clinical

Highly selective and sensitive detection of cardiac troponin I (cTnI) is a powerful complement to clinical diagnosis of acute myocardial infarction (AMI). In this study, a strategy for cTnI detection was developed by constructing a universal biosensing interface composed of zwitterionic peptides and aptamers. The peptides were self-assembled onto gold chips, and some of them were biotinylated. The cTnI-specific binding aptamers were immobilized through the streptavidin-biotin system. Surface plasmon resonance (SPR) measurements revealed the preparation process. The developed aptasensor presents a linear detection with cTnI ranging from 20 ng/ml to 600 ng/ml and a detection limit of 20 ng/ml. The high immobilization of the aptamer enhances the sensitivity of the aptasensor and the calculated KD was 6.75 nM. Due to the outstanding antifouling property of the zwitterionic peptide, the developed aptasensor possesses a high resistance towards protein fouling. Moreover, the aptasensor has excellent selectivity and specificity towards cTnI in complex media. Hence, the proposed peptide-based aptasensor shows great potential for practical application in medium sized Myocardial Infarction (MI).

The global virome: The viruses have a global distribution, phylogenetic diversity and host specificity. They are obligate intracellular parasites with single- or double-stranded DNA or RNA genomes, and afflict bacteria, plants, animals and human population. The viral infection begins when surface proteins bind to receptor proteins on the host cell surface, followed by internalisation, replication and lysis. Further, trans-species interactions of viruses with bacteria, small eukaryotes and host are associated with various zoonotic viral diseases and disease progression. Virome interface and transmission: The cross-species transmission from their natural reservoir, usually mammalian or avian, hosts to infect human-being is a rare probability, but occurs leading to the zoonotic human viral infection. The factors like increased human settlements and encroachments, expanded travel and trade networks, altered wildlife and livestock practices, modernised and mass-farming practices, compromised ecosystems and habitat destruction, and global climate change have impact on the interactions between virome and its hosts and other species and act as drivers of trans-species viral spill-over and human transmission. Zoonotic viral diseases and epidemics: The zoonotic viruses have caused various deadly pandemics in human history. They can be further characterized as either newly emerging or re-emerging infectious diseases, caused by pathogens that historically have infected the same host species, but continue to appear in new locations or in drug-resistant forms, or reappear after apparent control or elimination. The prevalence of zoonoses underlines importance of the animal–human–ecosystem interface in disease transmission. The present COVID-19 infection has certain distinct features which suppress the host immune response and promote the disease potential. Treatment for epidemics like covid-19: It appears that certain nutraceuticals may provide relief in clinical symptoms to patients infected with encapsulated RNA viruses such as influenza and coronavirus. These nutraceuticals appear to reduce the inflammation in the lungs and help to boost type 1 interferon response to these viral infections. The human intestinal microbiota acting in tandem with the host’s defence and immune system, is vital for homeostasis and preservation of health. The integrity and balanced activity of the gut microbes is responsible for the protection from disease states including viral infections. Certain probiotics may help in improving the sensitivity and effectivity of immune system against viral infections. Currently, antiviral therapy is available only for a limited number of zoonotic viral infections. Because viruses are intracellular parasites, antiviral drugs are not able to deactivate or destroy the virus but can reduce the viral load by inhibiting replication and facilitating the host’s innate immune mechanisms to neutralize the virus. Conclusion: Lessons from recent viral epidemics - Considering that certain nutraceuticals have demonstrated antiviral effects in both clinical and animal studies, further studies are required to establish their therapeutic efficacy. The components of nutraceuticals such as luteolin, apigenin, quercetin and chlorogenic acid may be useful for developing a combo-therapy. The use of probiotics to enhance immunity and immune response against viral infections is a novel possibility. The available antiviral therapy is inefficient in deactivating or destroying the infecting viruses, may help in reducing the viral load by inhibiting replication. The novel efficient antiviral agents are being explored.

