Uremic Research Articles

MO204CHRONIC KIDNEY DISEASE, SLEEPINESS, MILD COGNITIVE IMPAIRMENT AND FINE MOTOR CONTROL

Abstract Background and Aims Chronic kidney disease (CKD) is a systemic condition because it modifies all organs' function due to an imbalance in plasma volume, electrolytes, hormones, and proteins. Indeed, at the nervous system level, mild cognitive impairment (MCI), sleep disorders and depression often accompany CKD. MCI partially explains the low quality of life of CKD patients, comparable to that of metastatic cancer patients. Mild Cognitive Impairment (MCI) has a high prevalence in this cohort (27-62%). Nevertheless, scattered literature data suggest that CKD patients can also have poor motor control, evidenced by a higher risk of falls, postural instability, reduced gait speed. In this cohort, few data are available regarding the motor circuits called central pattern generators, which control physiological tremor. Specifically, uraemic encephalopathy accentuates physiological tremor, which is regulated by central and peripheral oscillators. Overall, subtle changes in motor control often accompany other forms of MCI. Therefore, this study aimed at evaluating the effects of chronic kidney disease on cognitive and motor functions using up-to-date technologies to record physiological tremor and innovative data analysis. Method This retrospective case-control study enrolled 313 patients (139 controls, 79 CKD patients stage III-IV, 35 kidney transplant (Tx), 60 dialysis (HD) patients). These groups were comparable for age and weight. Creatininemia, azotemia, LDL, HDL, hemoglobin, and proteinuria were used for correlative analyses. We evaluated the chronotype using the Morningness-Eveningness Questionnaire (MEQ) and the degree of sleepiness using the Epworth Sleepiness Scale (ESS). Cognitive impairment was assessed by the Montreal Cognitive Assessment test (MoCA). Cognitive domains of the MoCA score were projected onto brain regions using CerebroViz library in R and a new transformation matrix derived from fMRI literature data. UMAP algorithm was used to identify patients' subgroups. The physiological tremor was recorded on patients maintaining the dominant arm extended using the smartphone App Phyphox. The tremor frequency spectrum was extracted by Fourier analysis. Results The sleepiness score (ESS) was significantly increased in HD (ESS = 5±0.4) compared to the healthy controls (ESS= 4±0.41) whereas was not significantly modified in CKD patients (3.24± 0.32). The chronotype was also not significantly different among the various groups. The mean score of the MoCA test was significantly lower in CKD, Tx, and HD groups (CKD MoCA =24.5±0.3; Tx MoCA =25.4±0.6; HD MoCA =24.6±0.7) than controls (MoCA score=28±0.1). A different pattern of impairment in the cognitive domains of MoCA was evidenced in the various groups using the CerebroViz projection and UMAP tools. MoCA score was inversely correlated with proteinuria (Pearson coefficient=-0.47; p<0.05). The higher frequencies of the physiological tremor (11-13 Hz) were significantly more represented in Tx patients compared to controls (p<0.05). Conversely, the lower frequencies (1-4 Hz) were significantly less represented in the HD group compared to controls (p<0.05). The peak frequency was inversely correlated with age in all patients (Pearson coefficient= -0.45; p<0.05) and inversely associated with azotemia levels, particularly in HD patients (Pearson coefficient=0.43; p<0.05). Conclusion Our results suggest that CKD patients present altered cognitive and motor control patterns, linked in part to the proteinuria level, suggesting a pathogenetic role of endothelial dysfunction. The characteristic motor, sleepiness and cognitive patterns of HD patients might be due to the arteriovenous fistula or the other peculiarities of these patients. These results might help identify new early markers of brain dysfunction in these patients, with the possibility of delaying or reversing cognitive decay.

