Chronic Uremia Research Articles

Compositional characteristics of the gut microbiome in patients with uremia.

During acute or chronic uremia, the cumulative harmful effects of uremic toxins result in numerous health problems and, ultimately, mortality. Previous research has identified that uremic retention solutes originate from the gut microbiome, indicating that uremia may be closely associated with gut microbiome dysbiosis. To deepen our understanding of the compositional characteristics of the gut microbiome in patients with uremia and thereby promote precision medicine in the treatment of uremia, we conducted a study of the compositional characteristics of the gut microbiome in 20 patients with uremia. The gut microbiome diversity of uremic patients and the control group showed certain differences. Nonmetric multidimensional scaling analysis showed that the beta diversity of the gut microbiome of uremic patients was significantly different from that of the healthy control individuals, with a distinct clustering effect in the uremic patient group, and it also showed a similarly distinct clustering effect in the healthy control group. The Chao1 index and Sobs index were significantly lower in the uremic patient group than in the healthy control group (P < 0.05). By analyzing the composition and abundance distribution of the gut microbiome in the uremic patient group and healthy control group, we found that the relative abundance of the gut microbiome constituents Fusobacteriota, Enterobacteriaceae, Oscillospirales, Ruminococcaceae, and Lachnospiraceae was significantly increased in the intestines of uremic patients. We also detected the rare taxa Erysipelotrichaceae, which was present only in the uremic patient group. Predictive functional analysis suggested that an increased abundance of Ruminococcaceae and Lachnospirales, which are associated with indoxyl sulfate and phenylacetyl glutamine, and an increased abundance of Oscillospirales, which is associated with pyruvate metabolism, in uremic patients may strongly influence the gut environment according to renal function, resulting in dysbiosis associated with uremic toxin production. Rare taxa such as Erysipelotrichaceae have been suggested to be detrimental to intestinal disease. Further research into these gut microbiomes may provide new ideas for the prevention and treatment of uremia with the gut microbiome.

Uremic Leontiasis Ossea Secondary to Hyperparathyroidism in Three Patients with End Stage Renal Disease

Renal osteodystrophy is a common complication referring to the skeletal changes associated with the phosphocalcic disorders of chronic uremia in patients with end-stage kidney disease. Uremic leontiasis ossea (ULO) is a rare and severe form of renal osteodystrophy with characteristic overgrowth of the cranial vault and facial bones. Computed tomography (CT) findings are particularly characteristic and include serpiginous tunneling within the maxillofacial bones and cortical bone resorption. The recognition of its radiological appearance and abrupt management are essential to avoid its devastating esthetic and functional impairments. Today's better medical facilities have improved hemodialysis methods, and meticulous patient follow‐up has decreased the incidence of leontiasis. In this paper, we report three rare cases of patients with end stage renal failure who presented with multiple face swellings and were diagnosed with ULO.

Gut Dysbiosis in Experimental Kidney Disease: A Meta-Analysis of Rodent Repository Data.

