There is increased evidence that the prevalence of peripheral artery disease (PAD) in hemodialysed patients is higher than in general population [1,2]. According to ACC/AHA (American College of Cardiology / American Heart Association) guidelines, the following risk factors are associated with PAD [3,4]

Native arteriovenous fistulae (AVF) are the best options for chronic hemodialysis (HD) access. Unfortunately, not every patient fulfils the requirements necessary for this type of vascular access: the artery and the vein implicated in dialysis fistula creation must accomplish some criteria which makes them suitable for this procedure. If these criteria are not fully met, the chances to a successfully intervention and a quick and qualitative maturation of the fistula are dropping [1-5]. An artery that is suitable for AVF creation has an inner diameter > 2 mm, optimal initial flow and elastic walls allowing dilatation to accommodate a supplementary 10 - 20 fold blood flow increase after the AVF is performed [1,2,5-11]. The participating vein must be superficial enough (less than 5 mm from the skin surface), wide enough (a caliber bigger than 2.5 mm) and its walls must allow important dilatation (without fibrosis, injuries, and thickenings). In elderly, diabetics or patients with late initiation of HD some of these demands are frequently absent we need to adapt surgical procedures, taking advantage of any oppor tunity to overcame shortcomings and create a native dialysis access [1,2,5,9].

The prevalence of end stage renal disease (ESRD) is constantly increasing in worldwide population, as is the necessity of renal replacement therapy [1-3]. The improvements in dialysis techniques determined increasing quality and lifetime of dialysis patients and the need for a reliable vascular access that sustains the procedure for long periods of time. On the other hand, the progressive aging of dialyzed population and the emerging complications, as well as the rising prevalence of diabetes as a cause for chronic kidney disease (CKD), hampers the processes of obtaining and maintaining an adequate vascular access [1,4,5].

Angiodysplasia (AD), gastric antral vascular ectasia (GAVE or watermelon stomach), radiation-induced vascular ectasia and Dieulafoy's lesions are considered sporadic lesions and they can induce gastrointestinal bleeding (1). AD is the most common vascular abnormality of the gastrointestinal tract, probably the most common cause of recurrent gastrointestinal hemorrhage in patients with renal failure (2) and an important cause of erythropoiet-inresistant anaemia in dialyzed patients. Angiodysplasia injuries developed in the gastric antrum were first described in 1953 and named GAVE, being characterized as submucosal capillary dilatation and fibromuscular hyperplasia (3).

Chronic kidney disease (CKD) is a worldwide health problem [1,2] affecting between 7 - 10% of young individuals (30 - 64 years old) in Europe [2] and approximately 10 - 18% of the population in the USA [3]. In 2013, in Romania, the prevalence of CKD was approximately 13.1%, meaning about 1,900,000 persons, and 13,899 patients were on chronic dialysis [4].
CKD is associated with increased cardiovascular morbidity, even from early stages [5-8]. Decreased glomerular filtration rate (GFR) is a strong predictor of cardiovascular events, even in the absence of other cardiac risk factors [9]. Risk for cardiovascular disease in CKD patients is 10 - 30 times higher than in non-CKD individuals and mortality from cardiovascular diseases (CVD) accounts for approximately 50% from all causes of death in dialysis population [6,10,11,12]. Predisposing features for developing CVD in CKD patients include both traditional and nontraditional - uremia associated - factors [11,12].

Renal artery stenosis represents the main cause of secondary hypertension and, due to its progressive profile, leads to end-stage renal disease and important cardiovascular events (1). Despite the large number of trials in this particular field of interest, RAS therapy remains a complex challenge for clinicians with regard to interventional revascularization, eventually resulting in renal function preservation, improved blood pressure control (BP) and prevention of adverse cardiovascular events in selected patients (2).
In fact, the matter of debate is represented by the proper selection of patients which would benefit the most from renal revascularization with stent implantation, while also taking into account the outcomes of the recently emerging large clinical trials that were unable to confirm the clear benefits of endovascular therapy.

Protein-energy malnutrition is a frequent clinical condition in chronic hemodialysis patients (1). The causes of protein-energy malnutrition are: interaction between blood and dialyzer with subsequent activation of the complement, amino acids and peptides losses when undergoing hemodialysis, metabolic acidosis, chronic inflammation and anorexia (2). There are two types of protein-energy malnutrition. Type 1 protein-energy malnutrition is characterized by patients’ poor food intake. This occurs along with slow decrease of serum albumin and loss of muscle mass, the presence of normal levels of C-reactive protein and response to nutritional interventions. The second type of protein-energy malnutrition is characterized by an increased serum level of C-reactive protein and lower serum albumin level than in type 1, even with an optimal food intake. This type of protein-caloric malnutrition is strongly associated with chronic inflammation and does not respond to nutritional intervention (3).