Discontinuation of Complement-Inhibitor Therapy in Patients with Atypical Hemolytic Uremic Syndrome

The terminal complement inhibitor eculizumab has improved the outlook for patients with atypical hemolytic uremic syndrome (aHUS), especially with

POS1367 PROCALCITONIN IN RHEUMATOLOGY

Background:The differentiation between infection and aseptic inflammation is difficult and often a challenge in the daily practice of rheumatology.Procalcitonin (PCT) is a preferred marker for bacterial infections that allows the rheumatologist to make an early diagnosis, choose an appropriate antibiotic therapy for bacterial infection, and avoid unnecessary antibiotic therapy for inflammation.Objectives:To study the levels of PCT in various inflammatory states observed in a rheumatology department, and to assess its possible discriminating role in the differentiation of bacterial infection from other inflammatory processes.Methods:This is a preliminary monocentric retrospective study conducted from January 2018 to December 2020 in our rheumatology department. The inclusion criteria were all patients hospitalized in rheumatology for a rheumatic or autoimmune disease or a bone and joint infection.PCT samples from patients were analyzed along with general signs (fever/chills) and with routine assessment (blood count including white blood cell count(WBC), erythrocyte sedimentation rate (ESR)and C reactive protein(CRP)) in patients admitted to hospitalfor a fever or a biological inflammatory syndrome, or both, with a laboratory cut-off value of 0.5 ng/ml.Results:20 patients were included. Their mean age was 46.1 (extremes 19 – 66)and the with sex ratio was 1. Three patients had a history of autoimmune disease, 2 of neoplasia, 1 with chronic terminal kidney failure and hemodialysis, and 4 patients took antibiotics before hospitalization. The mean PCT was 100.01ng/ml (extremes 0.01-200), and Sensitivity at 57.44% and specificity at 100%, PPV: 100%, NPV: 81.25%.The patients were divided according to their final diagnosis into 3 groups: bacterial or fungal infection; inflammatory abacterian disease (autoimmune or rheumatic flare, neoplasia, metabolic, reactive arthritis); infection + inflammatory abacterian disease. Group 1 included 4 patients, their mean PCT was 6.92ng/ml (0.16-26.80),mean CRP was 131.725 mg/L, and mean ESR was 50 mm, and 25% had hyperleukocytosis.2 patients had already taken antibiotics before admission. Group 2 included 13 patients, their mean PCT was 0.025 ng/mL (0.01-0.13), mean CRP was 132.25mg/L, mean ESR was 84.38mm, and 30.77% of them had hyperleukocytosis. Group 3 included 3 patients, their mean PCT was 66.88 ng/mL (0.02-200), mean CRP was 560 mg/L, mean ESR was 107.33 mm, and 33.33% had hyperleucocytosis. The patient with the highest PCT was admitted for a sepsis with uremic encephalopathy that improved after hemodialysis. A control PCT was made in 2 patients with infection who received antibiotics,showing a decrease or negativation compared to the initial value of PCT.Conclusion:Our study showed that PCT levels only increased significantly in bacterial infections. The PCT values were more discriminating than the level of WBC and CRP in differentiating a bacterial infection from another inflammatory process, hence the value of using this marker in case diagnosis doubt.Group 1(n=4)Group 2(n=13)Group 3(n=3)Mean age4546.7744.67Sex ratio M/F2/28/50/3Reason for hospitalizationPhlegmon of the left shoulder and inflammatory gonalgia in a feverish context 25%Multiple vertebral fractures 25%Acute monoarthritis of the left knee 25%Pain in the left hip with functional impairment 25%Inflammatory polyarthralgia15.38%Inflammatory back pain 23.07%Activity of his autoimmune 15.38%diseaseChronic hip pain 7.69%Acute febrile polyarthralgia 30.77%Biarthritis 7.69%Acute febrile polyarthralgia 66.67%Flare of polymyalgia rheumatica 33.33%HistoryNeoplasia 25%Autoimmune disease 23.07%End-stage chronic renal disease with hemodialysis 33.33%PCT indicationSuspected septic arthritis 75%Exploration of inflammatory syndrome 25%Suspicion of arthritis 46.15%Exploration of inflammatory syndrome 53.85%Suspicion of sepsis 33.33%Exploration of inflammatory syndrome 66.67%Mean PCT value (ng/ml)6.920.02566.88fever/chills75%30.77%33.33%Biological parametersHyperleukocytosisESR (mm)CRP (mg/L)25%50131.72530.77 %84.38132.2533.33%107.33560Disclosure of Interests:None declared