The broad spectrum of heterozygous versus homozygous JAK2V617F mutated MPN consists ET, ET with early features of PV (prodromal PV), classical PV, masked PV, advanced PV and post-PV myelofibrosis. Combined use of bone marrow histology and increased erythrocyte counts above 5.8x1012/L can replace increased red cell mass at time of presentation as the pathognomonic clue for the correct diagnosis of hetero/homozygous or homozygous mutated PV. Erythrocyte counts are in the normal range below 5.8x1012/L in heterozygous JAK2V617F mutated ET and prodromal PV but above 5.8x1012/L in heterozygous-homozygous or homozygous mutated PV. The bone marrow cellularity and morphology in pre-fibrotic ET, prodromal PV and PV carrying the JAK2V617F mutation are overlapping showing clustered increase of large mature pleomorphic megakaryocytes (M) with no increase of cellularity (<60%) in ET. The bone marrow is hypercellular (60%-80%) due to increased erythropoiesis megakaryopoiesis (EM) in prodromal and classical PV and trilinear hypercellular (80%-100% due increased megakaryopoiesis, erythropoiesis and granulopoiesis (EMG) in advanced PV and masked PV. Bone marrow cellularity ranging from normal (<60%) in ET to increased erythropoiesis (EM) in prodromal PV to hypercellular (80-100%) in advanced PV and masked PV largely depends on increasing JAK2V617F mutation load from low to high on top of other biological MPN variables like constitutional symptoms during long-term follow-up. MPL515 mutated ET is featured by an increase of clustered small and giant megakaryocytes with hyper-lobulated staghorn-like nuclei in a normal cellular bone marrow. The third entity of pronounced JAK2/MPL wild type ET associated with primary megakaryocytic granulocytic myeloproliferation (PMGM) without PV features proved to be caused by calreticulin (CALR) mutation. CALR mutated thrombocythemia is characterized by dual proliferation of megakaryocytic and granulocytic bone marrow proliferation of dense clustered large to giant immature dysmorphic megakaryocytes with bulky (bulbous) hyperchromatic nuclei, which are not seen in MPL515-mutated Thrombocythemia and JAK2V617F-Thrombocythemia, prodromal PV and classical PV. 

The present article extends the PVSG-WHO criteria into a simplified set of Rotterdam and European Clinical, Molecular and Pathological (RCP/ECMP) criteria to diagnose and classify the myeloproliferative neoplasms (MPNs). The crude WHO criteria still miss the masked and early stages of ET and PV. Bone marrow histology has a near to 100% sensitivity and specificity to distinguish thrombocythemia in BCR/ABL positive CML and ET, and the myelodysplastic syndromes in RARS-T and 5q-minus syndrome from BCR/ABL negative thrombocythemias in myeloproliferative disorders (MPD). The presence of JAK2V617F mutation with increased erythrocytes above 6x1012/L and hematocrit (>0.51 males and >0.48 females) is diagnostic for PV obviating the need of red cell mass measurement. About half of WHO defined ET and PMF and 95% of PV patients are JAK2V617F positive. The combination of molecular marker screening JAK2V617F, JAK2 exon 12, MPL515 and CALR mutations and bone marrow pathology is 100% sensitive and specific for the diagnosis of latent, early and classical ECMP defined MPNs. The translation of WHO defined ET, PV and PMF into ECMP criteria have include the platelet count above 350 x109/l, mutation screening and bone marrow histology as inclusion criteria for thrombocythemia in various MPNs. According to ECMP criteria, ET comprises three distinct phenotypes of true ET, ET with features of early (“forme fruste” PV), and ET with a hypercellular erythrocythemic, megakaryocytic granulocytic myeloproliferation (EMGM or masked PV). The ECMP criteria clearly differentiate early erythrocythemic, prodromal and classical PV from congenital polycythemia and idiopathic or secondary erythrocytosis. The burden of JAK2V617F mutation in heterozygous ET and in homozygous PV is of major clinical and prognostic significance. JAK2 wild type MPL515 mutated normocellular ET and MF lack PV features in blood and bone marrow. JAK2/MPL wild type hypercellular ET associated with primary megakaryocytic granulocytic myeloproliferation (PMGM) is the third distinct CALR mutated MPN. The translation of WHO into ECMP criteria for the classification of MPNs have a major impact on prognosis assessment and best choice for first line non-leukemogenic approach to postpone potential leukemogenic myelopsuppressive agents as long as possible in ET, PV and PMGM patients.

