Acute Uremia Research Articles

Acute lung injury induced by acute uremia and renal ischemic-reperfusion injury: The role of toll-like receptors 2 and 4, and oxidative stress.

Objective(s):Acute lung injury (ALI) is a common complication of distant organ dysfunction induced by acute kidney injury (AKI). Toll-like receptors (TLRs) have a critical role in progression of AKI. The main goal of this study was to determine whether lung gene expression of TLR2 and TLR4 change by ischemic (renal bilateral ischemic-reperfusion; BIR) and uremic (bilateral nephrectomy; BNX) AKI.Materials and Methods: Forty male rats were divided into five groups. Two kidneys were removed in BNX, and renal pedicles were clamped in BIR for 45 min. The kidney and lung tissue, and blood samples were collected and saved after 24 hr in all groups. The bone marrow mesenchymal stem cells were immediately injected (1×106,IV) into the treated groups. The expression of TLR2, TLR4, TNF-α, and VEGF was checked by RT-PCR in the tissue samples. MDA level, SOD, and CAT activity were evaluated in the tissue samples.Results: Structural disturbance of ALI was detected as alveolar hemorrhage and vascular congestion after BIR and BNX. Lung TLR2 and TLR4 but not TNF-α and VEGF up-regulated in these groups. Oxidative stress stabilized after the BIR and BNX in the tissue samples. BMSCs reduce the expression of TLR2 and TLR4 and oxidative stress in the treated groups. Conclusion:Acutely gathering systemic mediators after renal ischemic or uremic injury induce ALI through overexpression of TLR2 and TLR4 and oxidative stress. Therefore, the Lung protective effect of BMSCs may be related to modulation of TLR2 and TLR4 and oxidative stress in the kidney and lung tissue.

Candida Administration in Bilateral Nephrectomy Mice Elevates Serum (1→3)-β-D-glucan That Enhances Systemic Inflammation Through Energy Augmentation in Macrophages.

Systemic inflammation, from gut translocation of organismal molecules, might worsen uremic complications in acute kidney injury (AKI). The monitoring of gut permeability integrity and/or organismal molecules in AKI might be clinically beneficial. Due to the less prominence of Candida albicans in human intestine compared with mouse gut, C. albicans were orally administered in bilateral nephrectomy (BiN) mice. Gut dysbiosis, using microbiome analysis, and gut permeability defect (gut leakage), which was determined by fluorescein isothiocyanate-dextran and intestinal tight-junction immunofluorescent staining, in mice with BiN-Candida was more severe than BiN without Candida. Additionally, profound gut leakage in BiN-Candida also resulted in gut translocation of lipopolysaccharide (LPS) and (1→3)-β-D-glucan (BG), the organismal components from gut contents, that induced more severe systemic inflammation than BiN without Candida. The co-presentation of LPS and BG in mouse serum enhanced inflammatory responses. As such, LPS with Whole Glucan Particle (WGP, a representative BG) induced more severe macrophage responses than LPS alone as determined by supernatant cytokines and gene expression of downstream signals (NFκB, Malt-1 and Syk). Meanwhile, WGP alone did not induced the responses. In parallel, WGP (with or without LPS), but not LPS alone, accelerated macrophage ATP production (extracellular flux analysis) through the upregulation of genes in mitochondria and glycolysis pathway (using RNA sequencing analysis), without the induction of cell activities. These data indicated a WGP pre-conditioning effect on cell energy augmentation. In conclusion, Candida in BiN mice accelerated gut translocation of BG that augmented cell energy status and enhanced pro-inflammatory macrophage responses. Hence, gut fungi and BG were associated with the enhanced systemic inflammation in acute uremia.