COVID‐19 Pneumonia and Exacerbation of Multiple Sclerosis Flares Necessitating Placement of Suprapubic Catheter and PEG Tube: A Case Study

One of the public health challenges posed by the COVID‐19 pandemic is the management of patients with chronic neurological conditions, including multiple sclerosis. Here, we present the case of a 45‐year‐old male patient with severe multiple sclerosis without disease‐modifying therapy who was admitted for COVID‐19 pneumonia, treated with dexamethasone and Remdesivir, and then discharged. Subsequently, the patient was readmitted twice in the next month for complications arising from worsening dysphagia, musculoskeletal weakness, and neurogenic bladder. On the first of these re‐admissions, the patient presented with altered mental status, secondary to uremic encephalopathy due to acute kidney injury precipitated by lack of adequate PO hydration. This admission was complicated by multiple pulmonary emboli necessitating transfer from the floor to the ICU, in addition to central line placement, candidemia, Pseudomonas urinary tract infection, and hemorrhagic cystitis. Despite this protracted course, the patient's mental function and orientation slowly improved as his renal function improved secondary to intravenous fluid administration. Because the patient's worsening dysphagia and weakness made adequate hydration by mouth untenable, the possibility of PEG tube placement was broached with the patient and his family. After consent was obtained, a PEG tube was placed, and the patient was subsequently discharged home under the care of his family. Two days after discharge, however, the patient presented to the Emergency Department, again with altered mental status due to uremic encephalopathy secondary to dehydration. During this admission, blood cultures also revealed Pseudomonal sepsis, likely secondary to recurrent UTI ultimately caused by neurogenic bladder. Accordingly, a suprapubic catheter was placed, and the care team worked with the patient's family to develop an adequate hydration regime before discharge. This case study suggests that COVID‐19 may exacerbate ongoing neuropathological processes in patients with chronic neurological disease, and illustrates strategies clinicians and patients use to grapple with these changes.

Concerted outcome of metformin and low dose of radiation in modulation of cisplatin induced uremic encephalopathy via renal and neural preservation

AimThe therapeutic expediency of cisplatin was limited due to its nephrotoxic side effects, so this study planned to assess the nephrotic and neuroprotective impact of metformin (MET) and low-dose radiation (LDR) in cisplatin-prompted kidney injury and uremic encephalopathy (UE). MethodsThe effect of the 10-day MET treatment (200 mg/kg, orally) and/or fractionated LDR (0.25 Gy, of the total dose of 0.5 Gy, 1st and 7th day, respectively) on (5 mg/kg, intraperitoneally) cisplatin as a single dose was administered at the 5th day. Serum urea, creatinine and renal kidney injury molecule-1 were measured for the assessment of kidney function. Furthermore, the antioxidant potential in the renal and brain tissues was evaluated through, malondialdehyde and reduced glutathione estimation. Moreover, renal apoptotic markers: AMP-activated protein kinase, lipocalin, B-cell lymphoma 2 associated X protein, B-cell lymphoma 2, P53 and beclin 1 were estimated. UE was evaluated through the determination of serum inflammatory markers: nuclear factor kappa B, tumor-necrosis factor-α and interleukin 1 beta likewise, the cognitive deficits were assessed via forced swimming test, gamma-aminobutyric acid, n-methyl-d-aspartate and neuronal nitric oxide synthases besides AMP-activated protein kinase, light chain 3 and caspase3 levels in rats' cerebella. Key findingsThe obtained results revealed a noticeable improvement in the previously mentioned biochemical factors and behavioral tasks that was reinforced by histopathological examination when using the present remedy. Significancemetformin and low doses of radiation afforded renoprotection and neuroprotection against cisplatin-induced acute uremic encephalopathy.

