Clinical nephrology最新文献

{"title":"De novo positive hepatitis B surface antigen after hepatitis B vaccination in dialysis patients.","authors":"Amelia Chien-Wei Chao, Winston Wing-Shing Fung, Cheuk Chun Szeto, Kai Ming Chow","doi":"10.5414/CN110937","DOIUrl":"https://doi.org/10.5414/CN110937","url":null,"abstract":"","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10067856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"On the earliest descriptions of the uremic syndrome in medical literature.","authors":"Anirban Ganguli","doi":"10.5414/CN111149","DOIUrl":"https://doi.org/10.5414/CN111149","url":null,"abstract":"<p><p>Uremic syndrome refers to the clinical manifestations of renal failure (acute or chronic) that results from the accumulation of several endogenous toxins normally excreted by the kidneys and can be fatal unless the primary cause is addressed and the toxins removed by dialysis. A historical description of the syndrome is traditionally believed to start in the 18^th - 19^th century through seminal works in the field of experimental medicine. This account, however, ignores the possibility of clinical apperception of this syndrome in ancient medical literatures. The <i>Sushruta Samhita (SS)</i>, a Sanskrit text whose authorship is attributed to the legendary ancient Indian surgeon <i>Sushruta</i> (6^th century BC), is well known for its pioneering descriptions of several surgical procedures, even though its contribution to the fields of internal medicine and especially nephrology is detailed. <i>Prameha</i>, a term that first appears in the <i>SS</i>, and subsequently in later historical Ayurvedic (traditional Indian medicine) texts, denotes a multi-systemic disease syndrome impacting the neurological, cardiac, dermatological, and gastrointestinal systems that is recognized through its intimate association with urinary abnormalities such as hematuria, frothy urine, or glycosuria. This construct is highly consistent with uremic syndrome originating from multiple renal disease processes such as acute glomerulonephritis, nephrotic syndrome, diabetes mellitus, etc. Furthermore, medical treatment of <i>prameha</i>, as detailed in the original text, reflects several recently validated approaches to managing chronic kidney disease, supporting the hypothesis that this historical entity may be one of the earliest descriptions of uremic syndrome in medical history.</p>","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10047106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical outcomes of ceftolozane-tazobactam dosing in patients with sepsis undergoing renal replacement therapies.","authors":"Wasim S El Nekidy,&nbsp;Mooza Al Ali,&nbsp;Emna Abidi,&nbsp;Islam M Ghazi,&nbsp;Nizar Attallah,&nbsp;Rania El Lababidi,&nbsp;Fadi Hijazi,&nbsp;Jihad Mallat","doi":"10.5414/CN111166","DOIUrl":"https://doi.org/10.5414/CN111166","url":null,"abstract":"<p><p>Ceftolozane-tazobactam (C/T) recommended dosing in patients undergoing renal replacement therapies (RRT) is lacking evidence. The objective of this study was to evaluate the clinical outcomes of C/T dosing in patients on RRT.</p><p><strong>Materials and methods: </strong>A retrospective descriptive study conducted at our institution between May 1, 2017, and March 15, 2022. The primary endpoint was to determine the clinical cure for patients who received C/T for documented infection while on RRT. The secondary endpoints were the microbiologic cure, 30-day infection recurrence, and 30-day crude mortality.</p><p><strong>Results: </strong>Of the 27 patients who met the inclusion criteria, 17 (63%) were males, median age was 69 (62 - 82) years, and weight 67 (57 - 79) kg. The majority of patients had pneumonia 19 (70.4%) followed by bacteremia 5 (18.5%). Multidrug resistant <i>Pseudomonas spp</i>. was the causative organism of infection in 22 subjects (81.5%). Clinical cure was achieved in 17 subjects (63%). Of the 14 subjects who had their culture repeated, 10 (71.4%) patients had microbiologic cure vs. 4 (28.5%) patients who had a microbiologic failure (p = 0.327). 