Tubular Interstitial Nephritis Research Articles

Fatal leptospirosis in endangered Barbary macaques (Macaca sylvanus) kept in captivity: Assessing the role of sympatric rodents

Between December 2020 and January 2021, an outbreak of acute mortality in endangered Barbary macaques (Macaca sylvanus) kept in captivity was detected in a zoo in Spain. The main findings observed in the two fatally affected animals at post-mortem evaluation were jaundice, renal tubular necrosis and interstitial nephritis. Leptospira spp. infection was confirmed by real time PCR (qPCR) in different tissues in both individuals. Analyses of secY gene from a positive individual showed 100% homology with a previously published sequence corresponding to Leptospira interrogans serovar Copenhageni. Free-living sympatric brown rats (Rattus norvegicus) from the affected zoo were also analyzed, and showed a prevalence and seroprevalence of Leptospira spp. of 18.2% (4/22; 95% CI: 2.1–34.3) and 41.9% (26/62; 95% CI: 29.7–54.2), respectively. We detected seropositive sera to five different serovars of Leptospira spp. (Copenhageni, Grippotyphosa, Pomona, Canicola and Hardjo) in the rodent population, with L. Copenhageni being the predominant one. This study describes for first time an outbreak of fatal leptospirosis in captive non-human primates in Europe. Our results show that Barbary macaques, an endangered species, are highly susceptible to Leptospira spp. infection, with sympatric wild rodents being the most likely reservoir animals involved in transmission in this outbreak. Our results suggest that rodent control could be an effective measure for minimizing exposure to Leptospira spp. in zoological collections. Given the potential implications for conservation, animal and public health, non-human primates and rodents should be included in surveillance programs for Leptospira spp. in zoos.

Tubular Interstitial Nephritis Secondary to Herbal Consumption: Case Report and Literature Review

Acute tubular interstitial nephritis is a form of immune-mediated renal injury characterized by infiltration of immune cells in the renal tubulointerstitium, leading to oliguric or non-oliguric acute kidney injury. It manifests with systemic arterial hypertension, foamy urine, and sometimes with secondary anemia if there is progression to chronic renal disease. The diagnosis of certainty is made by biopsy, the initial treatment consists of identifying and removing the triggering agent to avoid further exposure to toxins, management of the acute renal lesion and in some cases, it may be decided to start corticosteroids to avoid progression to end-stage chronic kidney disease. We present the case of a 24-year-old female patient with a history of consumption of unspecified herbal medicine for aesthetic purposes 3 years prior to our evaluation, who debuted with hypertensive emergency manifested by hypertensive retinopathy, hypertensive renal vasculopathy and tubulointerstitial nephritis, successfully treated with the withdrawal of the aggressor agent, angiotensin converting enzyme inhibitors, nitrates and corticosteroids. After 6 months of follow-up, the patient is asymptomatic and with total recovery of the renal disease documented by normal creatinine in laboratory tests.

Tubular basement membrane deposits after allogeneic hematopoietic stem cell transplantation

BackgroundExtraglomerular immune complex deposition is rare and only a few membranous nephropathy cases with tubular basement membrane deposits have been reported following allogeneic hematopoietic stem cell transplantation.Case presentationWe reported a 56-year-old man with increased serum creatinine after allogeneic hematopoietic stem cell transplantation who underwent a renal biopsy. Tubular interstitial nephritis was identified on light microscope. The unique histologic features were diffuse tubular basement membrane immune complex deposition detected by both immunofluorescence and electron microscopy, while the glomerular involvement was inconspicuous. The differential diagnosis from other forms of tubular basement membrane deposition is discussed.ConclusionDiffuse granular tubular basement membrane immune complex deposition with minimal glomerular involvement is also a manifestation of renal complication in hematopoietic stem cell transplantation recipient. However, the exact mechanism and target antigen remains unknown.