The clinical phenotypes in 268 JAK2V617F mutated MPN patients in the Seoul study were PV in 101, ET in 95 and MF in 78 and 56 CALR mutated MPN consisted of PV in none, ET in 40 and MF in 16 cases. CALR mutated MPN patients were younger than JAK2V617F mutated MPN patients (mean ages 57.5 and 66 years), had lower values for values for leukocytes (8.6 vs 11.9x109/L) and higher values for platelets (898 vs 643x109/L respectively). Bone marrow histopathology in 268 JAK2V617F mutated MPN patients in the Seoul study was featured by an increased erythropoiesis and megakaryopoiesis (EM) in 13.5%, an increased erythropoiesis, megakaryopoiesis and granulopoiesis (EMG) in 31.3%, a normocellular megakaryocytic (M) proliferation in 29,1%, a megakaryocytic and granulocytic (MG) proliferation with a relative reduction of erythropoiesis in post-ET and Post-PV myelofibrosis in 26.2%. The bone marrow histology in 56 cases of CALR mutated MPN show a predominantly increased megakaryopoiesis (M) in two thirds and an increased megakaryopoiesis and granulopoiesis (MG) with a decreased erythropoiesis in one third. Thirteen consecutive CALR MPN patients in the Belgian & Dutch cross sectional study presented with thrombocythemia associated with a typical PMGM bone marrow histology in 11 and myelofibrosis in 2 cases. All 11 thrombocythemia and 2 myelofibrosis CALR mutated MPN patients did not have constitutional symptoms and did not suffer from microvascular erythromelalgic disturbances, major thrombosis at platelet counts between 400 and 1000x109/L. There was an occurrence of hemorrhages at platelet counts above 1000x109/L in two CALR thrombocythemia cases. Bone marrow histology of CALR mutated thrombocythemia in the Seoul and Belgian/Dutch study showed loose clusters of large megakaryocytes (M) with bulky, cloud-like nuclei with a normal or a minor reduction of erythropoiesis and no increase in reticulin fibers grade 0 or 1 (RF 0 or 1). CALR thrombocythemia patients show various degrees of increased bone marrow cellularity due to dual megakaryocytic and granulocytic (MG) proliferation featured by large megakaryocytes with roundish bulky nuclear forms and cloud-like clumsy nuclei, which are almost never seen in JAK2V617F ET and PV. Assessment of allele burden is an independent and most important factor for all molecular variants MPN disease burden. Overt myelofibrosis with advanced post PV and or ET myelofibrosis at the bone marrow level occurred in one third (30%) of 208 evaluable JAK2 MPN patients and in 8 (14%) of 56 CALR MPN patients in the Seoul study.

Ailment repairing regiments has turn out to be arduous, despite a plenty of understanding and knowledge acquired in the past relating to the molecular underpinnings of Alzheimer’s disease (AD. Umpteen clinical experiments targeting the fabrication and accumulation have been turned fruitless to fit potency standards. The tests aiming beta-amyloid hypothesis also turned futile making it exigent for further handling tactics. The new emanation of a comparably candid, economical, and punctilious system known as gene editing have showed light in path of cure for AD by CRISPR/Cas9 gene editing. Being a straight approach this procedure has already shown assurance in other neurological disorders too such as Huntington’s disease. This review standpoint the immanent service of CRISPR/Cas9 as a remedial option for AD by aiming on specific genes inclusive of those that induce early-onset AD, as well as those that are substantial risk components for late-onset AD such as the apolipoprotein E4 (APOE4) gene.

Allogeneic hematopoietic stem cell transplant (alloHSCT) is a curative treatment for many hematologic malignancies. Unfortunately, about 30-50% of all recipients undergoing alloHSCT develop acute graft-versus-host-disease (aGVHD), which is associated with high morbidity and mortality [1,2]. Treatment of aGVHD involves the use of immune suppressive drugs such as high dose of steroids that leads to further immunosuppression and risk for opportunistic infections. Often patients are refractory to steroids therapy making the prognosis dismal. Thus, it is critical to identify robust biomarkers to detect aGVHD before onset of clinical symptoms so that therapeutic strategies can be implemented that may result in better treatment responses and less toxicity. 