Over the past few years, the conventional transurethral resection of bladder tumors (TURBT) has undergone increasing criticism among the international urological community due to its’ inability to achieve a complete tumor ablation [1]. This substantial oncologic drawback has been mainly related to the limited sensitivity of the classical white light cystoscopy (WLC) [2]. In other words, the standard endoscopic assessment of the bladder was often outlined as insufficiently capable of accurately identifying all of the existing tumor formations [3].

Digestive manifestations due to uremia and uremic toxins are multiple in patients with chronic kidney disease (CKD) on hemodialysis (HD). As much as 79 percent of these patients report gastrointestinal symptoms manifested as nausea, vomiting, dry mouth, dysgeusia, halitosis, pyrosis, abdominal pain, bloating, diarrhea (1,2). Due to many pathogenic mechanisms, the prevalence of gastro-duodenal peptic ulcer disease is higher in HD subjects than in general population, but comparable in frequency with nondialyzed CKD patients (3-5). A recent published 10 years-study presented that the incidence of peptic ulcer disease is 4 times higher in patients with CKD and 9.4 times higher in individuals on chronic HD compared to the general population (6). Regarding localization, gastric ulcers are twice more frequent documented than duodenal ulcers (6-8). An imbalance between protective and aggressive mucosal factors in favor of the last ones is noticed in HD patients. Chronic dialysis stress, intradialysis hypotension (causing mucosal hypo-perfusion), anemia, intra-dialysis anticoagulant, metabolic acidosis, potentially ulcerogenic medication (steroids, non-steroid anti-inflammatory and antiplatelet drugs) lead to high frequencies of peptic ulcer disease (9). Since the appearance of ulcerous lesions, the risk of their complications (e.g.: hemorrhages, perforations, penetrating injuries) is much higher than in general population. One recent cohort study in Taiwan showed that the incidence of gastro-duodenal bleedings is double in CKD patients and 5 times higher in HD ones (2). Subsequently, common comorbidities such as diabetes, liver cirrhosis and ischemic heart disease participate as pathogens in digestive bleedings (10).
An adequate diagnosis and monitoring of peptic ulcer disease in dialysis patients represent a constant concern of our clinical practice, because of the high prevalence of this kind of pathology, the life-threatening potential complications and the complexity of the treatment. Therefore, further on we discuss the case of an atypical peptic ulcer disease in a chronic HD patient.

Patients with chronic renal disease frequently display eso-gastro-duodenal associated pathology: anorexia, heartburn, nausea, vomiting, abdominal pain, gastric motility disorder so far as gastroparesis
some of these symptoms decline once the substitution therapy of the renal function is initiated through hemodialysis, and some persist because of the interdialytic metabolic acidosis, used anticoagulant in dialysis or complementary therapies.
The most severe clinical manifestation is superior digestive hemorrhage, with multiple intricate causes (mucosal lesions induced by gastrin, angiodysplasia including GAVE - gastric antral vascular ectasia, treatments with lesion potential - NSAIDs, corticoids, oral iron drugs, mucosa inflammation under uremic toxins or oxygen radicals, gastric and intestinal wall edema due to interdialytic hypervolemia, malnutrition). The gastric hyperacidity induced injuries in renal patients are often esophagitis, gastritis, duodenitis and gastro-duodenal ulcer.

Bladder cancer represents the most common malignancy of the urinary tract and the 7th most frequent cancer in men and 17th in women. The prevalence of this malignancy varies between regions and countries. In Europe for example, the highest age-standardized incidence rate has been reported in Spain and the lowest in Finland (1). In the United States, the incidence and mortality due to bladder cancer is also high (more than 60,000 new cases and up to 13,000 deaths annually) (2). Therefore, in the last decades, it has been noticed an increased prevalence of bladder cancer, probably caused by tobacco abuse, industrial carcinogens risk factors and overall aging process of the population (3). 75-85% of all newly diagnosed bladder tumors is represented by non-muscle-invasive bladder cancer (NMIBC), a multifocal disease, that includes stages pTa, pT1 and carcinoma in situ (CIS) (4). Furthermore, this pathology has a high recurrence rate within the first 5 years after the initial diagnosis (5), despite the recent technological advances (6).

Hyponatremia, with an incidence of 15 - 22%, is considered when serum sodium levels are < 135 mEq/L (in institutionalized geriatric patients, in 1 - 4% to 7 - 53% cases there have been reported values below 130 mEq/L) [1-3]. Additionally, according to expert panel recommendations the frequency of hyponatremia in hospitalized patients depends on the detected level of hyponatremia [2]. This special condition is highly important to be detected on time because it represents a recognized risk factor of morbidity and mortality, even in asymptomatic patients [1]. Furthermore, it was noticed that a swift correction can induce severe neurological disorders and even death [1]. Therefore, for an adequate treatment management (prophylaxis and therapy) is vital for understanding hyponatremia main causes and the incriminated pathophysiological mechanisms [1].