#5386 ONCO-NEPHROLOGY: THE ROLE OF KIDNEY BIOPSY IN THE MANAGEMENT OF SIDE EFFECTS OF TARGETED THERAPIES

Abstract Background and Aims The introduction of innovative therapies, resulting from revisiting cancer as a disease of the immune system, has changed the scenario of complications. These new classes of drugs, such as targeted therapies and immune checkpoint inhibitors, assure substantial advantages in cancer therapy, despite some side affecting various organs, including the kidney. Histological evaluations of kidney disorders induced by targeted/immunotherapy are limited. Method In this study we examined the histological features of patients treated with new cancer agents who underwent kidney biopsy for new onset kidney failure and/or urinary abnormalities. Results The cohort included 30 adult patients. The most frequently administered therapies were immunotherapy (30%), targeted therapy (26.7%), immunotherapy plus targeted therapy (13.3%), immunotherapy plus chemotherapy (13.3%), targeted therapy plus chemotherapy (16.7%). The most common histological finding was tubular interstitial nephritis (30%) that was associated with acute tubular necrosis in 4 cases, and thrombotic microangiopathy (23.3%). After kidney biopsy, 16 of the 30 patients were treated according to the histological diagnosis. Fourteen patients were treated with steroids. One patient with membranous nephropathy was treated with a single dose of rituximab. A patient with severe thrombotic microangiopathy requiring dialysis received a treatment with eculizumab for 3 months. Overall some renal response was obtained in all patients treated with glucocorticoids, while complete kidney response was achieved in the patient treated with rituximab. Cancer treatment was resumed without change in 21 out of 30 patients. Conclusion Kidney biopsy is critical for the management of kidney toxicities and should be strongly encouraged for patients showing adverse kidney effects of novel cancer agents.

Comment on "Determination of Orellanine in Human Biological Matrices Using Liquid Chromatography with High-Resolution Mass Spectrometry Detection: A Validated Method Applied to Suspected Poisoning Cases".

To the Editor, Following our recent published article presenting an analytical method to detect orellanine in human fluids (i.e., urine, plasma and whole blood) (1), we would like to provide additional information regarding the detection of orellanine in kidney biopsies. Indeed, renal biopsy analysis in order to demonstrate orellanine intoxication was proposed decades ago (2, 3), but the elements presented here make us consider this approach likely to be questionable. Some Cortinarius mushrooms contain a nephrotoxic mycotoxin called orellanine. Known since a massive poisoning in Poland in 1957, orellanus syndrome after a consumption of Cortinarius mushrooms is characterized by the long latency period (2–14 days) between intake and first symptoms (4). Renal damage observed from biopsies has shown acute tubular necrosis, interstitial nephritis and fibrosis (5). The mechanism of orellanine toxicity is not clearly understood. Proposed mechanisms include inhibition of different cellular enzymes, inhibition of RNA and DNA synthesis and production of oxygen free radicals generated via oxidated orellanine. It is also unclear whether it is orellanine that is toxic to kidney cells or a degradation product such as orellinine or an unidentified metabolite (1, 4, 5). Diagnosis of orellanine poisoning is based on a suspicion of ingestion of Cortinarius mushrooms and acute kidney injury. Therefore, the clinical diagnosis is difficult and deserves analytical confirmation. Some have proposed kidney biopsy to detect orellanine on the belief that orellanine or its metabolites persist in renal cells (2, 3). This was based on the postulate that the release of orellanine and its metabolites from renal cells was very slow, allowing for a greater detection window range.

The need for kidney biopsy in the management of side effects of target and immunotherapy.