POS-009 PREVALENCE AND ETIOLOGIES OF ACUTE KIDNEY INJURY IN ELDERLY

Acute renal failure in the elderly is a common phenomenon. It is favored by functional modifications of the kidney and the repercussions of many chronic diseases such as diabetes, hypertension or obstructive urological pathologies which incidence increases with age. The aim of our work was to study the epidemiological and clinical characteristics, to specify the etiological circumstances and the different therapeutic and evolutionary modalities of AKI in the elderly. It was a retrospective descriptive study conducted on 70 AKI files identified in the Nephrology department of Charles Nicolle Hospital in Tunis among 380 patients hospitalized over a period of one year. The incidence of AKI in the elderly was 44.8%. It was classified AKIN 1, 2 and 3 in 25%, 25.6% and 49.4% of cases, respectively. The average age was 75 years. The sex ratio was 1.12. The pathological history was dominated by cardiovascular pathology. High blood pressure and diabetes were noted in 56% and 32% of the cases, respectively. Patients were hospitalized through the emergency room in 47.1% of the cases or outpatient in 14.3% of the cases. The discovery of AKI was systematic in the face of an increase in serum creatinine and / or urea numbers in 60% of cases. Signs of acute uremia and changes in diuresis revealed ARI in 57.1% and 30% of the cases, respectively. The mean creatinine level was 515 μmol / l. Hypokalemia and hyperkalemia were observed in 14.4% and 21.4% respectively. AKI was organic in 42.8% of the cases, functional in 31.8% of the cases and related to an obstacle in 24.8% of the cases. Correction of hydroelectrolytic disorders was performed in 61.4% of our patients. Diuretics were used in 17.4% of patients. Hemodialysis was performed only in 18% of our patients. It was performed prophylactically in 7 cases and in an emergency context in 6 cases. In the latter case, the indication for hemodialysis was primarily hyperkalemia and / or metabolic acidosis. The average hospital stay was 19 days. The evolution was favorable in 64.2% of the cases, unfavorable in 35.8% of the cases with a passage to chronicity in 32.6% and a death in 12.8% of the cases. In the elderly, acute renal failure is a common morbid event. The structural and functional alterations of the nephron and the increase in the incidence of certain pathologies expose these patients to nephrotoxic accidents. Hence the interest of preventive measures of this AKI and especially the importance of an early diagnosis based on new biomarkers of AKI, in order to establish the most suitable therapeutic means.

Candida Administration Worsens Uremia-Induced Gut Leakage in Bilateral Nephrectomy Mice, an Impact of Gut Fungi and Organismal Molecules in Uremia.

The impact of gut fungi and (1→3)-β-d-glucan (BG), a major fungal cell wall component, on uremia was explored by Candida albicans oral administration in bilateral nephrectomy (BiNx) mice because of the prominence of C. albicans in the human intestine but not in mice. As such, BiNx with Candida administration (BiNx-Candida) enhanced intestinal injury (colon cytokines and apoptosis), gut leakage (fluorescein isothiocyanate [FITC]-dextran assay, endotoxemia, serum BG, and bacteremia), systemic inflammation, and liver injury at 48 h postsurgery compared with non-Candida BiNx mice. Interestingly, uremia-induced enterocyte apoptosis was severe enough for gut translocation of viable bacteria, as indicated by culture positivity for bacteria in blood, mesenteric lymph nodes (MLNs), and other organs, which was more severe in BiNx-Candida than in non-Candida BiNx mice. Candida induced alterations in the gut microbiota of BiNx mice as indicated by (i) the higher fungal burdens in the feces of BiNx-Candida mice than in sham-Candida mice by culture methods and (ii) increased Bacteroides with decreased Firmicutes and reduced bacterial diversity in the feces of BiNx-Candida mice compared with non-Candida BiNx mice by fecal microbiome analysis. In addition, lipopolysaccharide plus BG (LPS+BG), compared with each molecule alone, induced high supernatant cytokine levels, which were enhanced by uremic mouse serum in both hepatocytes (HepG2 cells) and macrophages (RAW264.7 cells). Moreover, LPS+BG, but not each molecule alone, reduced the glycolysis capacity and mitochondrial function in HepG2 cells as determined by extracellular flux analysis. Additionally, a probiotic, Lactobacillus rhamnosus L34 (L34), attenuated disease severity only in BiNx-Candida mice but not in non-Candida BiNx mice, as indicated by liver injury and serum cytokines through the attenuation of gut leakage, the fecal abundance of fungi, and fecal bacterial diversity but not fecal Gram-negative bacteria. In conclusion, Candida enhanced BiNx severity through the worsening of gut leakage and microbiota alterations that resulted in bacteremia, endotoxemia, and glucanemia.IMPORTANCE The impact of fungi in the intestine on acute uremia was demonstrated by the oral administration of Candida albicans in mice with the removal of both kidneys. Because fungi in the mouse intestine are less abundant than in humans, a Candida-administered mouse model has more resemblance to patient conditions. Accordingly, acute uremia, without Candida, induced intestinal mucosal injury, which resulted in the translocation of endotoxin, a major molecule of gut bacteria, from the intestine into blood circulation. In acute uremia with Candida, intestinal injury was more severe due to fungi and the alteration in intestinal bacteria (increased Bacteroides with decreased Firmicutes), leading to the gut translocation of both endotoxin from gut bacteria and (1→3)-β-d-glucan from Candida, which synergistically enhanced systemic inflammation in acute uremia. Both pathogen-associated molecules were delivered to the liver and induced hepatocyte inflammatory responses with a reduced energy production capacity, resulting in acute uremia-induced liver injury. In addition, Lactobacillus rhamnosus attenuated intestinal injury through reduced gut Candida and improved intestinal bacterial conditions.

