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.

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.

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.

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.

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.

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.

Acute kidney injury due to intravenous detergent poisoning:A case report

BACKGROUND Detergent poisoning mostly occurs through oral ingestion(>85%),ocular exposure(<15%),or dermal exposure(<8%).Reports of detergent poisoning through an intravenous injection are extremely rare.In addition,there are very few cases of renal toxicity directly caused by detergents.Here,we report a unique case of acute kidney injury caused by detergent poisoning through an accidental intravenous injection.CASE SUMMARY A 61-year-old man was intravenously injected with 20 mL of detergent by another patient in the same room of a local hospital.The surfactant and calcium carbonate accounted for the largest proportion of the detergent.The patient complained of vascular pain,chest discomfort,and nausea,and was transferred to our institution.After hospitalization,the patient’s serum creatinine level increased to 5.42 mg/dL,and his daily urine output decreased to approximately 300 mL.Renal biopsy findings noted that the glomeruli were relatively intact;however,diffuse acute tubular injury was observed.Generalized edema was also noted,and the patient underwent a total of four hemodiafiltration sessions.Afterward,the patient’s urine output gradually increased whereas the serum creatinine level decreased.The patient was discharged in a stable status without any sequelae.CONCLUSION Detergents appear to directly cause renal tubular injury by systemic absorption.In treating a patient with detergent poisoning,physicians should be aware that the renal function may also deteriorate.In addition,timely renal replacement therapy may help improve the patient’s prognosis.

Restoration of E-cadherin by compound 8J protects against cisplatin-induced acute kidney injury by attenuating inflammation and programmed cell death

OBJECTIVE E-cadherin is a major component of tubular adherent proteins which maintain intercellular contacts and cell polarity in epithelial tissue,it is involved in the pathological process of renal cell carcinoma and fibrotic diseases via epithelial-mesenchymal transition.Although we and others found that expression of E-cadherin was significantly down-regulated in kidney suffered acute kidney injury(AKI),its function in AKI was still unknown,which was explored in the current study.METHODS We disrupted E-cadherin or restored E-cadherin with compound 8J in cisplatin-stimulated tubular epithelial cell lines,the cell damage and inflammation were evaluated,additionally,the therapeutic potential of E-cadherin restoration was also determined in vivo.RESULTS We found that cisplatin reduced E-cadherin expression both in mouse kidney and tubular epithelial cell lines(m TECs).Administration of compound 8J restored the level of E-cadherin,thereby increased cell viability while attenuating programmed cell death,which may be mediated by deactivation of RIPK/MLKL axis,reduced membrane translocation of phosphor-MLKL and decreased cleavage of caspase 3.Compound 8J also suppressed inflammatory response in cisplatin-treated m TECs,which was correlated with suppressed NF-κB phorsphorylation and promoter activity.In contrast,disruption of E-cadherin enhanced cell damage and inflammation.Treatment of compound 8J failed to further attenuate kidney damage in E-cadherin knockdown cells,indicating compound 8J protected against mT ECs mainly through restoring E-cadherin.We also found that peritoneal injection of compound 8J protected against renal function and tubular damage by preventing NF-κB-driven renal inflammation and RIPK/MLKL-regulated programmed cell death,which was led by restoration of E-cadherin in cisplatin nephropathy.CONCLUSION More than a victim degraded after kidney injury,E-cadherin also has functional role in controlling tubule integrity,programmed cel death and renal inflammation.In this regard,restoration of E-cadherin by compound 8J should be considered as a novel therapeutic strategy for acute kidney injury.

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.

Predicting outcomes after kidney transplantation: Can Pareto’s rules help us to do so?

Kidney transplantation is the best option for kidney replacement therapy,even considering that most of the times the grafts do not survive as long as their recipients.In the Khalil et al's experience,published in this issue of the Journal,they analyze their second kidney graft survival and describe those significant predictors of early loss.This editorial comments on the results and put in perspective that most of the times,long-term graft survival could be inadvertently jeopardized if the immunosuppressive therapy is reduced or withdrawn for any reason,and that it could happen frequently if the transplant physician intends to innovate with the clinical care without proper evidence-based data.