Alterations in gut microbiota contribute to the pathophysiology of a diverse range of diseases, leading to suggestions that chronic uremia may cause intestinal dysbiosis that contributes to the pathophysiology of CKD. Various small, single-cohort rodent studies have supported this hypothesis. In this meta-analysis of publicly available repository data from studies of models of kidney disease in rodents, cohort variation far outweighed any effect of experimental kidney disease on the gut microbiota. No reproducible changes in animals with kidney disease were seen across all cohorts, although a few trends observed in most experiments may be attributable to kidney disease. The findings suggest that rodent studies do not provide evidence for the existence of "uremic dysbiosis" and that single-cohort studies are unsuitable for producing generalizable results in microbiome research. Rodent studies have popularized the notion that uremia may induce pathological changes in the gut microbiota that contribute to kidney disease progression. Although single-cohort rodent studies have yielded insights into host-microbiota relationships in various disease processes, their relevance is limited by cohort and other effects. We previously reported finding metabolomic evidence that batch-to-batch variations in the microbiome of experimental animals are significant confounders in an experimental study. To attempt to identify common microbial signatures that transcend batch variability and that may be attributed to the effect of kidney disease, we downloaded all data describing the molecular characterization of the gut microbiota in rodents with and without experimental kidney disease from two online repositories comprising 127 rodents across ten experimental cohorts. We reanalyzed these data using the DADA2 and Phyloseq packages in R, a statistical computing and graphics system, and analyzed data both in a combined dataset of all samples and at the level of individual experimental cohorts. Cohort effects accounted for 69% of total sample variance ( P <0.001), substantially outweighing the effect of kidney disease (1.9% of variance, P =0.026). We found no universal trends in microbial population dynamics in animals with kidney disease, but observed some differences (increased alpha diversity, a measure of within-sample bacterial diversity; relative decreases in Lachnospiraceae and Lactobacillus ; and increases in some Clostridia and opportunistic taxa) in many cohorts that might represent effects of kidney disease on the gut microbiota . These findings suggest that current evidence that kidney disease causes reproducible patterns of dysbiosis is inadequate. We advocate meta-analysis of repository data as a way of identifying broad themes that transcend experimental variation.

Mineralização, ulceração e epistaxe em um cão com uremia causada por insuficiência renal crônica

ABSTRACT: Soft tissue mineralization and epithelial ulceration are common findings in dogs with uremia, being commonly reported in the gastrointestinal tract, lungs and pleura. This report described a case of nasal mucosal mineralization and ulceration contributing to recurrent epistaxis in a dog with chronic renal failure and uremia. A dog with recurrent epistaxis accompanied by elevated urea and creatinine was hospitalized. Platelet count and coagulation tests were within normal limits. Chronic renal failure was diagnosed, and the dog was euthanized. On necropsy, the kidneys were small, with an irregular capsular surface. The nasal conchae were slightly reddish. Histopathology revealed chronic glomerulonephritis, with gastric mineralization and bilateral parathyroid hyperplasia. Vascular and basal lamina mineralization, epithelial ulceration and hemorrhage were seen in the nasal conchae. The observed findings indicated that nasal mineralization and ulceration were caused by uremia. The severity of histopathological findings suggested that nasal mineralization/ulceration may have caused or at least contributed to epistaxis in this dog. We hope to stimulate further investigations into possible association between uremia, nasal mucosa mineralization/ulceration and epistaxis in dogs.

Ntrk1 promotes mesangial cell proliferation and inflammation in rat glomerulonephritis model by activating the STAT3 and p38/ERK MAPK signaling pathways

BackgroundMesangial proliferative glomerulonephritis (MsPGN) accounts for a main cause of chronic kidney disease (CKD), chronic renal failure and uremia. This paper aimed to examine the effect of Ntrk1 on MsPGN development, so as to identify a novel therapeutic target for MsPGN.MethodsThe MsPGN rat model was constructed by single injection of Thy1.1 monoclonal antibody via the tail vein. Additionally, the Ntrk1 knockdown rat model was established by injection of Ntrk1-RNAi lentivirus via the tail vein. Periodic acid-schiff staining and immunohistochemistry (IHC) were performed on kidney tissues. Moreover, the rat urinary protein was detected. Mesangial cells were transfected and treated with p38 inhibitor (SB202190) and ERK inhibitor (PD98059). Meanwhile, the viability and proliferation of mesangial cells were analyzed by cell counting kit-8 (CCK-8) and 5-Ethynyl-2′-deoxyuridine assays. Gene expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western-blot (WB) assays.ResultsThe proliferation of mesangial cells was enhanced in glomerulus and Ki67 expression was up-regulated in renal tubule of MsPGN rats. The urine protein level increased in MsPGN rats. Pro-inflammatory factors and Ntrk1 expression were up-regulated in glomerulus of MsPGN rats. Ntrk1 up-regulation promoted the viability, proliferation, expression of pro-inflammatory factors and activation of the STAT3, p38 and ERK signaling pathways in mesangial cells. Ntrk1 knockdown reduced mesangial cell proliferation, urine protein, pro-inflammatory factors, activation of STAT3, p38 and ERK signaling pathways in glomerulus, and decreased Ki67 expression in renal tubule of MsPGN rats. Treatment with SB202190 and PD98059 reversed the effect of Ntrk1 on promoting the viability, proliferation and inflammatory response of mesangial cells.ConclusionNtrk1 promoted mesangial cell proliferation and inflammation in MsPGN rats by activating the STAT3 and p38/ERK MAPK signaling pathways.