First Consultation in Nephrology: Case of the Point G University Hospital (Bamako-Mali)

Understanding the first consultation of people with kidney disease seems to us to be essential to understand the attitude of the referring physician and the nephrologist. The aim was to find out to whom a patient with kidney disease should be referred in the first instance and for what reason? Hence the evaluation of the prevalence of the first consultation in the nephrology department of the Point G University Hospital in Bamako was made. Patients and Method: This was a prospective descriptive study which took place from July 2017 to June 2018 in the nephrology department of the Point G University Hospital. The study included all patients who came to the nephrology department for the first time during this period. Results: Between July 2017 and June 2018 at the nephrology and haemodialysis service of the G point University Hospital, we retained 643 out of 1031 patients who came for their first consultation, i.e. 62.36%. There were many patients aged between 41 and 50 years. The average age was 42.6 ± 5.03 years with extremes of 30 and 82 years. The sex ratio (M/F) was in favor of males, 1.14. The majority of patients were referred/evacuated from the referral health centres (57.6%). The majority of patients were referred/evacuated by general practitioners (70.5%). Cardiologists were the main specialists to refer/evacuate patients (21.2%). The main reasons for consultation that led to the first diagnostic hypotheses were: arterial hypertension for vascular nephropathy, glomerular syndrome for glomerular nephropathy, acute uraemia syndrome for acute renal failure, hydronephrosis for obstructive uropathy and finally diabetes for diabetic nephropathy. Conclusion: The first consultation in nephrology remains an important step in the management of renal disease, especially when the referral is an emergency. The percentage of referrals is dominated by general practitioners.

A case of hemodialysis and steroid therapy for carbamazepine-induced eosinophilic granulomatosis with polyangiitis: a case report with literature review

BackgroundCarbamazepine-induced acute kidney injury is mainly caused by acute tubulointerstitial nephritis. Only one case of carbamazepine-induced eosinophilic granulomatosis with polyangiitis (EGPA) with acute kidney injury has been reported. But the patient’s condition improved with the immediate discontinuation of carbamazepine. We present a case requiring hemodialysis and steroid therapy for carbamazepine-induced EGPA with acute kidney injury.Case presentationA 77-year-old man with allergic rhinitis was prescribed carbamazepine for trigeminal neuralgia 1 year ago. He developed rash and itching on the left forearm 1 month ago and was diagnosed with polymorphic exudative erythema and admitted to our hospital. Laboratory data revealed leukocytosis eosinophilia and renal failure (serum creatinine 9.2 mg/dL). Carbamazepine was discontinued, and hemodialysis was initiated because of acute uremia and oliguria. A lymphocyte stimulation test for carbamazepine was positive. Polyneuropathy in the upper and lower extremities was observed by electromyogram, and a renal biopsy indicated EGPA. The main clinical findings were allergic rhinitis, eosinophilia, and vasculitis symptoms, such as multiple mononeuritis and muscle weakness. Renal biopsy showed diffuse cellular infiltration dominated by eosinophils in the interstitium, with granulomatous changes in particular observed around the arteriole. Fibrinoid necrosis was also observed around the arteriole. We therefore made a diagnosis of carbamazepine-induced EGPA. Following steroid therapy after the discontinuation of carbamazepine, the patient was discharged from our hospital without hemodialysis. In contrast with the previous case of EGPA, the present case had the following characteristics: (1) elderly male patient, (2) hemodialysis required for acute kidney injury, and (3) improved renal function following steroid therapy after discontinuation of carbamazepine.ConclusionOur case report indicates that early diagnosis and appropriate therapy can improve acute kidney injury caused by carbamazepine and allow the patient to discontinue dialysis.