Dexamethasone protects the glycocalyx on the kidney microvascular endothelium during severe acute pancreatitis

Objective: This study demonstrated that dexamethasone(DEX) protects the endothelial glycocalyx from damage induced by the inflammatory stimulus tumor necrosis factor-α(TNF-α) during severe acute pancreatitis(SAP), and improves the renal microcirculation. Methods: Ninety mice were evenly divided into 3 groups(Sham, SAP, and SAP+DEX). The SAP mice model was established by ligature of pancreatic duct and intraperitoneal injection of cerulein. Renal perfusion and function, and morphological changes of the glycocalyx were evaluated by laser Doppler velocimetry, electron microscopy, and histopathology(hematoxylin and eosin(H&E) staining), respectively. Serum levels of syndecan-1 and TNF-α were assessed by enzyme-linked immunosorbent assay(ELISA). The proàtectiveì effects of dexamethasone on the glycocalyx and renal microcirculation were evaluated. Results: Significantly high levels of serum TNF-α were detected 3 h after the onset of SAP. These levels might induce degradation of the glycocalyx and kidney hypoperfusion, resulting in kidney microcirculation dysfunction. The application of dexamethasone reduced the degradation of the glycocalyx and improved perfusion of kidney. Conclusions: Dexamethasone protects the endothelial glycocalyx from inflammatory degradation possibly initiated by TNF-α during SAP. This is might be a significant discovery that helps to prevent tissue edema and hypoperfusion in the future.

Histopathological characteristics and causes of kidney graft failure in the current era of immunosuppression

BACKGROUND The histopathological findings on the failing kidney allograft in the modern era is not well studied. In this study, we present our experience working with kidney transplant recipients with graft failure within one year of the biopsy.AIM To report the histopathological characteristics of failed kidney allografts in the current era of immunosuppression based on the time after transplant, cause of the end-stage renal disease and induction immunosuppressive medications.METHODS In a single-center observational study, we characterized the histopathological findings of allograft biopsies in kidney transplant recipients with graft failure within one year after the biopsy.RESULTS We identified 329 patients with graft failure that met the selection criteria between January 1, 2006 and December 31, 2016. The three most common biopsy findings were interstitial fibrosis and tubular atrophy(IFTA, 53%), acute rejection (AR, 43%) and transplant glomerulopathy(TG, 33%). Similarly, the three most common causes of graft failure based on the primary diagnosis were AR(40%),TG(17%), and IFTA(13%). Most grafts failed within two years of post-transplant(36%). Subsequently, approximately 10%-15% of grafts failed every two years: >2-4 years(16%), > 4-6 years(13%), > 6-8 years(11%), > 8-10 years(9%) and > 10 years(16%). AR was the most common cause of graft failure in the first six years(48%), whereas TG was the most prevalent cause of graft failure after 6 years(32%) of transplant.CONCLUSION In the current era of immunosuppression, AR is still the most common cause of early graft failure, while TG is the most prevalent cause of late graft failure.

Anthrahydroquinone-2,6-disulfonate alleviates paraquat-induced kidney injury via the apelin-APJ pathway in rats