The introduction of innovative therapies, resulting from revisiting cancer as a disease of the immune system, has changed the scenario of complications. These new classes of drugs, such as targeted therapies and immune checkpoint inhibitors, assure substantial advantages in cancer therapy, despite some side effects affecting various organs, including the kidney. Histological evaluations of kidney disorders induced by targeted/immunotherapy are limited. In this study we examined the histological features of patients treated with new cancer agents who underwent a kidney biopsy for new onset kidney failure and/or urinary abnormalities. The cohort included 30 adult patients. The most frequently administered therapies were immunotherapy (30%), targeted therapy (26.7%), immunotherapy plus targeted therapy (13.3%), immunotherapy plus chemotherapy (13.3%), targeted therapy plus chemotherapy (16.7%). The most common histological finding was tubular interstitial nephritis (30%) that was associated with acute tubular necrosis in 4 cases, and thrombotic microangiopathy (23.3%). After kidney biopsy, 16 of the 30 patients were treated according to the histological diagnosis. Fourteen patients were treated with steroids. One patient with membranous nephropathy was treated with a single dose of rituximab. A patient with severe thrombotic microangiopathy requiring dialysis received a treatment with eculizumab for 3 months. Overall some renal response was obtained in all patients treated with glucocorticoids, while complete kidney response was achieved in the patient treated with rituximab. Cancer treatment was resumed without change in 21 out of 30 patients. Kidney biopsy is critical for the management of kidney toxicities and should be strongly encouraged for patients showing adverse kidney effects of novel cancer agents.

Glomerulonephritis Following Russell’s Viper Bite – 1st Case Report in Bangladesh

Russell’s viper bite causing coagulopathy, hypotension, DIC, rhabdomyolysis and acute kidney injury. Nephropathy usually is caused by RV having hemotoxic or myotoxic venom components. Multiple mechanism causes renal pathologic changes including tubular necrosis, cortical necrosis, interstitial nephritis, and glomerulonephritis. But above all glomerulonephritis is very rare. We report a case of Russell’s viper bite who died of renal failure due to focal segmental proliferative glomerulonephritis admitted int the Rajshahi Medical College Hospital, Rajshahi, Bangladesh.
 TAJ 2022; 35: No-2: 169-172

EFFECT OF SCORPION VENOM TOXINS ON STRUCTURAL AND FUNCTIONAL PARAMETERS OF INTERNAL ORGANS, INCLUDING KIDNEYS (REVIEW).

The aim: To establish patterns of structural and functional changes in internal organs, including kidneys, under the conditions of exposure to scorpion venom toxins. Materials and methods: A thorough literature analysis was conducted on the basis of PubMed, Google Scholar, Web of Science, and Scopus databases. When processing the search results, we chose the newest publications up to 5 years old or the most thorough publications that vividly described the essence of our topic. Conclusions: The venom of various species of scorpions exhibits a wide range of biological activity. Acting on the structures of the central and peripheral nervous system, the toxins of scorpion venom cause the development of paralysis, convulsions, brain inflammation, hemorrhagic and ischemic strokes. Under conditions of influence on the cardiovascular system, damage to the endothelial lining of the vascular wall, disturbances in heart rhythm, conduction, and the development of destructive changes in the myocardium are characteristic. Data on kidney damage due to scorpion bites require a more detailed study, as information on microscopic and submicroscopic changes in the structure of the organ is too limited. However, cases of the development of tubular necrosis, interstitial nephritis, and kidney infarction are currently known.

Acute Kidney Injury in Cancer Immunotherapy Recipients

Cancer immunotherapy has now entered clinical practice and has reshaped the standard of care for many cancer patients. With these new strategies, specific toxicities have emerged, and renal side effects have been described. In this review, we will describe the causes of acute kidney injury in CAR T cell, immune checkpoint inhibitors and other cancer immuno-therapy recipients. CAR T cell therapy and bispecific T cell engaging antibodies can lead to acute kidney injury as a consequence of cytokine release syndrome, tumor lysis syndrome, sepsis or specific CAR T cell infiltration. Immune checkpoint blockade most often results in acute tubular interstitial nephritis, but glomerular diseases have also been described. Although the pathophysiology remains mostly elusive, we will describe the mechanisms of renal damage in these contexts, its prognosis and treatment. As the place of immunotherapy in the anti-cancer armamentarium is exponentially increasing, close collaboration between nephrologists and oncologists is of utmost importance to provide the best standard of care for these patients.

