Clinical, Etiological and Progressive Aspects of Acute Tubular Necrosis of Toxic Origin at the Brazzaville University Hospital Center

Background and Objectives: Acute tubular necrosis (ATN) is the second cause of acute kidney injury (AKI) in an intra-hospital environment. The toxic origin is avoidable. Our objectives were to determine the toxic substances at the origin of ATN at the Brazzaville University Hospital and determine the evolving aspects and the factors associated with it. Patients and Methods: We carried out a 12-month from June 20, 2022 to June 30, 2023. It was a prospective observational study in the Nephrology Department of Brazzaville University Hospital Center. The diagnosis of ATN was done in the presence of AKI occurring in the context of taking nephrotoxic substances with negative albuminuria. Cases of ATN aggravating CKD were excluded. Data analysis was done with Epi-Info 7.2 software. Results: We identified 63 cases of AKI on toxic ATN. Their average age was 47 ± 19 years with a male predominance of 60.2%. The 3 main toxicants incriminated were: herbal medicine (49.2%), Gentamycin (17.5%) and non-steroidal anti-inflammatory drugs (14.3%). An indication for hemodialysis was made in 43 patients (68.2%), the evolution was marked by a cure in 29 patients (46.1%), 10 (15.9%) became chronic kidney failure, 19 (30.1%) died, 5 (7.9%) were lost to follow-up. The main factor for non-healing is anuria (p Conclusion: The main cause of toxic ATN at Brazzaville University Hospital is herbal medicine. The death rate is high there.

Prucalopride-associated acute tubular necrosis

We report the first case of acute renal failure secondary to prucalopride, a novel agent for the treatment of chronic constipation. The 75 years old male patient was initiated on prucalopride after many failed treatments for constipation following a Whipple's procedure for pancreatic cancer. Within four months of treatment his creatinine rose from 103 to 285 μmol/L(e GFR 61 decrease to 19 m L/min per 1.73 m2). He was initially treated with prednisone for presumed acute interstitial nephritis as white blood casts were seen on urine microscopy. When no improvement was detected, a core biopsy was performed and revealed interstitial fibrosis and tubular atrophy. The presence of oxalate and calcium phosphate crystals were also noted. These findings suggest acute tubular necrosis which may have been secondary to acute interstitial nephritis or hemodynamic insult. The use of prednisone may have suppressed signs of inflammation and therefore the clinical diagnosis was deemed acute interstitial nephritis causing acute tubular necrosis. There are no previous reports ofprucalopride associated with acute renal failure from the literature, including previous Phase Ⅱ and Ⅲ trials.

Changing picture of renal cortical necrosis in acute kidney injury in developing country

Renal cortical necrosis(RCN) is characterized by patchy or diffuse ischemic destruction of all the elements of renal cortex resulting from significantly diminished renal arterial perfusion due to vascular spasm and microvascular injury. In addition, direct endothelial injury particularly in setting of sepsis, eclampsia, haemolytic uremic syndrome(HUS) and snake bite may lead to endovascular thrombosis with subsequent renal ischemia. Progression to end stage renal disease is a rule in diffuse cortical necrosis. It is a rare cause of acute kidney injury(AKI) in developed countries with frequency of 1.9%-2% of all patients with AKI. In contrast, RCN incidence is higher in developing countries ranging between 6%-7% of all causes of AKI. Obstetric complications(septic abortion, puerperal sepsis, abruptio placentae, postpartum haemorrhage and eclampsia) are the main(60%-70%) causes of RCN in developing countries. The remaining 30%-40% cases of RCN are caused by non-obstetrical causes, mostly due to sepsis and HUS. The incidence of RCN ranges from 10% to 30% of all cases of obstetric AKI compared with only 5% in non-gravid patients. In the developed countries, RCN accounts for 2% of all cases of AKI in adults and more than 20% of AKI during the third trimester of pregnancy. The reported incidence of RCN in obstetrical AKI varies between 18%-42.8% in different Indian studies. However, the overall incidence of RCN in pregnancy related AKI has decreased from 20%-30% to 5% in the past two decades in India. Currently RCN accounts for 3% of all causes of AKI. The incidence of RCN in obstetrical AKI was 1.44% in our recent study. HUS is most common cause of RCN in non-obstetrical group, while puerperal sepsis is leading cause of RCN in obstetric group. Because of the catastrophic sequelae of RCN, its prevention and aggressive management should always be important for the better renal outcome and prognosis of the patients.