412.1: Lip Actinic Cheilitis and Its Relationship to Clinical Characteristics and Immunosuppression in Kidney Transplant Recipients

Introduction: Due to drug immunosuppression after kidney transplantation (KT), as well as factors such as chronic uremia and chronic sun exposure, Kidney Transplant Recipients (KTR) have a 46-fold increased incidence of Lip Cancer (LC). Because of the high prevalence of LC in KTR, there are concerns about its prevention, which can be accomplished by diagnosing Actinic Cheilitis (AQ) on lips, a potentially malignant oral lesion that can progress to LC. Aim: The purpose of this investigation was to see if there was a link between the clinical manifestations of AQ and the clinical profile of KTRs. Methods: Convenience sampling in a cross-sectional observational clinical study. An expert researcher completed the diagnosis and clinical staging of AQ in KTRs using Pointevin et al 2017 criteria and a clinical evaluation and photographic record of six different angulations of the lower lip were used to calibrate the researcher (Kappa intra-avaliador >0.8). Demographic data, time since KT, immunosuppressants, exposure to AQ risk factors such as alcoholism, smoking, chronic sun exposure, and exposure to volatile chemical agents, and history of positive serology for oncogenic viruses after KT were all obtained retrospectively from electronic medical records. For the association of variables, Chi-square and Macnemar tests were performed, with a significance value of (0.05). Results: The sample size was 48 (100%) KTR, with 29 people diagnosed with AQ (60.41 percent). Light-siknned KTR was linked with the most severe AQ staging in 9 subjects (18.75 percent; p=0.035). History of exposure to volatile chemical agents (16.33 percent; p=0.007), drunkenness (15.25 percent; p=0.008), and smoking (20.66 percent; p=0.05) were also risk factors for AQ. A history of prolonged sun exposure was linked to a higher severity of QA 22(45.83 percent; p<0.001). The prevalence of AQ was linked to the usage of tacrolimus 43 (89,58 percent; p<0.001) and azathioprine 11 (22,91 percent; p0.001). However, the use of Mycophenolate Mofetil was linked to the most severe cases of AQ in 7 patients (14.58 percent; p=0.05). Individuals who got sirolimus, on the other hand, showed less AQ expression, with 7 patients (14.58 percent; P=0.016) manifesting with lesser degrees. After TxR, positive Epstein-Barr Virus serology was linked to the existence of AQ 17 (35,41 percent; p=0.028). Conclusion: The presence and severity of AQ in KTR were linked to fair skin, chronic sun exposure, Epstein-Barr Virus infections, and the use of Mycophenolate Mofetil. Sirolimus appears to have a protective effect against the development of AQ. It is possible to select groups of patients at higher risk for AQ and, as a result, for LC using this clinical profile associated with the manifestation of AQ, allowing for prevention and early diagnosis. This study was approved by the Ethics and Research in Human Beings Committee under protocol CAAE12798019.3.0000.5417.

Glia as a key factor in cell volume regulation processes of the central nervous system.

Brain edema is a pathological condition with potentially fatal consequences, related to cerebral injuries such as ischemia, chronic renal failure, uremia, and diabetes, among others. Under these pathological states, the cell volume control processes are fully compromised, because brain cells are unable to regulate the movement of water, mainly regulated by osmotic gradients. The processes involved in cell volume regulation are homeostatic mechanisms that depend on the mobilization of osmolytes (ions, organic molecules, and polyols) in the necessary direction to counteract changes in osmolyte concentration in response to water movement. The expression and coordinated function of proteins related to the cell volume regulation process, such as water channels, ion channels, and other cotransport systems in the glial cells, and considering the glial cell proportion compared to neuronal cells, leads to consider the astroglial network the main regulatory unit for water homeostasis in the central nervous system (CNS). In the last decade, several studies highlighted the pivotal role of glia in the cell volume regulation process and water homeostasis in the brain, including the retina; any malfunction of this astroglial network generates a lack of the ability to regulate the osmotic changes and water movements and consequently exacerbates the pathological condition.