Project extension for community healthcare outcomes improves care and treatment for multidrug-resistant tuberculosis patients in Tanzania.

Project Extension for Community Healthcare Outcomes (Project ECHO) is a telementoring, case based virtual community of practice training and education model connecting experts to primary care clinicians (PCCs). Project ECHO has good evidence for favorable treatment outcomes on wide range of diseases. Since 2017, Tanzania hosts multidrug resistant tuberculosis (MDR TB) ECHO with hub at Kibong'oto Infectious Diseases Hospital. However, little is known on outcomes of MDR TB ECHO. This study aimed to describe the outcomes of MDR TB ECHO in managing MDR TB patients in Tanzania. Review of case studies was conducted at MDR TB ECHO hub in Tanzania. Up to June 2020, a total of 134 sessions and 60 patient cases were presented in MDR TB ECHO. This article describes outcomes of MDR TB ECHO in managing three selected complicated MDR TB patient cases presented. Case 1: Child with MDR TB, neck abscess, and anemia secondary to chronic illness. Case 2: Adult with MDR TB and end stage renal disease co morbidity. Case 3: Adult failing standard MDR TB treatment. Anemia resolved in Case 1; surgical dressing was done to neck abscess and neck healed. Case 2 was initiated with end stage renal disease management; uremic encephalopathy and lower limb edema resolved. Case 3 was initiated with individualized MDR TB treatment. All three patients attained smear and culture conversion and continue with MDR TB treatment. To our knowledge, this is the first report on effectiveness of project ECHO in supporting PCCs in bringing favorable treatment outcomes to MDR TB patients. We advocate adaptation and scale up of ECHO model as an effective approach for strengthening management of MDR TB and other infectious diseases.

Hepatorenal Sendrom Tanısı Olan Bireylerde Hemşirelik Bakımı

Hepatorenal sendrom, karaciğer yetmezliği olan hastalarda görülen en yaygın komplikasyonlardan biridir. Azotemi, oligüri, glomerüler filtrasyon hızının azalması ve inatçı assitin artmasıyla ortaya çıkan böbrek yetmezliği tablosudur. Böbreklerde yapısal bir sorun yoktur. Hepatorenal sendrom oluşumuna portal hipertansiyon, splenik arteriyel vazodilatasyon sebep olur. Sonuç olarak, renal hipoperfüzyona neden olan renal vazokonstrüksiyon gelişir. Karaciğer transplantasyonu gerçekleşen hastalarda ameliyat sırasındaki yetersiz perfüzyona bağlı gelişen akut tübüler nekroz, ameliyat sonrası hipovolemi ve ilaçlara bağlı gelişen nefrotoksisite, karaciğer nakli sonrası böbrek yetmezliğinin diğer önemli nedenlerindendir. Tedavide amaç, splenik ve sistemik vazokonstrüksiyonun düzeltilmesi, böbreklerin vazodilatasyonunun sağlanması ve sodyum dengesi ile birlikte normovoleminin sağlanmasıdır. Hemşirelik bakımında; klinikte hastanın hemodinamisinin stabil olması sağlanmalı, laboratuvar bulguları izlenmeli ve hastanın durumu sıklıkla değerlendirilmelidir. Ayrıca hasta sıvı-elektrolit dengesizlikleri yönünden izlenmelidir. Hepatorenal sendroma bağlı olarak hastanın saatlik diürez miktarı, ortalama arter basıncı, kreatinin klirensi ve serum kreatin gibi kritik değerlerindeki ani değişimler, su ve tuz tutulumuna bağlı olarak ortaya çıkan ödem hastanın hemodinamisinin olumsuz etkilenmesine neden olur. Özellikle yoğun bakım ünitelerinde hastaların izlemi önem taşımaktadır.