30-day infection recurrence occurred in 6 (35.3%) patients of the clinical cure group and 2 (20%) patients in the clinical failure group (p = 0.362), while mortality occurred in 5 (29.4%) subjects vs. 7 (70%) in both groups, respectively (p = 0.049). The most frequently used doses of C/T were 1.5 g IV q8h while undergoing continuous venovenous hemodiafiltration and 0.75 g IV q8h while undergoing hemodialysis (p = 0.209). The median duration of therapy was 9 (4.5 - 13) days in the clinically cured group vs. 5 (3.75 - 5.5) days in those who had clinical failure (p = 0.038). There was no adverse event reported using these doses during the study period.</p><p><strong>Conclusion: </strong>The used doses of C/T in this study were higher than those approved by the U.S. FDA, while clinical success is uncertain. Larger outcomes and pharmacokinetics studies are needed to establish effective dosing and therapy duration.</p>","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10057005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of FGF-23 and FGFR1 is increased in uremic rat skin.","authors":"Sema Tulay Koz,&nbsp;Ozge Ozkaynak,&nbsp;Suleyman Koz,&nbsp;Huseyin Aydin,&nbsp;O Fahrettin Goze","doi":"10.5414/CN111082","DOIUrl":"https://doi.org/10.5414/CN111082","url":null,"abstract":"<p><strong>Purpose: </strong>Alterations in skin structure and function are very common in uremic patients, but still there is no unifying hypothesis for uremic skin disorders. Fibroblast growth factor-23 (FGF-23) deficiency has been linked to skin disorders in non-uremic animals. We aimed to study alterations in FGF-23 and fibroblast growth factor-23 receptor 1 (FGFR1) expression in uremic rat skins.</p><p><strong>Material and methods: </strong>Wistar albino rats were divided into two groups: sham group (SG, n = 8) and uremic group (UG, n = 8). Uremia was induced by reduction of the total kidney mass in the UG. Animals were sacrificed after 14 weeks of the follow-up.</p><p><strong>Results: </strong>Serum creatinine and blood urea nitrogen levels in the UG increased significantly, compared to the SG, at the end of the experiment (0.69 ± 0.08 vs. 0.3 ± 0.04 Mann-Whitney U test (MWU), p = 0,003 and 55.2 ± 8.9 vs. 29.6 ± 6.8 MWU, p = 0.002, respectively). Serum FGF-23 level in the UG was increased non-significantly, compared to the SG (53.5 ± 20.9 vs. 37.2 ± 9.7 MWU, p = 0.072), whereas serum 1,25(OH)₂D₃ level was significantly lower in the UG (149.4 ± 33.5 vs. 213.8 ± 43.8 MWU, p < 0.05). Expression of FGF-23 in UG skins, assessed by western blot, was significantly higher than that in the SG (186.3 ± 16.8 vs. 148.9 ± 25.9, MWU, p < 0.01). FGFR1 expression was increased in almost all parts of the uremic skin. Receptor expression was most dense at the epidermis and hair follicles. Normal skin appendages and cells either expressed no receptor, or expressed it very weakly.</p><p><strong>Conclusion: </strong>This study shows increased FGF-23 levels and FGFR1 expression in uremic rat skins. It deserves further study to fully place this finding in the pathophysiology and clinical picture of uremic skin diseases.</p>","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10053651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Wide intra- and inter-racial variation of end-stage kidney disease risk and transplant rate in pre-emptively listed kidney transplant candidates.","authors":"Jamie S Hirsch,&nbsp;Kenar D Jhaveri,&nbsp;Mersema Abate,&nbsp;Ernesto Molmenti,&nbsp;Kevin Coppa,&nbsp;Vinay Nair","doi":"10.5414/CN111136","DOIUrl":"https://doi.org/10.5414/CN111136","url":null,"abstract":"","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10074054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk factors for infective endocarditis in patients receiving hemodialysis: A propensity score matched cohort study.","authors":"Saif Al-Chalabi,&nbsp;Tricia Tay,&nbsp;Rajkumar Chinnadurai,&nbsp;Philip A Kalra","doi":"10.5414/CN111117","DOIUrl":"10.5414/CN111117","url":null,"abstract":"<p><p>In patients receiving hemodialysis, infective endocarditis (IE) may present in a similar way to other causes of bacteremia, which may delay early diagnosis and can lead to worse outcomes. In this study, we aimed to identify the risk factors for IE in hemodialysis patients with bacteremia. This study was conducted on all patients diagnosed with IE and receiving hemodialysis between 2005 and 2018 in Salford Royal Hospital. Patients with IE were propensity score matched with similar hemodialysis patients with episodes of bacteremia between 2011 and 2015 (non-IE