Summary: Myelodysplastic Syndrome (MDS) is a heterogeneous group of clonal hematopoietic malignancies characterized by progressive cytopenias, ineffective hematopoiesis, bone marrow hypercellularity and transformation to acute myeloid leukemia (AML). Objectives: Identify plasma proteins from MDS patients and from two healthy controls groups (young and elderly) by SDS-Page. Methods: Plasma from 08 healthy young, 08 healthy elderly and 08 MDS patients were used for this study. Proteins were fractionated, precipitated, used for SDS-PAGE gel analysis, stained with comassie brilliant blue, scanned and bands were analyzed. Results: It was possible to identify in both, 20% fraction and supernatant, proteins that were differentially expressed in each group. The ones that have showed some clinical relevance. Fibronectin was highly expressed only in the young control group. α2-Macroglobulin was also expressed in both control groups, but it was not expressed in the MDS group. Haptoglobin was highly expressed only in the elderly control and SMD groups. Conclusion: Protein expression in plasma can be a biomarker for MDS, and may play a key role in the process of aging and hematologic malignancies development.

The Myeloproliferative Neoplasms (MPN) of trilinear polycythemia vera (PV) and megakaryocytic leukemia (ML = primary megakaryocytic granulocytic myeloproliferation: PMGM) and Essential Thrombocythemia (ET) in the studies of Dameshek and Michiels are caused by the MPN driver mutations JAK2V617F, JAK2exon12, CALR and MPL515 discovered by Constantinescu-Vainchenker, Green and Kralovics. The JAK2V617F mutated trilinear myeloproliferative neoplasms (MPN) include a broad spectrum of clinical laboratory and bone marrow features in essential thrombocythemia (ET), prodromal PV and erythrocythemic PV, classical PV and advanced stages of masked PV and PV complicated by splenomegaly and secondary myelofibrosis (MF). Heterozygous JAK2V617F mutated ET is associated with low JAK2 allele and MPN disease burden and normal life expectance. In combined heterozygous and homozygous or homozygous JAK2V617F mutated trilinear PV, the JAK2 mutation load increases from less than 50% in prodromal PV and classical PV to above 50% up to 100% in hypercellular PV, advanced PV and PV with MF. Bone marrow histology show diagnostic features of eryhrocytic, megakaryocytic and granulocytic (EMG) myeloproliferation in JAK2V617F mutated trilinear MPN, which clearly differs from monolinear megakaryocytic (M) myelproliferation in MPL and CALR thrombocythemia and dual megakaryocytic granulocytic (MG) myeloproliferation in CALR mutated thrombocythemia. The morphology of clustered large pleomorphic megakaryocytes with hyperlobulated nuclei are similar in JAK2V617F thrombocythemia, prodromal PV and classical PV patients. Monolinear megakaryocytic (M) myeloproliferation of large to giant megakaryocytes with hyperlobulated staghorn-like nuclei is the hallmark of MPL515 mutated normocellular thrombocythemia. CALR mutated thrombocythemia usually presents with high platelet count around 1000x109/l and normocellular megakaryocytic (M) proliferation of immature megakaryocytes with cloud-like hyperchromatic nuclei followed by dual megakaryocytic granulocytic (MG) myeloproliferation followed by various degrees of bone marrow fibrosis. Natural history and life expectancy of MPN patients are related to the response to treatment and the degree of anemia, splenomegaly, myelofibrosis and constitutional symptoms. The acquisition of epigenetic mutations at increasing age on top of MPN disease burden independently predict unfavorable outcome in JAK2V617F, MPL515 and CALR mutated myeloproliferative neoplasms (MPNs, which mutually exclude each other).