The Management of Heavy Menstrual Bleeding After Percutaneous Coronary Intervention in a Woman of Reproductive Age.

Heavy menstrual bleeding (HMB), previously known as menorrhagia, is in place with heavy flow and longer lasting days of bleeding during menstrual period, sequentially leading to anemia. We reported a rare case of HMB in a 33-year-old patient after percutaneous coronary intervention (PCI), who presented with acute coronary syndromes (ACS), uremia and systemic lupus erythematosus before PCI. This patient received three times of hemodialysis weekly (Monday, Wednesday, and Friday). On the next day after PCI, this patient began to have menstruation. On the fifth day of menstruation, the patient complained of HMB and physical discomfort, with an urgent need for consultation of gynecologist. After gynecologist consultation, this patient was under oxytocin treatment. However, 2 days of oxytocin treatment did not significantly improve HMB. Afterward, the menstrual volume of patients was significantly reduced on eighth day of menstruation after once therapy of testosterone propionate and norethindrone. Regarding the reasons of HMB, heparin in hemodialysis and antiplatelet drugs utilized (aspirin and clopidogrel) after PCI may be contributors to the HMB. In addition, uterine myoma, cervical canal cyst, renal insufficiency and CYP2C19∗2 heterozygous are also possible contributors to HMB. There is no such case of whom had HMB in reproductive age with ACS, uremia and systemic lupus erythematosus under hemodialysis and antiplatelet therapy. More clinical safety data on HMB of reproductive age women who are under antithrombotic therapy are required.

Acute Uremia and Aspirin: A Recipe for Disaster Leading to Post-Sphincterotomy Hemorrhage

Acute Uremia and Aspirin: A Recipe for Disaster Leading to Post-Sphincterotomy Hemorrhage

35) An unusual case of acute onset severe uremia presenting as gastrointestinal bleeding

Introduction We report a case of acute renal failure and severe uremia presenting as gastrointestinal bleeding in an 11-year-old girl with VATER syndrome. Case Report The patient is an 11 year old girl with CKD II secondary to solitary kidney with grade 5 reflux, re-implanted at 2 years and mild persistent RTA. The patient had been clinically well apart from a 1-year history of dysuria and ultrasound evidence of a non-obstructing renal cyst. She was being monitored as an outpatient. She presented to her local emergency department with three days of hematemesis, melena, and weakness. …

Sudden bilateral vision loss as the sole manifestation of posterior reversible encephalopathy syndrome from acute uremia

Rationale:Posterior reversible encephalopathy syndrome (PRES) is a cliniconeuroradiological entity associated with vasogenic edema. Symptoms may include headache, seizures, altered mental status, and visual impairment. Patients with PRES generally present with neurological deficits.Patient concerns:Here, we report an unusual case of a 42-year-old man who presented with sudden bilateral vision loss without any other neurologic symptoms.Diagnoses:He was diagnosed with PRES secondary to acute uremia.Interventions and outcomes:Our patient experienced a dramatic improvement in visual acuity, blood chemistry values, and magnetic resonance imaging findings following repeated hemodialysis.Lessons:Sudden bilateral vision loss may be the sole manifestation of PRES, particularly in patient with risk factors for PRES. Awareness of this variation of the clinical symptoms of PRES is important to facilitate its recognition.