Frequency of neurological involvement in patients with/without diarrhea hemolytic uremic syndrome: A Systematic review and meta-analysis

Frequency of neurological involvement in patients with/without diarrhea hemolytic uremic syndrome: A Systematic review and meta-analysis

Profil épidémiologique et clinique, et survie à 90 jours des patients incidents en hémodialyse chronique au cours de la pandémie à SARS-CoV2 au Cameroun : expérience de l’hôpital général de Douala

BackgroundThe effect of COVID-19 pandemic on end stage renal disease patient who should initiated dialysis are limited in Sub-Saharan Africa is unknown. We sought to describe the epidemiologic and clinical profile of newly admitted patient in chronic haemodialysis during the COVID-19 pandemic in Cameroon and evaluate their survival between 90days of dialysis initiation. Material and methodWe conducted a cohort study of 6months from April to October 2020. End stage renal disease patients newly admitted in the haemodialysis facility of the General Hospital of Douala were included. Patients with confirmed or suspected COVID-19 were identified. Socio-demographic, clinical and biological data at dialysis initiation as well as mortality between the 90days of dialysis initiation were registered. ResultsA total of 57 incident patients were recorded from April to October 2020 with a monthly mean of 9.5 patients. The mean age was 46.95±13.12years. Twenty-four COVID-19 were identified with a frequency of 49% among emergency admission. Pulmonary œdema (79.2% vs. 42.4%; P=0.006) and uremic encephalopathy (83.4% vs. 53.6%; P=0.022) were more common in COVID-19. The overall survival at 90days was 48% with a tendency to poor survival among COVID-19 and patients with low socioeconomic level. In Cox regression, low socioeconomic level increase the risk of instant death by 3.08. ConclusionSARS-CoV2 seem to increase nephrology emergency and poor survival in haemodialysis at 90days.

Evaluation of cerebral dysfunction in patients with chronic kidney disease using neuropsychometric and neurophysiological tests

Background Uremic encephalopathy is defined as cerebral dysfunction due to toxin accumulation in patients with chronic kidney disease (CKD). This condition is characterized by subtle to florid symptoms, and its clinical course is always progressive when untreated but partially reversible with renal replacement therapy. While no test exists to measure subclinical uremic encephalopathy, two tests have been validated to measure minimal hepatic encephalopathy: the critical flicker frequency (CFF) test and the psychometric hepatic encephalopathy score (PHES). Objective To use CFF and PHES to measure the prevalence of cerebral dysfunction in individuals with CKD. Methods This cross-sectional study included a total of 69 patients with stage-5 CKD. Cutoff points for minimal encephalopathy were established using existing clinical guidelines: ≤39 Hz for CFF and < −4 for PHES. All participants were also screened for cognitive function and depression. Results Eighteen cases (26.1%) of cerebral dysfunction linked to uremic encephalopathy were detected with CFF, while twelve (17.4%) were detected by PHES; only six cases (8.7%) were diagnosed by both methods. Half of the cases (50%) had diabetes, and 61% were on hemodialysis. Cognitive function scores did not differ significantly between those receiving dialysis, hemodialysis, or no renal replacement therapy. Conclusions It is essential to identify cerebral dysfunction when uremic encephalopathy is in early subclinical stages to reduce preventable events as traffic and work accidents.

Reactive seizures in 40 dogs: A clinical study

Seizures are the most common neurological disorders in dogs. Based on the etiology the epileptic dogs were classified as idiopathic epilepsy, reactive seizures and structural epilepsy. In this study 40/179 dogs were diagnosed with reactive seizures. They were grouped in to different age and sex. The different etiologies of reactive seizures in this study were hepatic encephalopathy, cardiomyopathy, uremic encephalopathy, infectious, hypothyroidism, hypocalcemia, verminous, hypoglycaemia, tetanus and anemia. This categorisation will guide the clinician to treat for the primary cause and plan the antiepileptic treatment accordingly.