Clinical benefits 1. To improve efficiency in Osteoporosis treatment 2. To adjust the dosage of medication for osteoporosis with BMK 3. To adjust bone life cycle as needed 4. To prevent bone necrosis which dentists have been worried. 5. To reduce cost of treatment 

Aim:The work was to perform a comparative study of the neuroprotective and nootropic activities of two pharmaceutical substances, the HLDF-6 peptide and its amide form (HLDF-6-NH2). Materials and Methods: We used in the study healthy adult male Wistar rats aged 180–200 days weighing 280–300 g. We modelled ischemic stroke in rats by chronical occlusion of carotid arteries. Solutions of the HLDF-6-NH2 and HLDF-6 peptides were administered intranasally. Cognitive functions we assessed with Novel object recognition test and Morris maze. Results: The amide form of HLDF-6 peptide is more efficient: the neuroprotective activity of HLDF-6-NH2, evaluated by improvement of cognitive functions in animals, surpassed that of the native HLDF-6 peptide. A dose of 250 µg/kg of HLDF-6-NH2 peptide resulted in practically complete restoration of the disturbed functions. In the model of ischemic stroke, the amide form of the peptide significantly excelled the reference substance mexidol both in the effective dose and biological activity. Conclusion: The results of study of the agent allow hoping for its success in further clinical investigation. In view of high demand for the agent and in case of successful clinical trials, it will surely become widely used in clinical practice in treatment of IS.

Tamsulosin is used to treat Benign Prostatic Hyperplasia (BPH), prescribed annually to about 12.6 million patients worldwide. It is an alpha-adrenergic antagonist that reduces the tone of the prostate smooth muscle involved in the pathophysiology of BPH. By acting on alpha 1A receptors, predominant in the prostate, tamsulosin also acts on receptors present in the brain. This study consisted of a literature review aimed at disseminating scientific knowledge about the relationship between the use of tamsulosin and the onset of dementia. PubMed, Scopus, Scielo, Embase, and Web of Science studies involving dementia in patients using tamsulosin in the last five years were selected. The review showed a risk correlation and a higher incidence of dementia in treated patients. The risk ratio, when compared to other medicines, approached 1.20. In conclusion, it was identified the need for clinical trials with higher sampling power to increase relational significance due to the high prevalence of BPH and the extensive use of tamsulosin in elderly patients with the disease.

Background: The acaricidal action of Ozonized sunflower oil (OSO) has demonstrated in different clinical cases of different animal species, such as psoroptic rabbits and pig sarcoptic scabies and recently in demodesic goat. Objectives: This study evaluated the effectiveness of OSO as treatment for generalized demodicosis mange in dogs. Animals: Twenty dogs of different breeds, between six months and one year of age with generalized demodicosic mange that attended to Veterinary Clinic “José Luis Callejas” Havana, Cuba, during the year 2015, were included in the study. Methods: The demodicosis diagnostic was based on its clinical history, the mite’s presence by deep scraping and clinical signs. All cases had a history of receiving before conventional treatments without solution. OSO treatment was topically applied daily, every 12 hours, after shaving all affected areas. Monitoring of clinical signs, mite counting on scaling, pruritus and capillary regrowth (7, 14, 28, 56 and 84 days) were performed. Results: The results showed a significant reduction of mite counts, clinical signs and pruritus since the 7th day of application. The animals recovered the fur on more than 90% of the body surface. All the animals (100%) recovered from generalized demodesic mange in 84 days of treatment. Conclusion: The effectiveness and safety of OSO as election treatment of generalized demodicosis mange in dogs was demonstrated.

Pleurothotonus, commonly known as Pisa Syndrome (PS), is a rare neurological disorder characterized by lateral bending of the trunk with a tendency to lean to one side. This is typically mobile and resolves in supine position. It often presents as an incapacitating symptom of underlying neurodegenerative conditions like Parkinson’s disease, alzheimer’s disease, multisystem atrophy, dementia with Lewy bodies, progressive supranuclear palsy and even subacute sclerosing panencephalitis. It is known to be associated with neuroleptics, dopaminergic agents, valproic acid and lithium. PS is also seen in neurosurgical disorders like subdural hematoma, normotensive hydrocephalus, or as a late complication of pallidotomy in patients with PD. It can present either as an acute emergency or can develop gradually over time.PS tend to happen in coronal plane and can be controlled and managed if diagnosed in early stage. However, a chronic form known as “camptocormia” occurs often in a combined fashion with anteroposterior flexion which can improve to some extent, remain stable or even get worse. Pathophysiologic mechanism is not completely understood. This review will discuss all the updated literatures published in PS in terms of prevalence, pathophysiology, clinical manifestation, and treatment modalities.