Lymphocryptovirus-dependent occurrence of lymphoma in SIV-infected rhesus macaques with particular consideration to two uncommon cases of non-Hodgkin's lymphoma

Abstract. Despite combination antiretroviral therapy, high-grade malignant non-Hodgkin's lymphoma (NHL) is still one of the most frequently acquired immunodeficiency syndrome (AIDS)-defining disorders in the end stage of infection with human immunodeficiency virus (HIV). NHL can also be observed in rhesus macaques infected with the simian immunodeficiency virus (SIV). Thus, they represent a useful model to study morphological characteristics and oncogenetic mechanisms of NHL in humans.When reviewing the occurrence of lymphoma at the German Primate Center over the past 25 years within the context of pathogenic SIV infection we noticed a strikingly high incidence (four out of seven animals) of these tumors in rhesus macaques infected with ex vivo derived SIVmac251/32H/spleen in AIDS-defining end-stage disease. Polymerase chain reaction analysis of this virus stock revealed the co-presence of rhesus lymphocryptovirus (rhLCV), which represents the monkey homologue to human Epstein–Barr virus (EBV), suggesting an association between co-application of SIV and rhLCV and increased tumorigenesis.In addition, we present two cases of NHL in rhesus macaques infected with a SIVmac239 nef-mutant variant because one exhibited an unusual immunophenotype and the other an uncommon organ manifestation. Histological and immunohistochemical examinations of tumors of the first animal revealed metastatic diffuse large B-cell lymphomas (DLBCL) affecting the stomach and the pancreaticoduodenal lymph nodes, of which the one in the stomach presented the rare dual expression of CD20 and CD3. Necropsy of the second animal revealed an obstructive DLBCL around the urinary bladder neck that led to urine backflow and eventually death due to acute uremia without any further AIDS-like manifestations. In the tumors of both animals, abundant Epstein–Barr nuclear antigen-2 expression was demonstrated, thus verifying concurrent rhLCV infection. Flow cytometric analyses revealed a high percentage of activation as well as proliferation in B cells from peripheral lymph nodes in both animals. Moreover, CD4+ T cells were depleted in blood, colon and lymphoid tissue. Concomitantly, CD8+ T cells showed an exhausted phenotype. The two case reports and the increased incidence of NHL following co-application of SIV and rhLCV underline the role of rhLCV in lymphomagenesis.

Key role of the kidney in the regulation of fibroblast growth factor 23

High circulating levels of fibroblast growth factor 23 (FGF23) have been demonstrated in kidney failure, but mechanisms of this are not well understood. Here we examined the impact of the kidney on the early regulation of intact FGF23 in acute uremia as induced by bilateral or unilateral nephrectomy (BNX and UNX, respectively) in the rat. BNX induced a significant increase in plasma intact FGF23 levels from 112 to 267 pg/ml within 15 min, which remained stable thereafter. UNX generated intact FGF23 levels between that seen in BNX and sham-operated rats. The intact to C-terminal FGF23 ratio was significantly increased in BNX rats. The rapid rise in FGF23 after BNX was independent of parathyroid hormone or FGF receptor signaling. No evidence of early stimulation of FGF23 gene expression in the bone was found. Furthermore, acute severe hyperphosphatemia or hypercalcemia had no impact on intact FGF23 levels in normal and BNX rats. The half-life of exogenous recombinant human FGF23 was significantly prolonged from 4.4 to 11.8 min in BNX rats. Measurements of plasma FGF23 in the renal artery and renal vein demonstrated a significant renal extraction. Thus the kidney is important in FGF23 homeostasis by regulation of its plasma level and metabolism.

In Process Citation

The first case was a 77-year-old man with 5.6 cm juxtarenal abdominal aortic aneurysm who presented with multiple comorbidities. The patient had a single left kidney. A custom-made, single fenestrated stent graft was implanted successfully. The one-month follow-up showed a patent left renal fenestration without evidence of any endoleaks. Four months after the operation the patient was admitted with acute uremia. Imaging studies revealed an occluded left renal stent, which was successfully reopened. The second case was a 71-year-old man with 8.0 cm juxtarenal aneurysm. He presented with severe coronary artery disease among other multiple comorbidities in his medical history. He was successfully treated with a 3-vessel custom-made fenestrated stent graft to the renal and the superior mesenteric arteries. The one-month CT imaging revealed patent fenestrations without endoleaks. With the development of fenestrated endograft technology, complex aneurysms with visceral artery involvement can be treated with complete endovascular approaches. The first fenestrated endovascular case in Hungary was treated in the Heart and Vascular Center of Semmelweis University, Budapest. The short and middle-term results are offering improved clinical results when compared with conventional surgery, but the long-term outcomes are difficult to ascertain from the current published series.