Therapeutic Strategies to Protect the Central Nervous System against Shiga Toxin from Enterohemorrhagic Escherichia coli.

Infection with Shiga toxin-producing Escherichia coli (STEC) may cause hemorrhagic colitis, hemolytic uremic syndrome (HUS) and encephalopathy. The mortality rate derived from HUS adds up to 5% of the cases, and up to 40% when the central nervous system (CNS) is involved. In addition to the well-known deleterious effect of Stx, the gram-negative STEC releases lipopolysaccharides (LPS) and may induce a variety of inflammatory responses when released in the gut. Common clinical signs of severe CNS injury include sensorimotor, cognitive, emotional and/or autonomic alterations. In the last few years, a number of drugs have been experimentally employed to establish the pathogenesis of, prevent or treat CNS injury by STEC. The strategies in these approaches focus on: 1) inhibition of Stx production and release by STEC, 2) inhibition of Stx bloodstream transport, 3) inhibition of Stx entry into the CNS parenchyma, 4) blockade of deleterious Stx action in neural cells, and 5) inhibition of immune system activation and CNS inflammation. Fast diagnosis of STEC infection, as well as the establishment of early CNS biomarkers of damage, may be determinants of adequate neuropharmacological treatment in time.

Neurophysiological and Neuroradiological Changes in Children With Chronic Kidney Disease.

Background: Patients with chronic kidney disease (CKD) on maintenance hemodialysis frequently present with neurological complications. These complications include peripheral neuropathy, encephalopathy, and stroke.Objectives: To detect the prevalence of neurological manifestations and complications in children with CKD through neurophysiological and neuro-radiological findings.Methods: The study included 50 patients with CKD admitted to a pediatric nephrology unit. Their history and complete physical and neurological examination findings had been recorded. All patients underwent nerve conduction, electromyography, electroencephalography, and magnetic resonance imaging of the brain.Results: Fifty children of both sexes (23 males and 27 females) with a mean age of (12.08 ± 3.46 year) were studied. Eleven (22%) patients with CKD developed polyneuropathy, mostly of an axonal polyneuropathy pattern, while 39 (78%) of them showed normal electrophysiological studies. No myopathy was detected. Abnormal electroencephalography findings were detected in 18% of patients, mostly generalized and focal (temporal, occipital, and frontal) epileptogenic activity. Abnormal MRI brain findings were detected in 16% of patients, mostly of encephalomalacia.Conclusion: Uremic neuropathy was highly prevalent in children with CKD on maintenance hemodialysis. They developed polyneuropathy, mostly of an axonal polyneuropathy pattern. EEG is a useful method for early recognition of subclinical uremic encephalopathy and/or epileptogenic activity. Early demonstration and management of uremic neurological conditions may decrease the physical disability of CKD patients.

Kidney Ischemia/Reperfusion Injury Induces Changes in the Drug Transporter Expression at the Blood-Brain Barrier in vivo and in vitro.