Nursing Safety Management and Countermeasures of Patients with Chronic Renal Failure and Uremia

Nursing Safety Management and Countermeasures of Patients with Chronic Renal Failure and Uremia

Uremic mouse model to study vascular calcification and “inflamm-aging”

Calcification and chronic inflammation of the vascular wall is a high-risk factor for cardiovascular mortality, especially in patients with chronic uremia. For the reduction or prevention of rapid disease progression, no specific treatment options are currently available. This study aimed to evaluate an adenine-based uremic mouse model for studying medial vessel calcification and senescence-associated secretory phenotype (SASP) changes of aortic tissue to unravel molecular pathogenesis and provide a model for therapy testing. The dietary adenine administration induced a stable and similar degree of chronic uremia in DBA2/N mice with an increase of uremia blood markers such as blood urea nitrogen, calcium, creatinine, alkaline phosphatase, and parathyroid hormone. Also, renal fibrosis and crystal deposits were detected upon adenine feeding. The uremic condition is related to a moderate to severe medial vessel calcification and subsequent elastin disorganization. In addition, expression of osteogenic markers as Bmp-2 and its transcription factor Sox-9 as well as p21 as senescence marker were increased in uremic mice compared to controls. Pro-inflammatory uremic proteins such as serum amyloid A, interleukin (Il)-1β, and Il-6 increased. This novel model of chronic uremia provides a simple method for investigation of signaling pathways in vascular inflammation and calcification and therefore offers an experimental basis for the development of potential therapeutic intervention studies.Graphical abstract

Gut Microbiota as a Source of Uremic Toxins.

Uremic retention solutes are the compounds that accumulate in the blood when kidney excretory function is impaired. Some of these compounds are toxic at high concentrations and are usually known as “uremic toxins”. The cumulative detrimental effect of uremic toxins results in numerous health problems and eventually mortality during acute or chronic uremia, especially in end-stage renal disease. More than 100 different solutes increase during uremia; however, the exact origin for most of them is still debatable. There are three main sources for such compounds: exogenous ones are consumed with food, whereas endogenous ones are produced by the host metabolism or by symbiotic microbiota metabolism. In this article, we identify uremic retention solutes presumably of gut microbiota origin. We used database analysis to obtain data on the enzymatic reactions in bacteria and human organisms that potentially yield uremic retention solutes and hence to determine what toxins could be synthesized in bacteria residing in the human gut. We selected biochemical pathways resulting in uremic retention solutes synthesis related to specific bacterial strains and revealed links between toxin concentration in uremia and the proportion of different bacteria species which can synthesize the toxin. The detected bacterial species essential for the synthesis of uremic retention solutes were then verified using the Human Microbiome Project database. Moreover, we defined the relative abundance of human toxin-generating enzymes as well as the possibility of the synthesis of a particular toxin by the human metabolism. Our study presents a novel bioinformatics approach for the elucidation of the origin of both uremic retention solutes and uremic toxins and for searching for the most likely human microbiome producers of toxins that can be targeted and used for the therapy of adverse consequences of uremia.