bacteremic (NIEB)). Logistic regression analysis was used to predict the risk factors associated with infective endocarditis. There were 35 cases of IE, and these were propensity matched with 70 NIEB cases. The median age of the patients was 65 years with a predominance of males (60%). The IE group had higher peak C-reactive protein compared to the NIEB group (median, 253 mg/L vs. 152, p = 0.001). Patients with IE had a longer duration of prior dialysis catheter use than NIEB patients (150 vs. 28.5 days: p = 0.004). IE patients had a much higher 30-day mortality rate (37.1% vs. 17.1%, p = 0.023). Logistic regression analysis showed previous valvular heart disease (OR: 29.7; p < 0.001), and a higher baseline C-reactive protein (OR: 1.01; p = 0.001) as significant predictors for infective endocarditis. Bacteremia in patients receiving hemodialysis through a catheter access should be actively investigated with a high index of suspicion for infective endocarditis, particularly in those with known valvular heart disease and a higher baseline C-reactive protein.</p>","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9860776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute tubulointerstitial nephritis possibly caused by vedolizumab for ulcerative colitis in a kidney transplant recipient: A case report.","authors":"Masatomo Ogata,&nbsp;Masahiko Yazawa,&nbsp;Maho Terashita,&nbsp;Kiyomi Osako,&nbsp;Sayuri Shirai","doi":"10.5414/CN111029","DOIUrl":"https://doi.org/10.5414/CN111029","url":null,"abstract":"<p><p>Vedolizumab, which is used to effectively treat ulcerative colitis (UC), is a humanized monoclonal antibody that specifically inhibits α4β7 integrin on lymphocytes and prevents lymphocyte migration into the intestinal tissues. Herein, we report a case of acute tubulointerstitial nephritis (ATIN) probably caused by vedolizumab in a kidney transplant recipient (KR) with UC. Approximately 4 years after kidney transplantation, the patient developed UC and was treated initially with mesalazine. Treatment continued with the addition of infliximab later; however, he was hospitalized because of poor symptom control and treated with vedolizumab. His graft function declined rapidly after vedolizumab was administered. Allograft biopsy revealed ATIN. Since no evidence of graft rejection was found, vedolizumab-associated ATIN was diagnosed. The patient was treated with steroids, and his graft function improved. Unfortunately, he finally underwent total colectomy considering that UC was refractory to medical treatment. Previously, cases of vedolizumab-induced acute interstitial nephritis have been reported; however, none were associated with KRs. This is the first report of ATIN in KR which was possibly induced by vedolizumab.</p>","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10245272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation between plasma long non-coding RNA MEG-3 and inflammatory cytokines in patients with diabetic nephropathy.","authors":"Xingrong Guo,&nbsp;Meishe Gan,&nbsp;Lianji Zhou,&nbsp;Qingchen Wei,&nbsp;Zheng Li,&nbsp;Zuojie Luo,&nbsp;Hua Wei","doi":"10.5414/CN110996","DOIUrl":"10.5414/CN110996","url":null,"abstract":"<p><p>To identify the correlation between the plasma long non-coding RNA maternally expressed gene 3 (lncRNA MEG-3) and inflammatory cytokines in patients with diabetic nephropathy (DN) and search for a potential index for the diagnosis of DN. Quantitative real-time PCR (qPCR) was used to assess lncRNA MEG-3 expression. The levels of plasma cytokines were detected via enzyme-linked immunosorbent assay (-ELISA). 20 patients with type 2 diabetes (T2DM) and DN (DM+DN+ group), 19 patients with T2DM (DM+DN- group), and 17 healthy subjects (DM-DN- group) were finally enrolled. The expression of lncRNA MEG-3 was significantly upregulated in the DM+DN+ group compared to the DM+DN- group (p < 0.05) and the DM-DN- group (p < 0.001). Pearson's correlation analysis showed a positive correlation of lncRNA MEG-3 levels with cystatin C (Cys-C) (r = 0.468, p < 0.05), albumin-creatinine ratio (ACR) (r = 0.532, p < 0.05), and creatinine (Cr) (r = 0.468, p < 0.05), and a negative correlation with estimated glomerular filtration rate (eGFR) (r = -0.674, p < 0.01). Furthermore, the expression level of plasma lncRNA MEG-3 had a significantly positive correlation with the level of interleukin 1β (IL-1β) (r = 0.524, p < 0.05) and interleukin 18 (IL-18) (r = 0.230, p < 0.05). Binary regression analysis showed that lncRNA MEG-3 was a risk factor for DN with odds ration (OR) value of 1.71 (p < 0.05). The area under receiver operation characteristic (ROC) curve (AUC) of DN identified by lncRNA MEG-3 was 0.724. LncRNA MEG-3 was highly expressed in DN patients and showed a positive correlation with IL-1β, IL-18, ACR, Cys-C, and Cr.