information on the risk factors and conversion rate of normal renal function to proteinuria in type 2 diabetes patients is sparse. In this report, we review risk factors of diabetic nephropathy progression in type 2 diabetes patients (Ref. 50).

[Obesity--the risk factor of cardiovascular disease in patients with chronic kidney disease?]. / Obezita--rizikový faktor kardiovaskulárnych ochorení u pacientov s chronickým ochorením obliciek?

In general population obesity is regarded as a predisposing factor for chronic disease such as type 2 diabetes and cardiovascular disease. Obesity increases the risk of kidney disease and adversely affects the progress of kidney disease among patients with diagnosed kidney disease. The main reason of mortality in chronic kidney disease patients is cardiovascular disease, however, the real meaning of obesity as a risk factor of cardiovascular diseases is still uncertain. While in a general population obesity causes higher cardiovascular mortality, many studies reflect inverse association in chronic kidney disease patients. Obesity is associated with better survival, contrary to general population obesity appears to be a protective factor of cardiovascular disease. The name of this phenomenon is "reverse epidemiology" or "obesity paradox", in dialysis patients known as a "risk-factor-paradox". Some studies do not confirm this paradox association in patients with chronic kidney disease.

[Purtscher-like retinopathy--a rare complication of acute pancreatitis]. / Purtscher-like retinopatia--zriedkavá komplikácia akútnej pankreatitídy: kazuistika.

The article reports the case of a 27-year old woman hospitalised in the internal medicine ward for acute pancreatitis after eating fat food and drinking alcohol. In addition to acute pancreatitis, the patient complained of vision problems. The ophthalmologist detected bilateral occurrence of large whitish nidi located primarily around the optic disc, intraretinal hemorrhage and a massive retinal oedema in the central field and diagnosed Purtscher-like retinopathy. After a month of treatment of acute pancreatitis, the clinical picture improved, the patient's vision sharpness improved and the laboratory parametres returned to normal. The finding on the ocular fundus also improved. Even though similar cases are rare, more patients with acute pancreatitis should be checked for eventual vision disorders. Ocular fundus examination should be included in the set of tests performed for acute pancreatitis, similarly to the practice in arterial hypertension or diabetes mellitus patients.

Effect of vitamin E supplementation on microalbuminuria, lipid peroxidation and blood prostaglandins in diabetic patients.

BACKGROUND: Oxidative stress is an important pathogenic factor in the development of diabetic vascular complications. AIMS: To study the effect of vitamin E supplementation on microalbuminuria, plasma levels of malondialdehyde (MLD) and metabolites of prostaglandins TXA2 (TXB2) and PGI2 (6-keto-PGF1alpha) and to evaluate the relation between plasma MLD and thromboxane B2 (TXB2) in diabetic patients. PATIENTS AND METHODS: Diabetic microalbuminuric patients were supplemented with vitamin E 1200 IU daily (EVIT, Rodisma, Germany) and measurements of microalbuminuria, MLD, TXB2 and 6-ketoPGF1alpha were repeated after 4 months of treatment. RESULTS: Vitamin E supplementation lowered microalbuminuria (93.8 +/- 45.6 vs 67.95 +/- 28.4 microg/min, p < 0.05), MLD (0.55 +/- 0.26 vs 0.32 +/- 0.16 micromol/l, p < 0.001) and also TXB2 level (115.14 +/- 22.7 vs 15.32 +/- 14.7 ng/l, p < 0.001) in diabetic microalbuminuric patients. The changes of 6-keto-PGF1alpha after treatment were not significant. CONCLUSIONS: Our results did not show any significant relationship between levels of MLD and TXB2. Vitamin E supplementation significantly lowered microalbuminuria, MLD and TXB2. (Tab. 2, Fig. 2, Ref. 35).

[Effect of vitamin E therapy on progression of diabetic nephropathy]. / Vplyv liecby vitamínom E na progresiu diabetickej nefropatie.

Pathogenesis of diabetic nephropathy, which belongs to most serious microangiopathic complications of diabetes, is still not completely clear. Thromboxan A2 and increased oxidation stress are new factors apparently associated with pathogenesis of diabetic nephropathy. It was the aim of the contribution to verify the participation of thromboxan A2 and oxidation stress in the pathogenesis of diabetic nephropathy, as well as to follow the effects of treatment with vitamin E on its progression. In 19 diabetic subjects with microalbuminemia (MA) (age 55.2 +/- 7.6 years), 10 diabetic subjects with normoalbuminemia (NA) (age 54.4 +/- 6.1 years) and in 10 healthy subjects (age 53.6 +/- 9.4) the authors examined the level of malondialdehyde (MLDA) in serum, metabolites of thromboxan A2 (thromboxan B2-TXB2) and prostacyclin PGI2 (6-keto-PGF1 alpha) in urine by means of an RIA method (Isotop, Hungary). The diabetic patients with microalbuminemia were subsequently administered natural vitamin E (EVIT, Rodisna, FRG) at the daily dose of 1200 IU for the period of four months. After two and four months, respectively, MA, MLDA, TXB2 and 6-keto-PGF1 alpha) were examined. The age of the subjects in the two groups was not significantly different. In diabetic subjects with MA, the authors observed significantly higher MLDA levels in serum than in the control individuals (0.55 +/- 0.26 vs. 0.22 +/- 0.02 mumol/l, P < 0.001) and a significant difference occurred also in TBX2 in urine (134.7 +/- 113.8 vs. 27.7 +/- 10.1 ng/12 h, P < 0.001). Increased levels of TXB2 in urine were already present in diabetic subjects with NA as compared with healthy individuals (69.1 +/- 38.8 vs. 27.7 +/- 10.1 ng/12 h, P < 0.05). The treatment with vitamin E caused a significant decrease of MA (93.8 +/- 45.6 vs. 67.95 +/- 28.4 micrograms/min, P < 0.05), MLDA in serum (0.55 +/- 0.26 vs. 0.32 +/- 0.16 mumol/l, P < 0.001). On the basis of our results it is possible to suppose the role of oxidation stress and increased level of thromboxan A2 in the pathogenesis of diabetic nephropathy. The authors also confirmed that the treatment with vitamin E favorably decreases microalbuminemia, while the nephroprotective effect is apparently mediated not only by the antioxidant action, but also the decrease of thromboxan A2 production.