Therapeutic effects of human umbilical cord-derived mesenchymal stem cells against acute tubular necrosis quantified through measures of iNOS, BMP-7 and Bcl-2

Introduction: Acute tubular necrosis (ATN) is the most prevalent cause of acute renal failure (ARF). Mesenchymal stem cell transplantation has been studied as a potential treatment for renal dysfunction due to ATN. Inducible nitric oxide synthase (iNOS), bone morphogenetic protein-7 (BMP-7) and B-cell lymphoma 2 (Bcl-2) are surrogate markers of renal tubular epithelial regeneration and subsequent recovery of renal function following ATN. Methods: Serum creatinine (Scr) and blood urea nitrogen (BUN), as well as expression of iNOS, BMP-7 and Bcl-2 in gentamycin-induced ATN rat kidneys was investigated after human umbilical cord-derived mesenchymal stem cell (HUC-MSC) transplantation. Immunohistochemical staining was performed in 3 groups of rats: gentamycin-induced ATN treated with HUC-MSC, gentamycin-induced ATN without HUC-MSC, and untreated rats not receiving any treatments. Results: HUC-MSC transplantation led to a reduction in Scr and BUN in the kidneys of rats with gentamycin-induced ATN. Expression of iNOS in the HUC-MSC treated group occurred later and the expression levels were much lower during gentamycin-induced ATN compared to rats with ATN that were not treated with HUC-MSC. The expression of BMP-7 and Bcl-2 in the MSC-transplanted group was significantly increased compared to both control groups of rats with injured and healthy renal tubules. Conclusions: HUC-MSCs induce renal protection in a rat model of gentamycin-induced ATN, which is associated with reduced iNOS expression and up-regulation of Bcl-2 and BMP-7.

Acute renal failure associated with acute non-fulminant hepatitis B

A 38-year-old female presenting with a high fever of 39 ℃ developed severe liver dysfunction and acute renal failure(ARF).In tests for a hepatitis associated virus,an Immunoglobulin M-anti-hepatitis B virus core antibody was the only positive finding.Moreover,the progression of ARF coincided with the pole period of liver damage and all the other assumed causes for the ARF were unlikely.Therefore,this case was diagnosed as ARF caused by acute hepatitis B.ARF associated with non-fulminant hepatitis has been infrequently reported,usually in association with acute hepatitis A.This case is considered to be an extremely rare and interesting case.

Approach to Acute Kidney Injury: Diagnosis and Management

Acute kidney injury is a critical but commonly occurring medical condition that presents with a sudden decline in kidney function. This comprehensive review article provides an in-depth examination of the risk elements, etiology, diagnosis, management, and preventive approach of AKI. The causes that contribute to the development of AKI include prerenal, intrinsic renal, and postrenal. The diagnostic approach to AKI includes clinical, laboratory, and imaging studies to evaluate the root cause analysis and to find out the severity of kidney injury. Timely and accurate diagnosis is crucial for initiating appropriate management strategies. The treatment strategies may include fluid and electrolyte management, medication adjustments, nutritional support, and renal replacement therapy. The prospect of recovery diverges as it relies on the individual factors, reasons, and gravity of the condition. This review highlights the importance of raising awareness among healthcare professionals and the public about AKI, early recognition of risk factors, and prompt management. Further research is needed to explore novel therapeutic approaches and refine existing management guidelines for this critical condition.

Clinicopathological spectrum of snake bite-induced acute kidney injury from India