Altered Renal Expression of Relevant Clinical Drug Transporters in Different Models of Acute Uremia in Rats. Role of Urea Levels

Background/Aims: Organic anion transporter 1 (Oat1) and 3 (Oat3) are organic anion transporters that play critical roles in the body disposition of numerous clinically important drugs. We investigated the effects of acute uremia on the renal expression of Oat1 and Oat3 in three in vivo experimental models of acute kidney injury (AKI): induced by ischemia, by ureteral obstruction and by the administration of HgCl₂. We also evaluated the influence of urea in the expression of these transporters in proximal tubular cells suspensions. Methods: Membranes were isolated from kidneys of each experimental group and from cell suspensions incubated with different urea concentrations. Oat1 and Oat3 expressions were performed by immunoblotting. Results: A good correlation between uremia and the renal protein expression of Oat1 and Oat3 was observed in vivo. Moreover, the incubation of isolated proximal tubular cells with different concentrations of urea decreases protein expression of Oat1 and Oat3 in plasma membranes in a dose-dependent manner. Conclusion: The more severe the renal failure, the more important is the decrease in protein expression of the transporters in renal membranes where they are functional. The in vitro study demonstrates that urea accounts, at least in part, for the decreased expression of Oat1 and Oat3 in proximal tubule plasma membranes.

Acute uremia suppresses leucine-induced signal transduction in skeletal muscle

Adequate nutrient intake in acute uremia is a key part of patient management especially as food utilization is usually impaired. Leucine is important as it comprises about one-fifth of essential amino acid needs and, apart from serving as a substrate, it directly activates the mTOR signaling pathway stimulating protein synthesis and inhibiting autophagy. Here we tested whether leucine activation of the mTOR signaling pathway in muscle is severely disrupted in acute uremia. Several abnormalities were identified in bilateral ureteral ligated (model of acute uremia) compared to sham-operated pair-fed control rats. Levels of several signaling proteins increased significantly while leucine-induced phosphorylation of mTOR and downstream proteins, 4e-BP1 and S6K1, was completely suppressed. Levels of LC3B-II, a specific autophagosomal membrane-associated protein used as a marker of autophagy, increased threefold in uremia. Furthermore, while leucine suppressed LC3B-II levels in controls, it failed to do so in uremic rats. Muscle IL-6 mRNA levels increased, while IGF-1 mRNA levels decreased in uremia. These findings establish that, in acute uremia, severe resistance to leucine-induced activation of the mTOR anabolic signaling pathway develops. Thus, leucine resistance, together with the reduction in IGF-1 and increase in IL-6 expression, may explain why the anabolic effect of nutritional therapy is diminished in acute uremic patients.

Gastric acid secretion in experimental acute uremia

This study was conducted to evaluate gastric acid secretion in acute renal failure, highlighting the roles of renal mass and gastrin hormone. Acute uremic rats were divided into bilateral nephrectomized and bilateral ureteric obstruction groups. Gastric juice was collected for 2 h and analyzed for volume, free acidity, total acidity, and total acid output. Plasma levels of creatinine, urea, and gastrin were also determined. Bilateral nephrectomized and bilateral ureteric obstruction groups showed a significant increase in levels of free acidity, total acidity, and plasma gastrin. Compared with the ureteric obstruction group, nephrectomized rats showed a significant increase in gastric juice volume, total acid output, and plasma gastrin levels. Following pentagastrin stimulation, gastric juice volume, total acid output, free acidity, and total acidity were increased in the bilateral nephrectomy and ureteric obstruction groups compared with the respective control groups. The free and total acidity and total acid output also increased compared with the respective non-stimulated groups. Plasma creatinine and urea levels were significantly positively correlated with plasma gastrin, free acidity, and total acidity. Creatinine was positively correlated with total acid output, and gastrin was positively correlated with total acidity. In conclusion, acute renal failure promotes gastric acid hypersecretion that could potentially be attributed to high levels of gastrin hormone and uremic state per se.