POS-125 Revisiting kidney injury in scrub typhus infection: A novel cause of infection-related glomerulonephritis

Kidney injury related to infections is one of the important preventable causes of morbidity and mortality, especially in tropical regions. Kidney involvement in scrub typhus infection ranges from bland urinary sediments to the requirement of renal replacement therapy (RRT). Earlier studies have shown renal histopathological findings consistent with acute tubular necrosis, interstitial nephritis, and mild mesangial glomerulonephritis in patients with scrub typhus and renal injury. We investigated patients with complicated scrub typhus for the pattern of renal involvement.

Disease surveillance in England and Wales, June 2022.

Disease surveillance in England and Wales, June 2022.

Clinicopathologic characteristics of severe COVID-19 patients in Mexico City: A post-mortem analysis using a minimally invasive autopsy approach.

ObjectiveDescribe the histological findings of minimally ultrasound-guided invasive autopsies in deceased patients with severe SARS-CoV-2 and compare the diagnostic yield with open autopsies.DesignObservational post-mortem cohort study. Minimally invasive ultrasound-guided autopsies were performed in fourteen deceased patients with a confirmed diagnosis of SARS-CoV-2 pneumonia. Histological and clinical findings of lung, kidney, and liver tissue are described and contrasted with those previously reported in the literature.SettingSingle-center COVID-19 reference center in Mexico City.ResultsFourteen minimally invasive autopsies revealed a gross correlation with open autopsies reports: 1) Lung histology was characterized mainly by early diffuse alveolar damage (12/13). Despite low lung compliances and prolonged mechanical ventilation, the fibrotic phase was rarely observed (2/13). 2) Kidney histopathology demonstrated acute tubular injury (12/13), interstitial nephritis (11/13), and glomerulitis (11/13) as the predominant features 3) Liver histology was characterized by neutrophilic inflammation in all of the cases, as well as hepatic necrosis (8/14) despite minimal alterations in liver function testing. Hepatic steatosis was observed in most cases (12/14). SARS-CoV-2 positivity was widely observed throughout the immunohistochemical analysis. However, endothelitis and micro thrombosis, two of the hallmark features of the disease, were not observed.ConclusionOur data represents the largest minimally invasive, ultrasound-guided autopsy report. We demonstrate a gross histological correlation with large open autopsy cohorts. However, this approach might overlook major histologic features of the disease, such as endothelitis and micro-thrombosis. Whether this represents sampling bias is unclear.

Kidney manifestations of mitochondrial disorders.

Mitochondria are intracellular organelles involved in a number of key biologic processes in the cell, including energy production, redox signaling, calcium homeostasis, inflammation, senescence, innate immune response, and mitophagy. Mitochondrial cytopathies include a heterogeneous group of diseases that are characterized by impaired oxidative phosphorylation, leading to multi-organ involvement and progressive clinical deterioration. Mitochondrial cytopathies can result from mitochondrial or nuclear DNA mutations. Mitochondrial defects play an important role in the pathogenesis of nephropathies as tubular syndromes, interstitial nephritis, focal and segmental glomerulosclerosis and diabetic nephropathy. Therole of mitochondria in apathogenesis of nephrotoxicity and kidney carcinogenesis is also discussed (Tab. 2, Fig. 7, Ref. 100). Keywords: mitochondrial nephropathy, interstitial nephritis, glomerulosclerosis, diabetic nephropathy, nephrotoxicity, mitochondrial cytopathies.

Moringa oleifera hydorethanolic leaf extract induced acute and sub-acute hepato-nephrotoxicity in female ICR-mice.