AIM To study the clinico-pathological spectrum of snake bite-induced acute kidney injury(AKI).METHODS A retrospective study of patients admitted at Indira Gandhi Medical College Hospital,Shimla with snake bite-induced AKI from July 2003 to June 2016.Medical records were evaluated for patient's information on demographic,clinical characteristics,complications and outcome.Outcomes of duration of hospital stay,requirement for intensive care unit support,treatment with dialysis,survival and mortality were analyzed.The survival and non survival groups were compared to see the difference in the demographic factors,clinical characteristics,laboratory results,and complications.In patients subjected to kidney biopsy,the findings of histopathological examination of the kidney biopsies were also analyzed.RESULTS One hundred and twenty-one patients were diagnosed with snake bite-induced AKI.Mean age was 42.2 ± 15.1 years and majority(58%) were women.Clinical details were available in 88 patients.The mean duration of arrival at hospital was 3.4 ± 3.7 d with a range of 1 to30 d.Eighty percent had oliguria and 55% had history of having passed red or brown colored urine.Coagulation defect was seen in 89% patients.The hematological and biochemical laboratory abnormalities were:Anemia(80.7%),leukocytosis(75%),thrombocytopenia(47.7%),hyperkalemia(25%),severe metabolic acidosis(39.8%),hepatic dysfunction(40.9%),hemolysis(85.2%) and rhabdomyolysis(68.2%).Main complications were:Gastrointestinal bleed(12.5%),seizure/encephalopathy(10.2%),hypertension,pneumonia/acute respiratory distress syndrome(ARDS) and disseminated intravascular coagulation(9.1% each),hypotension and multi organ failure(MOF)(4.5% each).Eighty-two percent patients required renal replacement therapy.One hundred and ten(90.9%) patient survived and 11(9.1%) patients died.As compared to the survival group,the white blood cell count(P = 0.023) and bilirubin levels(P = 0.006) were significant higher and albumin levels were significantly lower(0.005) in patients who died.The proportion of patients with pneumonia/ARDS(P = 0.001),seizure/encephalopathy(P = 0.005),MOF(P = 0.05) and need for intensive care unit support(0.001) was significantly higher and duration of hospital stay was significantly shorter(P = 0.012) in patients who died.Kidney biopsy was done in total of 22 patients.Predominant lesion on kidney biopsy was acute tubular necrosis(ATN) in 20(91%) cases.In 11 cases had severe ATN and in other nine(41%) cases kidney biopsy showed features of ATN associated with mild to moderate acute interstitial nephritis(AIN).One patient only had moderate AIN and one had patchy renal cortical necrosis(RCN).CONCLUSION AKI due to snake bite is severe and a high proportion requires renal replacement therapy.On renal histology ATN and AIN are common,RCN is rare.

Nephropathy in dietary hyperoxaluria:A potentially preventable acute or chronic kidney disease

Hyperoxaluria can cause not only nephrolithiasis and nephrocalcinosis,but also renal parenchymal disease histologically characterized by deposition of calcium oxalate crystals throughout the renal parenchyma,profound tubular damage and interstitial inflammation and fibrosis.Hyperoxaluric nephropathy presents clinically as acute or chronic renal failure that may progress to endstage renal disease(ESRD).This sequence of events,well recognized in the past in primary and enteric hyperoxalurias,has also been documented in a few cases of dietary hyperoxaluria.Estimates of oxalate intake in patients with chronic dietary hyperoxaluria who developed chronic kidney disease or ESRD were comparable to the reported average oxalate content of the diets of certain populations worldwide,thus raising the question whether dietary hyperoxaluria is a primary cause of ESRD in these regions.Studies addressing this question have the potential of improving population health and should be undertaken,alongside ongoing studies which are yielding fresh insights into the mechanisms of intestinal absorption and renal excretion of oxalate,and into the mechanisms of development of oxalate-induced renal parenchymal disease.Novel preventive and therapeutic strategies for treating all types of hyperoxaluria are expected to develop from these studies.

Experimental Study on Detached Renal Tubular Epithelial Cells in Urine of Nephropathia Epidemic Patients

To elucidate the pathogenesis of acute renal failure (ARF) with nephropathia epidemic (NE), provide experimental evidence for the new therapy to NE and observe the effects of Arg-Gly-Asp (RGD) peptides on adhesion of re-nal tubular epithelial cell (RTEC), urine specimens of patients were collected un-der sterile conditions. Detached RTECs were separated, cultured and identified.Hantan Virus antigen was determined by using indirect immunofluorescence method and effects of RGD on adhesion of RTECs was observed by subgroup counting as well as by flow cytometry. This study showed that: (1) sublethal RTECs existed in the urine of NE-ARF patients, which could be cultured in monolayer form; (2 ) there was NE antigen in RTECs; and (3) adhesion of RTECs could be inhibited by RGD.