Ischemia/reperfusion injury is a major cause of acute kidney injury (AKI). AKI is characterized by a sudden decrease in kidney function, systemic inflammation, oxidative stress, and dysregulation of the sodium, potassium, and water channels. While AKI leads to uremic encephalopathy, epidemiological studies have shown that AKI is associated with a subsequent risk for developing stroke and dementia. To get more insights into kidney–brain crosstalk, we have created an in vitro co-culture model based on human kidney cells of the proximal tubule (HK-2) and brain microvascular endothelial cells (BMEC). The HK-2 cell line was grown to confluence on 6-well plates and exposed to oxygen/glucose deprivation (OGD) for 4 h. Control HK-2 cells were grown under normal conditions. The BMEC cell line cerebED was grown to confluence on transwells with 0.4 μm pores. The transwell filters seeded and grown to confluence with cereEND were inserted into the plates with HK-2 cells with or without OGD treatment. In addition, cerebEND were left untreated or treated with uremic toxins, indole-3-acetic acid (IAA) and indoxyl sulfate (IS). The protein and mRNA expression of selected BBB-typical influx transporters, efflux transporters, cellular receptors, and tight junction proteins was measured in BMECs. To validate this in vitro model of kidney–brain interaction, we isolated brain capillaries from mice exposed to bilateral renal ischemia (30 min)/reperfusion injury (24 h) and measured mRNA and protein expression as described above. Both in vitro and in vivo systems showed similar changes in the expression of drug transporters, cellular receptors, and tight junction proteins. Efflux pumps, in particular Abcb1b, Abcc1, and Abcg2, have shown increased expression in our model. Thus, our in vitro co-culture system can be used to study the cellular mechanism of kidney and brain crosstalk in renal ischemia/reperfusion injury.

Lentiform fork sign in a uremic patient with a high anion gap metabolic acidosis with seizures: a case report from North West of Ireland

BackgroundLentiform fork sign is a neuroradiological abnormality which is encountered in the clinical practice associated with uremic encephalopathy, dialysis disequilibrium syndrome and metabolic acidosis.Case presentationWe describe here a case of this neuro-radiological abnormality which was encountered in a patient with uraemia and high anion gap metabolic acidosis who presented with generalised convulsion and later had some tremor in her hands. In our patient, there were few predisposing factors which might have possibly resulted in this abnormality chronic kidney disease, diabetes mellitus, and metabolic acidosis.ConclusionThe Lentiform fork sign is a rare occurrence which can be related to a long list of toxic and metabolic causes but in conjunction with metabolic acidosis in chronic kidney disease patients, it can narrow down this list of alternate diagnosis.

Uraemic Encephalopathy in a Persian Cat with Chronic Kidney Disease

Uraemic encephalopathy (UE) is rarely associated with acute kidney injury or chronic kidney disease in domestic animals, and we now report the first case in a cat. The animal presented with hypothermia, apathy, lethargy, depression, severe dehydration, uraemic breath, elevated serum urea nitrogen and creatine concentrations, and eventual seizures and coma prior to death. Gross necropsy findings included severe bilateral renal scarring, ulcerative stomatitis and glossitis, and uraemic gastropathy. Microscopic lesions of diffuse interstitial fibrosis, multifocal mineralization and lymphoplasmacytic interstitial nephritis were seen in the kidneys. There was symmetrical, bilateral spongy vacuolation of the white matter of the basal nuclei and cerebellum and Alzheimer type II astrocytes in the cerebral cortex and hippocampus. Glial fibrillary acid protein immunolabelling was absent or faint in astrocytes of the cerebral grey matter. UE should be included in the differential diagnosis in animals with chronic kidney disease and neurological signs.

N-acetylcysteine modulates effect of the iron isomaltoside on peritoneal mesothelial cells.