MO713ENCAPSULATING PERITONEAL SCLEROSIS IN KIDNEY TRANSPLANT RECIPIENTS

Abstract Background and Aims Encapsulating peritoneal sclerosis (EPS) is a life-threatening complication of long-term peritoneal dialysis (PD). Causative factors are the chronic exposure to bioincompatible PD and peritonitis episodes. Pro-inflammatory state and oxidative stress associated with chronic uremia may further accelerate these pathomechanisms. Clinical symptoms are, essentially, signs of intestinal obstruction. Treatments commonly used are corticosteroids, tamoxifen, immunosuppressants like azathioprine, mycophenolate mofetil (MMF), or mTOR inhibitors which has fibrinolytic properties and may help with reducing inflammation. In the last ten years, the incidence of SEP in kidney transplant recipients has increased, but few cases have been reported. Given the rare nature of this pathology, we decided to publish the cases of two EPS happening after kidney transplantation (KT). Case report We report the cases of two male patients aged 46 and 25 with a history of chronic renal failure, who benefited of continuous ambulatory peritoneal dialysis (CAPD) for three years. The first patient was switched to haemodialysis (HD) for sub-dialysis, with one episode of peritonitis and one episode of catheter infection. The second patient had three episodes of peritonitis complicated by asymptomatic EPS, hence its transfer to HD. Our two patients presented, at 30 and 40 days post KT, an episode of acute intestinal obstruction with abdominal scans fitting with a mechanical bowel obstruction on an encapsulating peritonitis without signs of complication. Both patients were on corticosteroid therapy (15 and 17.5 mg/day) combined with MMF and Calcineurin inhibitors (CNIs) (Tacrolimus). Medical measures were not effecient. Surgical treatment was then considered. During the operation, a classical picture of EPS was found characterized by a thin cocoon-like sclerotic membrane encasing the small bowel. A complete resection of the encapsulating sclerotic membrane and total adhesiolysis were performed, with an immediate improvement on the clinical level. No recurrence was noted for both patients at 5 and 24 months respectively. Conclusion The specificities of our patients compared to the reported cases were the short duration of the PD and the relatively young age. In fact, some studies demonstrated an increased incidence of EPS in younger patients. In addition, this complication has declared itself despite corticosteroid therapy. Some case reports have demonstrated an increase in the incidence of SEP in kidney transplant patients, suggesting the possible implication of CNIs which have a profibrotic effect and may promote peritoneal matrix accumulation.

The kidney in COVID-19: protagonist or figurant?

The etiology of injury in COVID-19 patients is diverse and multifactorial. Autopsy and biopsy studies reveal, alongside podocyte and tubular cell anomalies, the presence of virion within the cells. Evidence suggests that, in addition to the direct cytopathic effect of SARS-CoV-2 on the glomeruli and renal tubules, there is also the indirect effect of cell-mediated immunity, the cytokines storm and the cross-talk between organs with possible systemic effects of the disease. These mechanisms are interconnected and have profound therapeutic implications involving extracorporeal removal of inflammatory cytokines. Dialysis patients, and children, in particular, should be classified as "at high risk" of contracting the disease. Infections are one of the most frequent causes of death in children with chronic renal failure who undergo dialysis. The reasons for this particular susceptibility are to be found in the compromised immune system, secondary to chronic malnutrition, immunosuppressive therapy, and uremia, frequent contact with healthcare personnel and other patients attending the dialysis unit and in need of the presence of other family members during treatment.

Differences and Effects of Metabolic Fate of Individual Amino Acid Loss in High-Efficiency Hemodialysis and Hemodiafiltration

The objective of the study was to quantify the loss and arterial blood concentration of the three main classes of amino acids (AAs)-nonessential amino acids (NEAAs), essential amino acids (EAAs), and branched-chain amino acids-as resulting from high-efficiency hemodialysis (HED) and hemodiafiltration (HDF). We moreover aimed to identify the different fates and metabolic effects manifested in patients undergoing hemodialysis and the consequences on body composition and influence of nutritional decline into protein energy wasting. Identical dialysis monitors, membranes, and dialysate/infusate were used to ensure consistency. Ten patients were recruited and randomized to receive treatment with on-line modern HED and HDF. Arterial plasma concentrations of individual AAs were compared in healthy volunteers and patients undergoing hemodialysis, and AA levels outflowing from the dialyzer were evaluated. Baseline AA plasma levels of patients undergoing hemodialysis were compared with findings obtained 1year later. A severe loss of AA with HED/HDF was confirmed: a marked loss of total AAs (5g/session) was detected, corresponding to more than 65% of all AAs. With regard to individual AAs, glutamine displayed a consistent increase (+150%), whereas all other AAs decreased after 12months of HD/HDF. Only a few AAs, such as proline, cysteine, and histidine maintained normal levels. The most severe metabolic consequences may result from losses of EAAs such as valine, leucine, and histidine and from NEAAs including proline, cysteine, and glutamic acid eliciting the onset of hypercatabolism threatening muscle mass loss. Dialysis losses, together with the effect of chronic uremia, resulted in a reduction of fundamental EAAs and NEAAs, which progressively led our patients after 12months to a deterioration of lean mass toward sarcopenia. Therefore, the reintroduction of a correctly balanced AA supplementation in patients undergoing HD to prevent or halt decline of hypercatabolism into cachexia is recommended.