Renal Cortical Necrosis: An Unusual Complication of <i>Plasmodium malariae</i>Malaria

Renal cortical necrosis (RCN) is anecdotal in malaria. To our knowledge, RCN secondary to Plasmodium malariae has not yet been published. We report a case of severe malaria complicated by RCN. A 29 year old Senegalese patient was transferred to our department for anuria in a context of severe malaria. The diagnosis was RCN secondary to a severe Plasmodium malariae malaria. Physical examination showed anuria, anaemic syndrome, haemorrhagic syndrome and a generally impaired condition. There was a normocytic normochromic anaemia aplastic, thrombocytopenia leukocytosis of 11.580/mm3, serum creatinine of 12.45 mg/dl and blood urea of 252 mg/dl. The Plasmodium malariae had been shown to thick blood film with high parasite density. The molecular study was able to confirm the infestation of this parasite. Treatment consisted of four haemodialysis sessions and antimalarial molecules. Initial evolution was favourable with a recovery through diuresis and a partial improvement in renal function. Given the persistence of impaired renal function, a renal biopsy was performed. This confirmed the RCN. At last consultation, he had no symptoms and his last glomerular filtration rate (GFR) was 30 mL/min/1.73 m2.

Acute renal artery occlusion following infliximab infusion

We report the case of a 44-year-old male patient who presented with acute renal artery occlusion, 3 d after frst injection of infiximab for steroid refractory attack of ulcerative colitis. Extensive work-up provided no evidence of predisposing factors for arterial thrombosis. Infiximab was thus suspected in the genesis of throm-bosis, based on both intrinsic and extrinsic criteria. At month 3 after thrombosis with ongoing anticoagulation, angio-tomodensitometry showed complete revascularization of the left renal artery with renal atrophy. Renal function remained normal and the patient was still in steroid free remission on mercaptopurin monotherapy at maximal follow-up. Few thromboembolic events have been described with anti- tumor necrosis factor （TNF） agents, but it is the frst case reported of renal artery thrombosis after infiximab infusion. In addition, we re-view thrombosis associated with anti-TNF agents.

近端肾小管上皮细胞代谢重编程在急性肾损伤中的研究进展

肾脏是一个高代谢器官,尤其是近端肾小管上皮细胞,在生理情况下主要依赖脂肪酸氧化供能,但是在急性肾损伤(AKI)期间,线粒体和过氧化物酶体功能障碍,近端肾小管上皮细胞发生代谢重编程,能量供应转向糖酵解,生成乳酸,并伴脂肪酸氧化紊乱及糖异生受损,短期内代谢重编程可能是对肾脏有益的能量代偿,但是该过程中也会加重肾损伤。本文就近端肾小管上皮细胞代谢重编程在AKI中的作用进行综述。

川芎嗪对脂多糖处理大鼠肾小管上皮细胞S1PR3的抑制作用

目的探讨川芎嗪对脂多糖(LPS)处理大鼠肾小管上皮细胞(NRK-52E)中1-磷酸鞘氨醇受体(S1PR)3的影响以及S1PR3在脓毒症相关急性肾损伤(S-AKI)中的作用及机制。方法将培养好的大鼠NRK-52E细胞分为对照组、LPS组、川芎嗪+LPS组。对照组不予处理;LPS组予川芎嗪等量0.9%氯化钠溶液预处理30 min后,予LPS 20μg/mL刺激12 h后离心收集细胞待检;川芎嗪+LPS组先用川芎嗪200 ng/mL预处理30 min后再予LPS 20μg/mL刺激12 h后离心收集细胞待检。采用流式细胞术检测3组细胞凋亡率及钙离子、半胱氨酸天冬氨酸蛋白酶-3(Caspase-3)表达的差异,ELISA法检测钙蛋白酶(Calpain)1、Calpain 2表达的差异,Western blot法检测各组细胞中S1PR3表达的差异。结果经LPS处理后脓毒症NRK-52E细胞模型成功建立。与对照组比较,LPS组的细胞凋亡率、钙离子表达、Caspase-3表达、S1PR3表达、Calpain 1、Calpain 2表达均明显增加(均P<0.01);与LPS组比较,川芎嗪+LPS组的细胞凋亡率、钙离子表达、Caspase-3表达、S1PR3表达、Calpain 1、Calpain 2表达均明显下降(均P<0.05)。结论川芎嗪可以抑制S1PR3的表达,能够降低肾小管上皮细胞内的钙离子浓度,从而抑制Caspase-3细胞凋亡信号通路,减少肾小管细胞凋亡。S1PR3可能在S-AKI的发生、发展中起到重要作用。

