The aim of this review was to highlight the most important complications of arteriovenous fistulas (AVFs) for hemodialysis (HD). The quality of vascular access for HD should be suitable for repeated puncture and allow a high blood flow rate for high-efficiency dialysis with minimal complications. The dialysis staff must be well versed in manipulation of the AVF, and there should be a minimal need for corrective interventions. Construction of an AVF creates conditions for increasing the flow of blood through the venous system. Fulfillment of these conditions reduces the risk of turbulence and endothelium injury, which, in turn, minimizes the potential for stenosis. An AVF is closest to the ideal model of vascular access. The most important complications of fistulae for HD are lymphedema, infection, aneurysm, stenosis, congestive heart failure, steal syndrome, ischemic neuropathy and thrombosis. In HD patients, the most common cause of vascular access failure is neointimal hyperplasia. It is important to gain information about early clinical symptoms of AVF dysfunction in order to prevent and adequately treat potential complications.

The role of xanthine oxidase (XOD) in patients undergoing chronic hemodialysis treatment (HD) is poorly understood. Geriatric nutritional risk index (GNRI) ≤ 90 could be linked with malnutrition-inflammation complex syndrome. This study measured XOD, myeloperoxidase (MPO), superoxide dismutase (SOD), lipid hydroperoxides, total free thiol groups, and advanced oxidation protein products (AOPP) in 50 HD patients before commencing (pre-HD) and immediately after completion of HD session (post-HD) and in 22 healthy controls. Pre-HD serum hydroperoxides, AOPP, XOD, and SOD were higher and total thiol groups were lower in patients than in controls (P < 0.05, resp.). Compared to baseline values, serum MPO activity was increased irrespective of GNRI status. Serum XOD activity was increasing during HD treatment in the group with GNRI ≤ 90 (P = 0.030) whilst decreasing in the group with GNRI > 90 (P = 0.002). In a multiple regression analysis, post-HD serum XOD activity was independently associated with GNRI ≤ 90 (β  ± SE: 0.398 ± 0.151; P = 0.012) and HD vintage (β  ± SE: −0.349 ± 0.139; P = 0.016). These results indicate that an upregulated XOD may be implicated in HD-induced oxidative injury contributing to accelerated protein damage in patients with GNRI ≤ 90.

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Compared to men, women have worse preoperative and postoperative QOL. Female sex was an independent predictor of QOL worsening six months after CABG.

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Cerebrovascular insult (CVI) is a known and important risk factor for the development of diabetic ketoacidosis (DKA); still, it seems that the prevalence of DKA among the patients suffering CVI and its influence on stroke outcome might be underestimated. Diabetic ketoacidosis itself has been reported to be a risk factor for the occurrence of stroke in children and youth. A cerebral hypoperfusion in untreated DKA may lead to cerebral injury, arterial ischemic stroke, cerebral venous thrombosis, and hemorrhagic stroke. All these were noted following DKA episodes in children. At least some of these mechanisms may be operative in adults and complicate the course and outcome of CVI. There is a considerable overlap of symptoms, signs, and laboratory findings in the two conditions, making their interpretation difficult, particularly in the elderly and less communicative patients. Serum pH and bicarbonate, blood gases, and anion gap levels should be routinely measured in all type 1 and type 2 diabetics, regardless of symptomatology, for the early detection of existing or pending ketoacidosis. The capacity for rehydration in patients with stroke is limited, and the treatment of the cerebrovascular disease requires intensive use of osmotic and loop diuretics. Fluid repletion may be difficult, and the precise management algorithms are required. Intravenous insulin is the backbone of treatment, although its effect may be diminished due to delayed fluid replenishment. Therefore, the clinical course of diabetic ketoacidosis in patients with CVI may be prolonged and complicated.

Hypomagnesemia is a significant pro-atherogenic factor and an important predictor of arteriovenous fistula complications.

Background. Increased lactate production is frequent in unregulated/complicated diabetes mellitus. Methods. Three groups, each consisting of 40 patients (type 2 diabetics with myocardial infarction, DM+AMI, nondiabetics suffering myocardial infarction, MI, and diabetics with no apparent cardiovascular pathology, DM group), were tested for pH, serum bicarbonate and electrolytes, blood lactate, and CK-MB. Results. Blood lactate levels were markedly higher in AMI+DM compared to MI group (4.54 ± 1.44 versus 3.19 ± 1.005 mmol/L, p < 0.05); they correlated with the incidence of heart failure (ρ = 0.66), cardiac rhythm disorders (ρ = 0.54), oxygen saturation (ρ = 0.72), CK-MB levels (ρ = 0.62), and poor short-term outcome. Lactic acidosis in DM+AMI group was not always related to lethal outcome. Discussion. The lactate cutoff value associated with grave prognosis depends on the specific disease. While some authors proposed cutoff values ranging from 0.76 to 4 mmol/L, others argued that only occurrence of lactic acidosis may be truly predictive of lethal outcome. Conclusion. Both defective glucose metabolism and low tissue oxygenation may contribute to the lactate production in diabetic patients with acute myocardial infarction; high lactate levels indicate increased risk for poor outcome in this population comparing to nondiabetic patients. The rise in blood lactate concentration in diabetics with AMI was associated with increased incidence of heart failure, severe arrhythmias, cardiogenic shock, and high mortality rate.