Nephrology Dialysis Transplantation 

About: Nephrology Dialysis Transplantation is an academic journal published by Oxford University Press. The journal publishes majorly in the area(s): Kidney disease & Medicine. It has an ISSN identifier of 0931-0509. Over the lifetime, 22328 publications have been published receiving 625120 citations. The journal is also known as: Nephrology, Dialysis, Transplantation & Nephrology Dialysis Transplantation : an International Basic Science and Clinical Renal Journal.

Gadolinium—a specific trigger for the development of nephrogenic fibrosing dermopathy and nephrogenic systemic fibrosis?

Abstract: Nephrogenic fibrosing dermopathy (NFD) is an acquired, idiopathic disorder that is observed in patients with renal disease. Most patients with NFD have undergone dialysis for renal failure [1,2]. It tends to affect mostly the middle-aged. An association of NFD with coagulation abnormalities, recent vascular surgery or intervention (e.g. shunt/fistula and angioplasty), and presence of antiphospholipid antibodies has been discussed by several authors thus far [1,3], but the origin of the disease is still unknown. A more widespread variant of this fibrosing skin disease with involvement of other organs (e.g. lungs, liver, muscles and the heart) is described as nephrogenic systemic fibrosis (NSF) by Leboit [4], Ting et al. [5] and Daram et al. [6]. NFD is characterized clinically by thickening, induration and hardening of the skin. Distinct nodules also can be seen. The (distal) extremities are the most common area of involvement, followed by the trunk, and the face is almost never involved [1]. The diagnosis of NFD is confirmed in a skin biopsy by specific histopathologic features, namely thickened collagen bundles with surrounding clefts, mucin deposition and a proliferation of fibroblasts and elastic fibers. Signs of inflammation are absent, which makes this disorder a distinct entity [1,7]. In this report, nine end stage renal disease patients undergoing magnetic resonance (MR) angiography are presented, in five of whom skin changes of nephrogenic fibrosing dermatopathy became apparent about 2–4 weeks after the administration of gadolinium (Gd)-containing contrast agent for MR. Patients with and without NFD were compared for possible risk factors to develop this skin disease. Gd is thought to be safe as a contrast agent in renal failure. This case series however, demonstrates that Gd–DTPA possibly plays a triggering role in the development of NFD under certain circumstances.

Arterial media calcification in end-stage renal disease: impact on all-cause and cardiovascular mortality

Abstract: Background Cross-sectional and follow-up studies on end-stage renal disease patients showed that arterial calcifications are associated with cardiovascular (CV) morbidity and are an independent predictor of all-cause and CV mortality. However, these studies did not examine the impact on prognosis according to the type of calcification, i.e. intimal vs medial. Arterial media calcification (AMC), a non-occlusive condition, affects haemodynamics differently from arterial intima calcification (AIC), which occurs in atherosclerotic plaques. The aim of this study was to investigate the prognostic value of AMC in relationship to all-cause or CV mortality for stable haemodialysis (HD) patients. Methods We included 202 such patients in the present study. At baseline, soft-tissue native radiograms of the pelvis and the thigh were analysed for the presence and type (AMC vs AIC) of arterial calcifications. All patients underwent B-mode ultrasonography of the common carotid artery to determine the presence of atherosclerotic calcified plaques, measurement of aortic pulse wave velocity and echocardiography. Results AIC was usually observed in older patients with a clinical history of atherosclerosis before starting HD treatment and typical risk factors associated with atherosclerotic disease. AMC was observed in young and middle-aged patients without conventional atherosclerotic risk factors. AMC was closely associated with the duration of HD and calcium-phosphate disorders, including the oral dose of elemental calcium prescribed as phosphate binder (CaCO(3)). Compared to patients with AIC, patients with AMC had a longer survival, but in turn their survival was significantly shorter than that of patients without calcifications. Conclusions AMC is a strong prognostic marker of all-cause and CV mortality in HD patients, independently of classical atherogenic factors. The principal effect of AMC on arterial function is increased arterial stiffness.