肾小管HIF-1α/miR-23a通路在脓毒血症急性肾损伤中的作用机制

目的探讨肾小管低氧诱导因子-1α(HIF-1α)/MicroRNA-23a(miR-23a)通路在脓毒血症急性肾损伤(SA-AKI)中的作用及相关作用机制。方法体外培养人近曲小管上皮细胞(HK-2细胞),采用脂多糖(LPS)处理HK-2细胞构建SA-AKI细胞模型。LPS处理的HK-2细胞分为LPS组、NC siRNA组、HIF-1αsiRNA组、anti-miR-NC组、anti-miR-23a组、HIF-1αsiRNA+miR-NC组、HIF-1αsiRNA+miR-23a组,以正常培养的HK-2细胞作为空白对照组(Control组)。采用qRT-PCR法检测细胞中HIF-1α、miR-23a基因表达;CCK-8法检测细胞活力;流式细胞术检测细胞凋亡;ELISA法检测细胞中炎性因子[白介素-1β(IL-1β)、白介素-6(IL-6)、肿瘤坏死因子α(TNF-α)]水平;Western blot法检测细胞中HIF-1α蛋白、NF-κB通路蛋白表达。结果与Control组比较,LPS组HK-2细胞中HIF-1α蛋白和mRNA表达水平、miR-23a mRNA表达水平均升高,细胞活力降低,细胞凋亡率、细胞中IL-6、IL-1β和TNF-α水平均升高(P<0.05)。与LPS组比较,HIF-1αsiRNA组HK-2细胞中HIF-1α蛋白和mRNA表达水平、miR-23a mRNA表达水平均降低,细胞活力升高,细胞凋亡率、细胞中IL-6、IL-1β和TNF-α水平均降低(P<0.05)。与LPS组比较,anti-miR-23a组HK-2细胞中miR-23a mRNA表达水平降低,细胞活力升高,细胞凋亡率、细胞中IL-6、IL-1β和TNF-α水平均降低(P<0.05)。与HIF-1αsiRNA组比较,HIF-1αsiRNA+miR-23a组HK-2细胞中miR-23a mRNA表达水平升高,细胞活力降低,细胞凋亡率、细胞中IL-6、IL-1β和TNF-α水平均升高(P<0.05)。与Control组比较,LPS组HK-2细胞p-NF-κB-p65/NF-κB-p65、p-IκBα/IκBα比值均升高(P<0.05)。与LPS组比较,HIF-1αsiRNA组和anti-miR-23a组HK-2细胞p-NF-κB-p65/NF-κB-p65、p-IκBα/IκBα比值均降低(P<0.05)。与HIF-1αsiRNA组比较,HIF-1αsiRNA+miR-23a组HK-2细胞p-NF-κB-p65/NF-κB-p65、p-IκBα/IκBα比值均升高(P<0.05)。结论肾小管HIF-1α通过调控miR-23a表达调节NF-κB信号通路,从而参与LPS诱导的肾小管上皮细胞损伤。

Acute Kidney Injury (AKI) in the Setting of Multi-Organ Dysfunction Syndrome (MODS) Secondary to Yellow Fever Infection (YFI) in a 19-Year-Old Woman

Background: Outbreak of yellow fever infection (YFI), a mosquito-borne disease, occurs sporadically worldwide especially in tropical nations. Acute kidney injury (AKI) commonly results from YFI and could be associated with a poor prognosis for victims even under intensive care unit (ICU). Pathophysiologic mechanisms for AKI include hypovolemic shut down, cytotoxicity, acute tubular necrosis (ATN), hemolysis, or coagulopathy. Early diagnosis, prompt and effective treatment modalities including dialysis improve treatment outcome. Aim: We report the case management of a 19-year-old woman who had yellow fever infection complicated by acute kidney injury in the setting of multi-organ dysfunction syndrome (MODS). Case Presentation: A 19-year-old woman who presented with fever, headache and vomiting for 2 weeks. In the course of the illness, urine volume became reduced and coke colored, followed by body swelling, yellowness of the eyes bleeding from the orifices. Examination revealed an acutely ill looking woman, icteric, and with pedal edema. Her pulse was 100/min and blood pressure was 120/80 mmHg. Liver was enlarged, soft and tender. She had proteinuria 3+ and polymerase chain reaction (PCR) confirmed yellow fever infection. She had markedly deranged serum biochemical parameters for which she had a three-hour session of hemodialysis with Heparin anticoagulation. The urea reduction ratio (URR) was 46.9%. Barrier nursing was commenced. She had 7 units of whole blood and a pint of fresh frozen plasma (FFP) with antibiotics, Rabeprazole, Tranexamic acid, Vitamin K and Frusemide. She had the second dialysis session of HD and entered into the recovering phase of AKI and was subsequently discharged after 18th days on admission. Conclusion: Yellow fever infection occurs sporadically and could lead to MODS involving the kidneys, liver and hematologic system. Prompt initiation of dialysis, correction of coagulopathy, and antibiotics use are measures needed to arrest progression and death. Vaccination, destruction of the natural habitat of the carrier and infective organisms are necessary particularly in endemic regions of the world.