Comparison of clinical effect of different dialysis frequency and methods in the treatment of chronic renal failure uremic patients

Objective To observe the clinical efficacy of different dialysis frequency and methods in the treatment of chronic renal failure uremia patients, and to provide a reliable reference for clinical practice. Methods From February 2016 to February 2017, 140 chronic renal failure uremic patients who admitted to the Department of Nephrology at Taizhou Central Hospital were selected and divided into the observation group and the control group by complete random distribution method, with 70 cases in each group.The patients in the control group received 3 times of regular hemodialysis treatment per week, while the observation group received 3 times of regular hemodialysis combined with 1 time of hemodiafiltration treatment per week.The clinical treatment effects and complications of the two groups were compared. Results Compared with blood uric acid(BUA)[(532.09±71.05)mmol/L], serum creatinine(Scr)[(734.34±63.08)μmol/L], blood urea(BUN)[(23.84±2.58)mmol/L], serum phosphorus[(1.98±0.37)mmol/L], parathyroid hormone(PTH)[(464.37±113.92)ng/L], β2 microglobulin(β2-MG)[(13.48±6.38)mg/L]in the control group, BUA[(495.89±58.23)mmol/L], Scr[(684.34±77.32)μmol/L], BUN[(20.62±1.77)mmol/L], serum phosphorus[(1.74±0.44)mmol/L], PTH[(352.14±123.25)ng/L], β2-MG[(9.58±5.45)mg/L] were significantly lower in the observation group, the differences were statistically significant (t=3.29, 4.19, 8.61, 3.49, 5.59, 3.88, all P 0.05). Conclusion Hemodialysis 3 times combined with 1 time of hemodiafiltration per week has significant advantage in the treatment of chronic renal failure uremia patients, which can effectively remove urine toxin molecules and reduce the incidence of complications, and it is worthy of clinical application. Key words: Renal failure, chronic; Uremia; Hemodialysis; Hemodiafiltration; Comparative effectiveness research

Analysis of clinical characteristics of severe and critically ill influenza A (H1N1)