Arterial stiffening and vascular calcifications in end‐stage renal disease

Abstract: Background Epidemiological studies have identified aortic stiffness as an independent predictor of cardiovascular mortality in end-stage renal disease (ESRD) patients. In these patients, aortic pulse wave velocity (PWV) was associated with mediacalcosis, but the influence of arterial calcifications on the viscoelastic properties of large arteries was not well characterized. The purpose of the present study was to analyse the influence of arterial calcifications on arterial stiffness in stable haemodialysed patients. Methods We studied 120 stable ESRD patients on haemodialysis. All patients underwent B-mode ultrasonography of common carotid artery (CCA), aorta, and femoral arteries to determine CCA distensibility, the elastic incremental modulus (Einc), and the presence of vascular calcifications. All patients underwent measurement of aortic PWV and echocardiogram. The presence of calcifications was analysed semiquantitatively as a score (0 to 4) according to the number of arterial sites with calcifications. Results Our observations indicate that arterial and aortic stiffness is significantly influenced by the presence and extent of arterial calcifications. The extent of arterial calcifications is in part responsible for increased left ventricular afterload, and is inversely correlated with stroke volume. The influence of calcifications is independent of the role of ageing and blood pressure. Arterial calcifications density increases with age, duration of haemodialysis, the fibrinogen level, and the prescribed dose of calcium-based phosphate binders. Conclusions The results of this study showed that the presence of vascular calcifications in ESRD patients was associated with increased stiffness of large capacity, elastic-type arteries, like the aorta and CCA. The extent of arterial calcifications increased with the use of calcium-based phosphate-binders.

Are there two types of malnutrition in chronic renal failure? Evidence for relationships between malnutrition, inflammation and atherosclerosis (MIA syndrome)

Abstract: Many methods have been used to assess the presence It is believed that malnutrition is common in patients with chronic renal failure (CRF). They have reduced of malnutrition in patients with CRF. A history of weight loss and symptoms such as anorexia, nausea body weight, depleted energy (fat tissue) stores, loss of somatic protein ( low muscle mass) and low levels of and vomiting may indicate impending or established malnutrition. Anthropometric measurements, such as serum albumin, transferrin, pre-albumin and other visceral proteins. Various studies show signs of malnumid-arm muscle circumference, skinfold thickness and hand-grip strength may all be useful tools for estimattrition in 23–76% of haemodialysis (HD) and 18–50% of peritoneal dialysis (PD) patients [1–4]. Such variing malnutrition. Hand-grip strength, in particular, has been shown to be an inexpensive, reliable and easily ations in the prevalence of malnutrition may be related to factors such as age, case mix, co-morbid conditions performed parameter of nutrition [4,8] that also predicts mortality in CRF patients (unpublished observaand quality of dialysis therapy. The aetiology of malnutrition in CRF is complex and may include many tion). Creatinine kinetics have also been advocated as a method to assess nutritional status. However, recent factors, e.g. poor food intake because of anorexia, nausea and vomiting due to uraemic toxicity, hormonal evidence suggests that it is unreliable in individual CRF patients [8,9]. More sophisticated methods used derangements, acidosis and increased resting energy expenditure. to evaluate nutritional status include bio-electrical impedance, dual-emission X-ray absorptiometry While malnutrition by definition is caused by poor nutritional intake, laboratory or anthropometric meas(DXA), nuclear magnetic resonance, computerized tomography, total body potassium and total body urements are generally used to define it clinically. Other factors can cause the same changes in body and plasma nitrogen, but mostly as research tools. Finally, several biochemical markers [e.g. serum albumin, pre-albumin, protein composition, especially inflammatory and infectious complications [5,6 ] and chronic heart failure insulin-like growth factor-1 (IGF-1) and transferrin] have been used to evaluate nutritional status. Of these (CHF). In addition, factors directly associated with the dialytic procedure, such as bio-incompatibility, biochemical markers, serum albumin so far has been the most common to assess malnutrition, and hyponutrient losses in the dialysate and, during PD, poor appetite due to abdominal discomfort and uptake of albuminaemia has sometimes, perhaps erroneously (see below), been used to diagnose malnutrition [10]. glucose may also contribute to what we define as malnourishment in CRF. These may exert their action either by direct nutrient loss or by triggering the Protein and energy requirements in chronic renal inflammatory response. However, since malnutrition failure also occurs in pre-dialysis patients [7], it is evident that dialysis-unrelated factors, e.g. infectious and The protein requirements in maintenance dialysis inflammatory complications as well as co-morbidity, patients are not well defined. It can be assumed that may also be important contributors to malnutrition the variation in protein requirements is much greater in CRF. among dialysis patients than in healthy subjects, due to additional causes of variation, such as endocrine Correspondence and offprint requests to: Peter Stenvinkel, MD, and biochemical abnormalities, anaemia, drugs, physDepartment of Renal Medicine, K56, Huddinge University Hospital, S-141 86 Huddinge, Sweden. ical inactivity and co-morbid conditions, e.g. cardiovas-