Excessive consumption of fructose (FR) leads to obesity, metabolic syndrome (MS) and insulin resistance, which are known risk factors for kidney stones. The epidemiological study has suggested the association between fructose consumption and urolithiasis, but the precise mechanism is still not well understood. Male Wistar rats were assigned for 8 weeks to three groups with different FR content in diet: RD ( = 5)-regular diet with a FR < 3%; F10 ( = 6)-regular diet with an addition of 10% Fr in drinking water; F60 ( = 5)-60% FR as a solid food.
View Article and Find Full Text PDFObjectives: This study was designed to evaluate the impact of fructose-rich diet and chronic kidney disease (CKD) on the in vitro function of pancreatic islets.
Methods: Fifty-four rats were divided into 3 equal groups as follows: control, rats with CKD 1/2 that underwent surgical uninephrectomy, and rats with CKD 5/6 that underwent uninephrectomy and kidney cortex mass resection. Each group was further assigned to 3 diet protocols--regular diet, regular diet with 10% fructose (F10), and 60% fructose-rich diet (F60).
Background/aims: Hypoxia-inducible factor (HIF)-1α is responsible for increased expression of genes engaged in angiogenesis. Our previous study indicated capillary rarefaction and atrophy of glycolytic fibers, mainly in locomotor muscles of uremic animals. Perhaps these changes are secondary to disturbances of HIF-1α in skeletal muscles.
View Article and Find Full Text PDFBackground: Fructose has been strongly linked with hypertension, hyperuricemia and inflammation in experimental models and humans. However, the effect of low-fructose diet on inflammation, hyperuricemia and the progression of renal disease has not yet been evaluated in patients with chronic kidney disease (CKD).
Methods: Twenty-eight patients (age 59 ± 15 years, 17 males/11 females) with Stages 2 and 3 CKD were switched from a regular (basal) (60.
We report a case of a 52-year-old male who has been diagnosed for many years because of chronic diarrhea and proteinuria with concomitant gradually progressing chronic kidney disease. Diagnostic problems associated with the initial diagnosis of amyloidosis as a primary cause of the patient's complaints have been described. Anderson-Fabry disease (AFD) was suspected following comprehensive evaluation that resulted eventually in the exclusion of amyloidosis and the echocardiographic examination showing hypertrophic cardiomyopathy in the patient with no history of hypertension and aortic valve defects.
View Article and Find Full Text PDFBackground: Chronic kidney disease (CKD) is associated with muscle excess fatigue and diminished maximal whole body oxygen consumption, which in part could be depended on poor muscle microcirculatory network. The aim of this study was to assume the influence of different stages of CKD on microcirculation vessels in functionally different skeletal muscles--locomotor, the gastrocnemius muscle, and postural, the longissimus thoracis muscle.
Methods: Male Wistar rats underwent sham operation (CON), uninephrectomy (CKD 1/2) and subtotal nephrectomy (CKD 5/6).
Background: Cardiac troponin I (cTnI) has been shown to be a specific marker of myocardial damage in the general population. In patients suffering from chronic kidney disease (CKD) cTnI may be increased in serum without other signs of acute myocardial damage confusing the diagnosis.
Aim: To compare cTnI concentration in CKD patients, treated conservatively or with haemodialysis, with healthy controls, and to evaluate the cardiovascular risk factor profile in these groups.
Background: Inflammation is a well-defined factor influencing the development of cardiovascular complications in chronic renal failure. The aim of this study was to examine systemic inflammatory state defined by the level of serum haptoglobin, local inflammation defined by monocyte chemoattractant protein-1 (MCP-1) level and arterial response to phenylephrine in different stages of renal failure.
Methods: Experiments were performed on male Wistar rats, weighing 290-380 g.