To investigate the clinical features, laboratory results, chest CT imaging manifestations and treatments of severe and critical influenza A (H1N1), and to analyze the relationship with the prognosis. The clinical data of 54 adult patients with severe and critical H1N1 admitted to the Fourth People's Hospital of Nanning from November 2018 to February 2019 were analyzed retrospectively. Throat swab specimens of the patients were determined for nucleic acid detection of influenza A (H1N1) virus, and all of the patients were confirmed. The gender, age, course of disease, underlying diseases, symptoms, body temperature, hospital stays, chest CT findings and laboratory results were collected, and the treatments and prognosis were recorded. Of 54 patients, 38 patients were enrolled in severe group, and 16 in critical group. Fever, cough, sputum, shortness of breath and so on could be found in the two groups. The CD4+T lymphocytes were less than normal reference value (410-1 590/μL) in both groups. The chest CT findings manifestations of severe group were scattered patchy shadows and ground glass appearance, all of them were cured and discharged after antiviral, antibiotics, and oxygen treatment. In critical group, the time in hospital was longer, the disease progresses varied faster, the shortness of breath was more apparent, and a large patch of fuzzy and real change shadows on both lungs could be found from CT findings. Compared with the severe group, creatine kinase (CK), lactic dehydrogenase (LDH), C-reactive protein (CRP) and procalcitonin (PCT) levels in the critical group were increased more significantly [CK (U/L): 704.50 (908.50) vs. 146.00 (220.75), LDH (U/L): 614.50 (492.25) vs. 217.00 (142.75), CRP (mg/L): 85.65 (56.13) vs. 18.80 (50.63), PCT (μg/L): 1.30 (5.00) vs. 0.10 (0.16), all P < 0.01], white blood cells count (WBC) and neutrophil ratio were also increased more significantly [WBC (×109/L): 12.37±7.63 vs. 8.29±3.32, neutrophil ratio: 0.81±0.11 vs. 0.75±0.11] without statistical differences (both P > 0.05). Nine patients in critical group were cured with cure rate of 56.25%. Seven patients died with mortality of 43.75%, including 2 patients with acquired immunodeficiency syndrome (AIDS) and uremia respectively, who had multiple organ failure (MOF) on admission and waive the mechanical ventilation treatment; 3 patients complicated with acute renal failure but abandon hemodialysis; 1 patient with nasopharyngeal carcinoma radiotherapy after operation; and 1 patient with chronic renal failure uremia period combined multiple drug-resistant bacteria infection, and died from MOF finally. The patients with severe and critical influenza A (H1N1) show fever, cough, dyspnea, and organ dysfunction in varying degrees. Severe patients were mainly pulmonary lesions, while critical patients show MOF such as heart, lung and kidney, and the lesions progressed rapidly. The major cause of death for critical influenza A (H1N1) may be chronic underlying diseases and MOF.

Metabolic syndrome and cardiovascular risk in patients on chronic hemodialysis of University Hospital of Annaba

While cardiovascular diseases are the leading cause of death in chronic hemodialysis patients the prevalence of the metabolic syndrome in these patients is currently poorly explored. The metabolic syndrome is composed of various abnormalities, which considered separately can be considered as innocuous. However, if they are found together in the same patient, they represent a major cardiovascular risk. The objective of the study was to evaluate the prevalence of the metabolic syndrome in chronic hemodialysis patients in the nephrology service of Annaba University Hospital. A prospective study was conducted on 60 patients with end-stage renal failure treated by hemodialysis recruited from the nephrology and hemodialysis unit of Annaba University Hospital in Algeria. The mean patients’ age was 41.55 ± 14.1 years old with a slight male predominance, the sex ratio M/F was 1.14. The data were collected by using a questionnaire including the patient size, weight, waist circumference and blood pressure. The biochemical parameters included: blood glucose, total cholesterol, HDL-C, LDL-C and triglycerides. The metabolic syndrome was present in 47% of the study population. Arterial hypertension was the most common abnormality with a prevalence of 70% followed by the decrease in HDL-C and abdominal obesity in 65% and 52% of the study population, respectively. Hypertriglyceridemia was present in 40%, and hyperglycemia in 35% of the patients. The cardiovascular risk was predominantly multifactorial: 58% of patients had at least 2 risk factors associated with their hypertension. The frequency and severity of cardiovascular and coronary complications, particularly in chronic uremia, necessitates a correction of risk factors, some of which are inherent in chronic renal failure. The evaluation of the metabolic syndrome is a mean of screening so as to prevent its complications, in particular the cardiovascular ones, the main cause of death in these patients.

HBV vaccination with Fendrix is effective and safe in pre-dialysis CKD population