Moringa oleifera (M. oleifera) Lam belongs to the family Moringaceae. It is an important multipurpose tree that is largely distributed globally and has been used almost in every aspect of traditional medicine for the treatment of various illnesses including cancers, diabetes mellitus, asthma, arthritis, etc. This study investigated the effects of oral acute and sub-acute administration of M. oleifera hydroethanolic leaf extract (MOHE) in ICR-mice. Its major phenolic compounds were also determined. Ten (10) female, 8-week old mice were grouped into control and treatment groups for acute toxicity study. A dose of 2000 mg/kg MOHE was given once to the treatment group via oral gavage. However, for the sub-acute toxicity study, 25 mice were grouped into groups A (control), B (125 mg/kg), C (250 mg/kg), D (500 mg/kg) and E (1000 mg/kg). MOHE was given via oral gavage to groups B, C, D and E daily for 28 days. Group A received only distilled water. The mice were sacrificed at the end of the experiments and samples were collected for evaluation. The results of the chemical profiling of MOHE revealed the presence of glucomoringin, niaziminine, quercetin and kaempferol as the major compounds. The treated mice in the acute toxicity study were slightly anaemic and showed evidence of stress leukogram. Moreover, a slight increase in creatinine, significant increases in AST and CK, hepatic degeneration and necrosis, none-obstructive sinusoidal dilatation, renal tubular necrosis, interstitial nephritis and renal interstitial oedema were observed. It is concluded that the LD50 of MOHE is higher than 2000 mg/kg. However, oral administration of MOHE causes acute mild anaemia and moderate hepato-nephrotoxicity in ICR-mice. Its major phenolic compounds are glucomoringin, niaziminine, quercetin and kaempferol.

Automobile Paint Reducer Induced Acute Kidney Injury

The various aspects of the automobile industry also carry with it the risk for occupational health hazards with it. Toluene has also evolved as a commonly used drug by substance abusers. Accidental exposure or self-poisoning with these substances has been reported in literature. These substances can also cause distal renal tubular acidosis (RTA), acute tubular necrosis, glomerulonephritis and interstitial nephritis, rhabdomyolysis and myoglobinemia.In this series, we report about three patients who developed renal manifestations because of organic solvents. Two of the three patients had ingested the paint reducer substance and the third one was addicted to sniffing the toluene based paint reducer. All the patients had in taken these substances with suicidal intent and developed acute kidney injury (AKI) and severe metabolic acidosis. One of the patients had features of rhabdomyolysis as well. The third patient was a substance abuser and had inhaled higher than usual dose and developed severe and refractory acidosis and mild kidney injury and required Renal Replacement Therapy (RRT) for acidosis. All the patients eventually recovered their kidney functions and were doing well during their follow-up.Toluene based organic solvents lead to acute neurological symptoms, accompanied by severe metabolic alterations, organ injury and dysfunc-tion. An association of the development of hypokalemic paralysis and metabolic acidosis with toluene intoxication has been observed. The management of acute toluene toxicity is mainly conservative, consisting of electrolytes correction, acid-base and fluid abnormalities and renal replacement therapy in severe AKI.Organic solvent exposure may result in acute tubular necrosis, rhabdomyolysis, RTA and AKI irrespective of the intake route. Clinical suspicion of organ dysfunction and failure and timely induction of supportive care leads to a good outcome.