Objective:To explore the protective effects of anthrahydroquinone-2,6-disulfonate(AH_(2)QDS)on the kidneys of paraquat(PQ)poisoned rats via the apelin-APJ pathway.Methods:Male Sprague Dawley rats were divided into four experimental groups:control,PQ,PQ+sivelestat,and PQ+AH_(2)QDS.The PQ+sivelestat group served as the positive control group.The model of poisoning was established via intragastric treatment with a 20%PQ pesticide solution at 200 mg/kg.Two hours after poisoning,the PQ+sivelestat group was treated with sivelestat,while the PQ+AH_(2)QDS group was given AH_(2)QDS.Six rats were selected from each group on the first,third,and seventh days after poisoning and dissected after anesthesia.The PQ content of the kidneys was measured using the sodium disulfite method.Hematoxylin-eosin staining of renal tissues was performed to detect pathological changes.Apelin expression in the renal tissues was detected using immunofluorescence.Western blotting was used to detect the expression levels of the following proteins in the kidney tissues:IL-6,TNF-α,apelin-APJ(the apelin-angiotensin receptor),NF-κB p65,caspase-1,caspase-8,glucose-regulated protein 78(GRP78),and the C/EBP homologous protein(CHOP).In in vitro study,a PQ toxicity model was established using human tubular epithelial cells treated with standard PQ.Twenty-four hours after poisoning,sivelestat and AH_(2)QDS were administered.The levels of oxidative stress in human renal tubular epithelial cells were assessed using a reactive oxygen species fluorescence probe.Results:The PQ content in the kidney tissues of the PQ group was higher than that of the PQ+AH_(2)QDS group.Hematoxylin-eosin staining showed extensive hemorrhage and congestion in the renal parenchyma of the PQ group.Vacuolar degeneration of the renal tubule epithelial cells,deposition of crescent-like red staining material in renal follicles,infiltration by a few inflammatory cells,and a small number of cast formation were also observed.However,these pathological changes were less severe in the PQ+sivelestat group and the PQ+AH_(2)QDS group(P<0.05).On the third day after poisoning,immunofluorescence assay showed that the level of apelin in the renal tissues was significantly higher in the PQ+AH_(2)QDS group than in the PQ group.Western blotting analysis results showed that IL-6,TNF-α,NF-κB p65,caspase-1,caspase-8,GRP78,and CHOP protein levels in the PQ group were higher than in the PQ+AH_(2)QDS group(P<0.05).The expression of apelin-APJ proteins in the PQ+AH_(2)QDS group was higher than in the PQ+sivelestat and PQ groups(P<0.05);this difference was significant on Day 3 and Day 7.The level of oxidative stress in the renal tubular epithelial cells of the PQ+AH_(2)QDS group and the PQ+sivelestat group was significantly lower than in the PQ group(P<0.05).Conclusions:This study confirms that AH_(2)QDS has a protective effect on PQ-poisoned kidneys and its positive effect is superior to that of sivelestat.The mechanism of the protective effects of AH_(2)QDS may be linked to reduction in cellular oxidative stress,PQ content of renal tissue,inflammatory injury,endoplasmic reticulum stress,and apoptosis.AH_(2)QDS may play a role in the treatment of PQ poisoning by upregulating the expression of the apelin-APJ.

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.

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。

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。

NGAL尿血比值在肝硬化急性肾损伤中的鉴别诊断价值

背景中性粒细胞明胶酶相关脂质运载蛋白(neutrophil gelatinase-associated lipocalin,NGAL)在肝硬化合并急性肾损伤(acute kidney injury,AKI)患者中对于急性肾小管坏死(acute tubular necrosis,ATN)与其他类型的AKI有重要的鉴别诊断价值,但血NGAL与尿NGAL直接相关,现有研究中对于NGAL尿血比值在ATN的鉴别诊断中的作用的研究很少,本试验意在评估其比值的临床作用.目的分析血尿NGAL及其尿血比值在肝硬化合并AKI患者中对于ATN的鉴别诊断价值.方法选取失代偿期肝硬化患者180例,其中合并AKI患者98例,根据AKI病因分成不同亚组,包括33例肾前性氮质血症,25例肝肾综合征急性肾损伤型及40例ATN,探讨血尿NGAL及其尿血比值在不同类型AKI中鉴别作用.结果尿NGAL对于肝硬化合并AKI患者中ATN的鉴别诊断价值较高,受试者工作曲线下面积(area under the curve,AUC)是0.964,诊断临界值为271.35 ng/mL时,敏感度为87.5%,特异性为96.6%.NGAL尿血比值对于ATN诊断价值也较高,AUC为0.953,诊断临界值在2.96时,敏感度为92.5%,特异性为91.4%.结论尿NGAL和NGAL尿血比值对于鉴别肝硬化合并AKI患者中ATN与其他类型AKI有重要价值,值得进一步研究及临床推广.