Patients with chronic kidney disease have a poor response to hepatitis B vaccine due to the immunodeficiency conferred from chronic uremia. A recombinant HB vaccine containing an improved adjuvant system AS04 (HBV-AS04) has been manufactured but scarce evidence exists on HBV-AS04 use among patients with CKD. To assess efficacy and safety of an adjuvanted recombinant vaccine (HBV-AS04) in a large cohort of CKD patients at pre-dialysis stage (with susceptibility to HBV infection). Patients were prospectively enrolled to receive four 20-mcg doses of HBV-AS04 by intramuscular route (deltoid muscle) at months 1, 2, 3, and 4. Anti-HBs surface antibody concentrations were tested at intervals of 1, 2, 3, 4, and 12months. Multivariate analyses were performed to assess the parameters, which predicted immunologic response to HBV-AS04 vaccine. One hundred and seven patients were included and 102 completed the study. At completion of vaccine schedule, the frequency of responders (anti-HBs titers≥10mIU/mL) was 95% (97/102) (mean anti-HBs antibody titers, 688.9±385mIU/mL), according to per-protocol analysis. Serum haemoglobin levels were greater in responder than non- or low-responder patients to HBV-AS04 (P=0.04) and this was confirmed by multivariate analysis. The seroprotection rate at month 50 was 88% (30/34) with lower anti-HBs antibody titers (218.5±269.6mIU/mL, P=0.001). No major side effects were observed. Our prospective study performed in a real-world setting showed a high immunogenicity and safety of HBV-AS04 vaccine in patients with CKD not yet on maintenance dialysis. Studies provided with longer follow-ups are under way to assess the durability of seroprotection in responders.

Treatments for Iron Deficiency (ID): Prospective Organic Iron Fortification.

Iron deficiency, one of the most common nutritional deficient disorders, frequently affects infants, adolescents and pregnant women and impairs growth, development and immune responses. Iron deficiency may also be secondary to gastrointestinal conditions such as gastrectomy and inflammatory bowel disease, as well as cancer and chronic uremia. Iron supplementation is the most commonly selected treatment option for iron deficiency. This review summarizes the iron compounds currently recommended for the iron fortification of foods and for clinical use. Additionally, this review discusses and compares the important aspects of high-quality iron compounds/products and classes of compounds that enhance iron bioavailability. The development of efficient iron fortification methods remains the most cost-effective and long-term approach to the treatment of iron deficiency or related anemia. To date, no orally administered options for iron fortification can sufficiently replace the parenteral administration of iron supplements, which includes the intramuscular injection of iron-dextran to neonatal piglets and intravenous injection of iron supplements to patients with gastrointestinal disorders. Iron bioavailability may be enhanced by encouraging customers to ingest iron-enriched foods together with dietary sources of vitamin C, folic acid and/or oligosaccharides.

The role of the intestinal microbiota in uremic solute accumulation: a focus on sulfur compounds.

The gut microbiota is considered to be a novel important factor to take into account in the pathogenesis of chronic kidney disease and uremia. Much attention has been paid to specific uremic retention solutes of microbial origin, such as indoxyl sulfate, p-cresyl sulfate, and trimethylamine-N-oxide. However, other novel less well studied compounds, such as hydrogen sulfide and related sulfur metabolites (sulfane sulfur, lanthionine, etc.), should be included in a more comprehensive appraisal of this topic, in light of the potential therapeutic opportunities for the future.

Urocystitis, pyelonephritis, renal papillary necrosis and chronic tubulointerstitial disease causing chronic renal insufficiency in a Siberian tiger (Panthera tigris altaica): a case report

The present case report describes a case of chronic renal failure characterised by renal medullary fibrosis and renal papillary necrosis in a male Siberian tiger (Panthera tigris altaica). A 12-year-old male Siberian tiger presented with depression, anorexia and weight loss. Blood urea nitrogen (&amp;gt; 50.4 mmol/l) and ammonia (71.7 µmol/l) were increased, suggesting chronic renal failure and uraemia. The tiger died secondary to gastric haemorrhage. At necropsy, the kidneys had yellow lesions in the medulla and renal papillae and petechiae in the cortex. The stomach had multiple mucosal ulcers and haemorrhage. Microscopically, marked renal medullary fibrosis and renal papillary necrosis were observed with tubular atrophy, degeneration, coagulative necrosis, calcification and chronic inflammatory cell infiltration. The renal cortex showed moderate interstitial inflammation. The urinary bladder exhibited epithelial desquamation and submucosal fibrosis. The tiger was diagnosed with chronic renal failure secondary to renal papillary necrosis and medullary fibrosis.