Kidney involvement and histological findings in two pediatric COVID-19 patients

BackgroundHistological findings of kidney involvement have been rarely reported in pediatric patients with SARS-CoV-2 infection. Here, we describe clinical, laboratory, and histological findings of two pediatric cases with almost exclusive kidney involvement by SARS-CoV-2.ResultsA 10-year-old girl with IgA vasculitis nephritis underwent kidney biopsy, showing diffuse and segmental mesangial-proliferative glomerulonephritis, and steroid therapy was initiated. After the worsening of the clinical picture, including an atypical skin rash, she was diagnosed with SARS-CoV-2. The re-evaluation of initial biopsy showed cytoplasmatic blebs and virus-like particles in tubular cells at electron microscopy. Despite SARS-CoV-2 clearance and the intensification of immunosuppression, no improvement was observed. A second kidney biopsy showed a crescentic glomerulonephritis with sclerosis, while virus-like particles were no longer evident.The second patient was a 12-year-old girl with a 3-week history of weakness and weight loss. Rhinitis was reported the month before. No medications were being taken. Blood and urine analysis revealed elevated serum creatinine, hypouricemia, low molecular weight proteinuria, and glycosuria. A high SARS-CoV-2-IgG titre was detected. Kidney biopsy showed acute tubular-interstitial nephritis. Steroid therapy was started with a complete resolution of kidney involvement.ConclusionWe can speculate that in both cases SARS-CoV-2 played a major role as inflammatory trigger of the kidney damage. Therefore, we suggest investigating the potential kidney damage by SARS-CoV-2 in children. Moreover, SARS-CoV-2 can be included among infectious agents responsible for pediatric acute tubular interstitial nephritis.

Protective Effect of Camel Milk on Gentamicin-inducedNephrotoxicity:From Renal Biomarkers to Histopathology Evidence

BACKGROUND: Gentamicin is an effective antibiotic with some important side effects, such as nephrotoxicity. There is evidence of renoprotective effects and antioxidant properties for camel milk. OBJECTIVES: In this study, the impact of camel milk on the nephrotoxicity induced by gentamicin was evaluated. METHODS: The present study was performed on four groups of six Wistar rats. Group 1(C), as the control group, received exclusively normal saline injections and the rats in group 2 (GM) received intraperitoneal gentamicin injections at the dose of 100 mg/kg for the last ten days. The animals in group 3 (CM) were fed by 5 mL/rat/day of camel milk through gavage for 15 days. Group 4 (MGM) was fed camel milk only for the first five days followed by gentamicin injections for 10 days. Serum urea, creatinine, and superoxide dismutase (SOD) were measured and kidneys were studied histopathologically. RESULTS: Increased concentrations of urea and creatinine along with the decreased level of SOD were found in the GM group. Histopathologic changes, such as eosinophilic casts in the tubular lumen, capillary congestion, glomerulonephritis, necrosis, interstitial nephritis, and edema were more common in the GM group, in comparison with the C, CM, and MGM groups (p <0.05). The elevations in serum urea and creatinine (p <0.05) were significantly prevented by the co-administra-tion of camel milk and gentamicin. Moreover, a significant increase in the serum activity of SOD was revealed in the GM group (p <0.05). Camel milk significantly prevented tissue injury, in comparison with the GM group (p <0.05). CONCLUSIONS: Our results demonstrated that gentamicin-induced histological and biochemical alterations in the kid-ney decreased significantly due to camel milk consumption

Methyl jasmonate reduces the inflammation and apoptosis of HK-2 cells induced by LPS by regulating the NF-κB pathway

Background: Methyl jasmonate is a bioactive oxylipid that participates in the defense-related mechanisms of plants. The anti-inflammatory and anti-oxidative capacities of methyl jasmonate against lipopolysaccharide (LPS) induced arthritis have been widely investigated. However, the role of methyl jasmonate in LPS-induced cell model of tubular-interstitial nephritis (TIN) has not been reported. Methods: LPS (5 µg/mL) was applied to treat human renal tubular epithelial cell line (HK-2) for the establishment of TIN cell model. LPS-induced HK-2 was incubated with 10 or 20 µM methyl jasmonate, cell viability and apoptosis were assessed by MTT and flow cytometry. ELISA and qRT-PCR were performed to determine the levels of interleukin (IL)-1 beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). The downstream pathway was investigated by western blot. Results: LPS induced cytotoxicity in HK-2 cell accompanied by decrease of cell viability and increase of cell apoptosis. Methyl jasmonate dosage dependently enhanced the cell viability and reduced cell apoptosis to ameliorate the cytotoxicity. LPS also induced inflammatory response in HK-2 cell with increased IL-1β, IL-6, IL-8 and TNF-α. Methyl jasmonate attenuated LPS-induced inflammation in HK-2 cell. Protein expression of IκBα was down-regulated, p65 and IκBα phosphorylation were up-regulated in LPS-induced HK-2. Methyl jasmonate attenuated LPS-induced decrease of IκBα and increase of p65 and IκBα phosphorylation in HK-2 cell. Conclusion: Methyl jasmonate demonstrated anti-apoptotic and anti-inflammatory effects on LPS-induced HK-2 cell through suppression of NF-κB activation.