</p>","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9852032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Penile and digital calciphylaxis: A case report and literature review.","authors":"Gonçalo Ávila,&nbsp;Patrícia Matias,&nbsp;Ivo Laranjinha,&nbsp;Ana Carina Ferreira,&nbsp;Célia Gil,&nbsp;Aníbal Ferreira","doi":"10.5414/CN110990","DOIUrl":"https://doi.org/10.5414/CN110990","url":null,"abstract":"<p><p>Calcific uremic arteriolopathy (CUA) represents a rare but severe disease with high morbimortality. The authors present the case of a 58-year-old male patient with chronic kidney disease due to obstructive uropathy, on hemodialysis (HD). He started HD due to uremic syndrome with a severe renal dysfunction, dysregulation of calcium and phosphate metabolism, and he presented with distal penile ischemia, which was treated with surgical debridement and hyperbaric oxygen therapy. Four months later, painful distal digital necrosis of both hands was observed. Extensive arterial calcification was observed on X-ray. A skin biopsy confirmed the presence of CUA. Sodium thiosulfate was administered for 3 months, HD was intensified, and hyperphosphatemia control was achieved, with progressive improvement of the lesions. This case illustrates an uncommon presentation of CUA in a patient on HD for a few months, non-diabetic and not anticoagulated, but with a severe dysregulation of calcium and phosphate metabolism.</p>","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9867478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A single-center experience of post-transplant atypical hemolytic uremic syndrome.","authors":"Bassam G Abu Jawdeh,&nbsp;Muhammad A Khan","doi":"10.5414/CN111160","DOIUrl":"https://doi.org/10.5414/CN111160","url":null,"abstract":"<p><strong>Purpose: </strong>Atypical hemolytic uremic syndrome (aHUS) is a genetic-based thrombotic microangiopathy (TMA) that is mediated by the activation of the alternative complement pathway. Heterozygous deletion in CFHR3-CFHR1 occurs in 30% of the general population and has not been classically linked to aHUS. Post-transplant aHUS has been associated with a high rate of graft loss. Herein, we report our case series of patients who developed aHUS after solid-organ transplantation.</p><p><strong>Materials and methods: </strong>Five consecutive cases of post-transplant aHUS were identified at our center. Genetic testing was performed in all but one.</p><p><strong>Results: </strong>One patient had a presumed TMA diagnosis before transplant. One heart and 4 kidney (KTx) transplant recipients were diagnosed with aHUS based on the clinical picture of TMA, acute kidney injury, and normal ADAMTS13 activity. Genetic mutation testing revealed heterozygous deletion in CFHR3-CFHR1 in 2 patients and a heterozygous complement factor I (CFI) variant of uncertain clinical significance (VUCS) (Ile416Leu) in a third. Four patients were on tacrolimus, 1 had anti-HLA-A68 donor-specific antibody (DSA), and another had borderline acute cellular rejection at the time of aHUS diagnosis. Four responded to eculizumab, and 1 out of 2 patients came off renal replacement therapy. One KTx recipient died from severe bowel necrosis in the setting of early post-transplant aHUS.</p><p><strong>Conclusion: </strong>Calcineurin inhibitors, rejection, DSA, infections, surgery, and ischemia-reperfusion injury are common triggers that could unmask aHUS in solid-organ transplant recipients. Heterozygous deletion in CFHR3-CFHR1 and CFI VUCS may be important susceptibility factors acting as the first hit for alternative complement pathway dysregulation.</p>","PeriodicalId":10396,"journal":{"name":"Clinical nephrology","volume":null,"pages":null},"PeriodicalIF":1.1,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9867987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}