Histopathological and ultrastructural studies of renal tissues after severe steam inhalation burns in dogs

This paper is to report the pathological changes of canine renal tissuesin the period of 48h after severe steam inhalation burns.All the specimens from84 male mongrel dogs were observed with light microscopy,and 30 out of the 84with electron microscopy additionally.The morphological changes of the glomeriwere characterized by hypertrophy and/or hyperplasia,and retrogressive changesof glomerular cells.The former manifested itself as cell enlargement and an in-crease of the amount of cytoplasm and of the number or organelles.The latterwas evidenced as intracellular edema.The renal tubules showed a varying degreeof degeneration,necrosis,and cast formation.Tubular necrosis affected more fre-quently the proximal convoluted tubules,of which the etiological factors were dis-cussed briefly.

超声影像组学对移植肾实质性病变鉴别诊断的价值

目的探讨超声影像组学对移植肾实质性病变组织学的诊断价值。方法选取186例因血肌酐异常而行肾穿刺活检的同种异体肾移植患者,根据活检结果分为急性排斥反应组(AR组)135例和肾小管坏死组(ATN组)51例。收集移植肾穿刺活检结果和超声资料,由2位医师根据常规超声参数进行诊断;应用影像组学进行超声图像特征提取,对获得的全部组学特征数据采用独立样本t检验进行初次筛选,再使用最小绝对值收敛和选择算子(LASSO)算法从已筛选特征中选择最优有效特征,并利用随机森林、K近邻法、逻辑回归、支持向量机分类器建立预测模型。所有患者按照7∶3的比例分配到训练队列和验证队列,采用5折交叉验证策略分析各组学模型在验证队列的准确度、敏感度、特异度、ROC曲线下面积(AUC)。结果医师组以常规超声参数为特征对AR和ATN鉴别诊断的敏感度为56.2%,特异度为60.7%,准确度为57.5%。应用影像组学方法每幅图像提取137个组学特征,经过筛选后最终保留6个有意义的特征,分别为2D形状-平坦度、一阶-最小值、直方图-最小值、直方图-体素计数、梯度-标准差、灰度共生矩阵-集群阴影。随机森林、支持向量机、逻辑回归和K近邻法4种模型的AUC分别为0.931(95%CI:0.779~0.997)、0.762(95%CI:0.604~0.897)、0.721(95%CI:0.582~0.808)和0.713(95%CI:0.508~0.796),其中随机森林模型敏感度为97.60%,特异度为80.00%,准确度为85.80%,综合表现最优。结论超声影像组学可以提取更多的超声图像特征,各组学模型对移植肾实质性病变组织学分型均具有较好的鉴别诊断价值,优于常规超声方法。

血清MCP-1、TRAF-6水平在脓毒症严重程度和急性肾损伤评估的作用

目的探讨血清单核细胞趋化蛋白-1(MCP-1)、肿瘤坏死因子受体相关因子-6(TRAF-6)水平在脓毒症严重程度和急性肾损伤评估中的作用。方法回顾性分析2021年6月至2022年6月在新疆维吾尔自治区人民医院重症医学科接受治疗的110例脓毒症患者的病例资料,依据脓毒症相关急性肾损伤发生情况分为发生组(50例)、未发生组(60例)。统计分析两组患者基线资料、血清MCP-1、TRAF-6水平,并分析脓毒症患者血清MCP-1、TRAF-6水平与序贯多器官功能障碍(SOFA)评分、急性生理和慢性健康Ⅱ(APACHEⅡ)评分的相关性,多因素Logistic回归分析脓毒症相关急性肾损伤影响因素。结果110例患者中,脓毒症相关急性肾损伤发生50例,未发生60例,发生率为45.45%。发生组患者的高血压、肺部感染比例均高于未发生组(P<0.05),SOFA评分、APACHEⅡ评分均高于未发生组(P<0.05),氧合指数低于未发生组(P<0.05),肾小球滤过率(eGFR)、血肌酐(SCr)、尿素氮(BUN)水平均高于未发生组(P<0.05),动脉血乳酸水平高于未发生组(P<0.05),但两组患者的性别、年龄、糖尿病比例的差异无统计学意义(P>0.05)。发生组患者的血清MCP-1、TRAF-6水平均高于未发生组(P<0.05)。脓毒症患者血清MCP-1、TRAF-6水平与SOFA评分、APACHEⅡ评分均呈显著的正相关关系(P<0.05)。多因素Logistic回归分析显示,脓毒症相关急性肾损伤影响因素包括高血压、肺部感染、SOFA评分、APACHEⅡ评分、肾小球滤过率(eGFR)、动脉血乳酸、MCP-1、TRAF-6(P<0.05),不包括氧合指数、尿素氮(BUN)、SCr(P>0.05)。结论血清MCP-1、TRAF-6水平和脓毒症严重程度和关系密切,可作为急性肾损伤的诊断参考指标。