Post-ischemic azotemia as a partial ‘brake’, slowing progressive kidney disease

Recent experimental work suggests a paradox: although uremia evokes systemic toxicities, in the setting of AKI, it can induce intrarenal cytoprotective and anti-inflammatory effects. Whether these influences can attenuate post-ischemic kidney disease progression remains unknown. To explore this possibility, male CD-1 mice were subjected to a 30-min unilateral (left) kidney ischemia model, previously shown to reduce renal mass by ∼50% over 2-3 weeks. Stepwise azotemia/acute uremia was superimposed by inducing different lengths of contralateral (right) kidney ischemia (0, 15, 18, 20 min). Subsequent loss of left renal mass (kidney weight) was assessed 2 weeks later and contrasted with the degree of initial azotemia 24-h BUN. A striking correlation between 24-h BUNs and 2-week left renal mass was observed (r, 0.77; P < 0.001). With 20 min of right kidney ischemia, left kidney size was completely preserved. This preservation did not result from increased tubular cell proliferation or decreased microvascular loss, as gauged by KI-67 and CD-34 immunohistochemistry, respectively. Rather, an early reduction in proximal tubule cell dropout (as judged by renal cortical N-acetyl-glucosaminidase content), with a subsequent preservation of tubule mass, was observed. In summary, these findings advance a novel concept: acute uremia can confer early post-ischemic cytoprotection resulting in a slowed progression of post-ischemic kidney disease.

Etiology of renal failure and peritoneal dialysis complications in Isfahan

Introduction: Worldwide specific diseases are jeopardizing people’s health in the world as well as in Iran. Chronic renal failure as a developed and irreversible failure is usually progressive. End Stage Renal Disease (ESRD) is a situation when renal function is not sufficient to preserve one’s life leading to acute uremia resulting in dialysis and/or kidney transplantation for the patients. Although dialysis methods bring about complications for the patients, peritoneal dialysis is relatively cost-effective and more convenient to survive. The present study aimed to investigate (the) Etiologic factor of renal failure and imposed complications of peritoneal dialysis in the patients of Isfahan Alzahra hospital. Materials and Methods: It was a cross-sectional descriptive study conducted on 67 patients in Isfahan Peritoneal Dialysis Center. The data from the patients were collected through a two-section questionnaire whose first section was allocated to demographic information and the second part was related to the disease and complications of peritoneal dialysis. The collected data were analyzed by SPSS version 18. Results: The findings showed that there were 39 (58%) males and 28 (42%) females. Mean age of the subjects was 48 (18.8) years old. Regarding marital status, 65% were married and 35% were single. Considering complications, 28 subjects (53.5%) had infectious complications while 24 subjects (46.2%) had non-infectious complications. The highest frequency in etiologic factor of renal failure was diabetes mellitus in 29 subjects (43.9%) and the lowest for polycystic kidney in 2 subjects (3%); in addition, hypertension was observed in 51 subjects (77.3%). Discussion: The most frequent and important complication of peritoneal dialysis catheters is infection, which may result in catheter loss and discontinuation of peritoneal dialysis (PD). Diabetes and hypertension were found as the most important etiologic factors for renal failure. They should also be considered as two major risk factors in prevention of renal diseases.

Klinische Probleme der Urämie

Uremia describes the consequences of intoxication in chronic renal failure with substances that are renally cleared in healthy individuals. Acute uremia is a syndrome of gastrointestinal symptoms, pericarditis, pleuritis, and central nervous system alterations ending with coma. These symptoms can be resolved by renal replacement therapy. In addition, chronic uremia can result in damage of multiple organ systems, which continues to advance despite dialysis therapy. This is caused by retention of toxins that cannot be adequately removed due to insufficient treatment time or a molecular weight range hampering elimination. Uremic toxins can be generated by the energy or nucleic acid metabolism, they can be proteins or large molecules that are altered chemically by the uremic milieu. Chronic uremia can influence the majority of long-term complications of chronic renal failure: systemic microinflammation, cardiovascular disease, immunodeficiency, malnutrition, anemia, bone metabolism, and polyneuropathy. There are few therapeutic options other than kidney transplantation.

Defective neutrophil rolling and transmigration in acute uremia

Circulating neutrophils are essential for innate immunity and undergo rapid, stepwise adhesion to and transmigration through the endothelium following tissue injury and microbial invasion. Neutrophil dysfunction may contribute to morbidity and mortality in acute kidney injury but has not frequently been studied at a mechanistic level. Rossaint et al. provide experimental evidence in mice and humans that acute uremia causes discrete intracellular signaling abnormalities that interfere with specific stages of neutrophil trafficking during inflammation.