Methyl jasmonate reduces the inflammation and apoptosis of HK-2 cells induced by LPS by regulating the NF-κB pathway

Background: Methyl jasmonate is a bioactive oxylipid that participates in the defense-related mechanisms of plants. The anti-inflammatory and anti-oxidative capacities of methyl jasmonate against lipopolysaccharide (LPS) induced arthritis have been widely investigated. However, the role of methyl jasmonate in LPS-induced cell model of tubular-interstitial nephritis (TIN) has not been reported. Methods: LPS (5 µg/mL) was applied to treat human renal tubular epithelial cell line (HK-2) for the establishment of TIN cell model. LPS-induced HK-2 was incubated with 10 or 20 µM methyl jasmonate, cell viability and apoptosis were assessed by MTT and flow cytometry. ELISA and qRT-PCR were performed to determine the levels of interleukin (IL)-1 beta (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α). The downstream pathway was investigated by western blot. Results: LPS induced cytotoxicity in HK-2 cell accompanied by decrease of cell viability and increase of cell apoptosis. Methyl jasmonate dosage dependently enhanced the cell viability and reduced cell apoptosis to ameliorate the cytotoxicity. LPS also induced inflammatory response in HK-2 cell with increased IL-1β, IL-6, IL-8 and TNF-α. Methyl jasmonate attenuated LPS-induced inflammation in HK-2 cell. Protein expression of IκBα was down-regulated, p65 and IκBα phosphorylation were up-regulated in LPS-induced HK-2. Methyl jasmonate attenuated LPS-induced decrease of IκBα and increase of p65 and IκBα phosphorylation in HK-2 cell. Conclusion: Methyl jasmonate demonstrated anti-apoptotic and anti-inflammatory effects on LPS-induced HK-2 cell through suppression of NF-κB activation.

Snake Bite Presenting as Haemolytic Uremic Syndrome: A Rare Case Report

Snake bite is predominantly an occupational hazard and causes severe health issues. Snake poisoning in India is a significant and prevalent cause of Acute Kidney Injury (AKI). In India, the occurrence of AKI after snake bite is 13-32%. All over the world every year, 1,50,000 people die as a result of it. Multiple mechanisms such as haemodynamic disturbances, direct tubular toxicity, coagulopathy, haemoglobinuria, and myoglobinuria can cause AKI after bites by snakes belonging to the Elapidae, Viperidae, and Colubridae families. Renal pathologic findings include acute tubular necrosis, cortical necrosis, interstitial nephritis, glomerulonephritis, and vasculitis. Thrombotic Microangiopathy (TMA) as a cause of snakebite-induced AKI is rarely reported in literature. Fewer details are known about the clinical course, optimal management, and overall prognosis of this entity. Haemolytic Uremic Syndrome (HUS) is a clinical disease that includes TMA, thrombocytopenia, and AKI as a triad. The HUS is a heterogeneity of illnesses with diverse aetiology which results in presentation, therapy and outcomes variance. Hereby, authors report a case of a 55-year-old female who was bitten by Russell’s viper and developed HUS. Patient eventually progressed to end stage renal disease and was advised lifelong haemodialysis. TMA should be taken into account as a probable cause of AKI following a snake bite. Plasma exchanges have yet to be determined in snake bite TMA.