司库奇尤单抗联合预防性抗结核治疗斑块型银屑病致急性肾损伤1例报告

1病例资料患者男,54岁,因“恶心、呕吐2周,血肌酐升高4 d”于2022年8月12日收入我科治疗。2022年7月初患者因全身皮肤弥漫性红色丘疹、斑块,伴脱屑、瘙痒就诊于我院皮肤科门诊,诊断为斑块型银屑病(中重度),因既往激素等治疗无效,拟给予司库奇尤单抗(可善挺®,辉瑞制药有限公司)治疗,用药前肝肾功能和尿常规检查均未见异常,血肌酐72μmol/L。因患者既往有肺结核病史,结核感染T细胞检测阳性,胸部CT示“两肺多发实性小结节,右上肺为著,右上肺索条影”,2022年7月18日上海市肺科医院肺结核科会诊后建议给予预防性抗结核治疗。

急性肾小管间质性肾炎与急性肾小管坏死的临床鉴别分析

目的:分析急性肾小管间质性肾炎(acute tubulointerstitial nephritis,ATIN)患者的临床及实验室检查特征,探讨该病与急性肾小管坏死(acute tubular necrosis nephritis,ATN)的鉴别诊断要点。方法:纳入2009年1月至2018年12月间在上海交通大学医学院附属瑞金医院肾脏科经肾活检病理诊断为ATIN、ATN的患者,收集其临床表现和实验室检查数据,并对两者进行比较分析。结果:10年间我院肾脏科行经肾活检的病例总计5537例,其中诊断为ATIN的患者共135例(2.4%,135/5537),诊断为ATN的患者109例(2.0%,109/5537)。ATIN占急性肾脏病(acute kidney disease,AKD)肾活检患者的21.4%(135/630)。ATIN患者的中位确诊年龄为53岁,女性占57.0%,临床主要表现为发热、皮疹、关节痛,常见诱因为感染、药物应用和毒物接触。与ATN组相比,ATIN患者中女性占比高(57.0%比33.9%),平均体重指数(body weight index,BMI)低(22.9±3.6比24.6±3.9,P<0.01),且发生急性肾损伤(acute kidney injury,AKI)(14.8%比64.2%)、少尿(17.0%比48.6%)及入院后需紧急透析(19.3%比39.4%)的百分比低(P<0.01)。ATIN患者入院时,血红蛋白(hemoglobin,Hb)[(100.9±20.9)g/L比(116.7±29.8)g/L]和血尿素氮/肌酐比值(blood urea nitrogen/creatinine ratio,BCR)(11.8±5.4比14.6±11.0)均较ATN组低(P<0.01)。多因素回归分析显示,入院时高白蛋白(>55 g/L)、低血清肌酐(serum creatine,Scr)(<62μmol/L)、低血清尿酸(urine acid,UA)(<208μmol/L)、低Hb水平(<130 g/L)与ATIN相关,联合这4项指标建立的预测模型,其诊断ATIN的受试者操作特征曲线下面积为0.798(95%CI为0.742~0.853),灵敏度为74.4%,特异度为71.4%。结论:ATIN在上海地区人群接受肾活检的AKD患者中占比高,好发于中年女性,半数患者诱因不明。患者入院时的白蛋白、Scr、Hb及UA水平有助于ATIN与AIN间的鉴别,基于上述4项指标构建的ATIN患者诊断预测模型具有较好的特异度和灵敏度。