Intravenous (i.v.) iron supplementation is used in patients on chronic peritoneal dialysis (pd). Iron induced intraperitoneal inflammation observed in our previous studies with iron sucrose may deteriorate the function of the peritoneum as the dialysis membrane. We evaluated effect iron compound, iron-isomaltoside-100 (IIS) on the peritoneal mesothelial cells (MC). We studied the effect of iv treatment with IIS ± N-acetylcysteine (NAC) on the dialysate parameters and function of MC. In 7 uremic pd patients IIS 200 mg was infused i.v. ± NAC 600 mg. Afterward, a 4 hours exchange was performed with Dianeal 1.5%. As a control dialysate exchange preceding IIS treatment was used. Inflammatory parameters of the drained dialysates as well as the dialysates and IIS effects on MC were evaluated in ex vivo experiments. Intravenous infusion of IIS resulted in an increase of the dialysate Fe (+147%, P < 0.01). Concentrations of the dialysates inflammatory mediators were increased: interleukin-6 (IL-6) +39%, P < 0.02, monocyte chemoattractant protein-1(MCP1) +50%, P < 0.02, and hyaluronan (HA) +64%, P < 0.02. Simultaneous i.v. infusion of NAC prevented increase of the dialysate inflammatory mediators. Dialysates collected after IIS treatment induced oxidative stress in MC (+29%, P < 0.05) and stimulated IL-6 synthesis (+64%, P < 0.05) in MC; no such effect was seen in dialysates obtained after simultaneous IIS and NAC i.v. treatment. IIS used as the additive to culture medium stimulated synthesis in MC of IL6 (+76%, P < 0.001) and plasminogen activator inhibitor-1 (PAI-1) (28%, P < 0.001) whereas synthesis of tissue plasminogen activator (t-PA) was reduced (-16%, P < 0.001). These changes were prevented in the presence of NAC 1 mmol/L. Intravenous administration of IIS results in the mild stimulation of intraperitoneal inflammation. IIS changes MC phenotype to the inflammatory one with reduced fibrinolytic activity. These effects are prevented by NAC.

Mechanisms of star fruit (Averrhoa carambola) toxicity: A mini-review

The star fruit (Averrhoa carambola) is consumed in high amounts in Asia and Central/South America. It contains oxalic acid and caramboxin. In some individuals, its ingestion may lead to nephrotoxicity and neurotoxicity. The nephrotoxic effect is due to oxalate deposition in renal tubules resulting in acute tubular necrosis and interstitial nephritis. Although uraemic encephalopathy secondary to acute kidney injury may play a role, a shift to an excitatory state of the central nervous system (CNS) by caramboxin through activation of excitatory neuroreceptors and inhibition of GABA receptors leads to mental confusion, seizures and status epilepticus seen with star fruit intoxication. In this mini-review, we discuss the mechanisms of star fruit-related toxicity.

Uraemia disarms neutrophils against Candida.

Uraemia disarms neutrophils against Candida.

Comparative study between drug-coated balloon angioplasty vs plain balloon angioplasty in management of venous stenosis in hemodialysis access circuit

Introduction Juxta-anastomotic venous stenosis is a major concern associated with arteriovenous fistulas, which is mainly a result of neointimal hyperplasia. Although balloon angioplasty remains the cornerstone treatment for vascular access stenosis, the combination of venous anatomy and physiology, with the pre-existing endothelial dysfunction of uremic patients, generally leads to poor mid-term and long-term results. Theoretically, vascular access patency may be optimized by a technology that would both block negative vessel wall remodeling and inhibit fibromuscular hyperplasia. One such approach could be the use of angioplasty with drug-coated balloon (DCB) angioplasty. Patients and methods Within a 10-month period, 80 patients with different types of hemodialysis access stenosis in whom percutaneous transluminal angioplasty (PTA) was indicated were prosTectively, randomized to have either DCB or plain balloon angioplasty (PBA). This study was designed to compare primary patency rates and target lesion revascularization of DCB vs PBA to preserve the patency of the vascular access circuit in patients undergoing hemodialysis after 1 year of follow-up. Results All patients enrolled in the study completed the 1-year follow-up period. Access circuit primary patency results were also significantly in favor of DCB angioplasty (DCB, 287 days, and PBA, 156 days; P=0.04). Target lesion revascularization-free survival was significantly superior in the DCB group according to the Kaplan–Meier survival analysis curve (DCB, 316 days, and PBA, 172 days; P=0.041). There was no statistically significant difference in this subgroup analysis (P>0.1). Conclusion In this two-center study, DCB angioplasty results in improved vessel patency and is superior to plain balloon dilation in the treatment of venous stenoses of failing native or prosthetic arteriovenous shunts used for dialysis access.