Introduction: Visual evoked potentials (VEPs) are potential differences recorded on the scalp in response to visual stimulation. They are obtained with slowly repeated stimuli. The aim of this study was to determine the normative values of the visual evoked potentials in our setting. Methodology: We conducted a cross-sectional study from February 1 to April 30, 2019 at the Clinical Neurophysiology laboratory of the I.P. Ndiaye Clinic at CHNU Fann in Dakar (Senegal). Results: We found that men had high averages of N75, P100 and N145 wave latencies and low averages of P100 wave amplitude (p>0.05). However, neither age nor body mass index influenced the parameters of VEPs. Conclusion: Sex is important physiological variable in establishing laboratory normative values for VEPs. There is a marked difference between the sexes for the VEPs parameters.

Introduction: Neurocysticercosis (NCC) is a common helminthic infection of the nervous system that occurs when humans become intermediate hosts in the life cycle of the pig tapeworm (Taenia solium) after ingesting its eggs. The objective of this study was to analyze socio-demographic, clinical and paraclinical features of patients with NCC in Lubumbashi, DRC. Methods: This is a cross-sectional study conducted over a period of 2 years within the Neuropsychiatric Center of Lubumbashi. Socio-demographic, clinical, paraclinical and therapeutic features were studied. Results: A total of 18 patients with NCC were listed. Epilepsy was found in 72.2% (13/18) of the cases. The mean age of the patients was 30.2 ± 13.5 years; males accounted for 61.2% of the cases. 84.6% were consumers of pork. Generalized epilepsy was found in 84.6% of the cases and hypereosinophilia in 38% of the cases. On the neuroimaging, the parietal location of lesions represented 92.3%; calcifications were the type of lesion in 53.8% of the cases and 69.2% of the cases presented lesions in the 4th evolutionary stage. Electroencephalogram was normal in 84.4% of the cases. Phenobarbital was the antiepileptic drug used in 69.3%; albendazole and prednisone were used in 53.9% of the cases. Conclusion: This study shows that NCC is one of the causes of epilepsy in Lubumbashi. Generalized tonic-clonic seizures are the most common form of presentation and calcified parenchymal lesions are the most common radiological feature of NCC. So, any patient with acute onset of afebrile seizure should be screened for NCC provided other common causes been ruled out.

Objective: Atlantoaxial subluxation (AAS) occurs when there is misalignment of the atlantoaxial joint. Several etiologies confer increased risk of AAS in children, including neck trauma, inflammation, infection, or inherent ligamentous laxity of the cervical spine. Methods: A single-center, retrospective case review was performed. Thirty-four patients with an ICD-10 diagnosis of S13.1 were identified. Demographics and clinical data were reviewed for etiology, imaging techniques, treatment, and clinical outcome. Results: Out of thirty-four patients, twenty-two suffered cervical spine trauma, seven presented with Grisel’s Syndrome, four presented with ligamentous laxity, and one had an unrecognizable etiology. Most diagnoses of cervical spine subluxation and/or instability were detected on computerized tomography (CT), while radiography and magnetic resonance imaging (MRI) were largely performed for follow-up monitoring. Six patients underwent cervical spine fusion, five had halo traction, twelve wore a hard and/or soft collar without having surgery or halo traction, and eight were referred to physical therapy without other interventions. Conclusion: Pediatric patients with atlantoaxial subluxation may benefit from limited 3D CT scans of the upper cervical spine for accurate diagnosis. Conservative treatment with hard cervical collar and immobilization after reduction may be attempted, but halo traction and halo vest immobilization may be necessary. If non-operative treatment fails, cervical spine internal reduction and fixation may be necessary to maintain normal C1-C2 alignment.

A 61-year-old Brazilian black woman consulted with a nephrologist due to proteinuria identified on a routine urine test. She has a personal history of thymoma resection five years ago, followed by multiple episodes of pulmonary infections including mycobacteriosis, recurrent mucocutaneous candidiasis, and paraneoplastic pemphigus. Physical examination showed no edema or hypertension and laboratory tests identified proteinuria of 2.43 g/day without hematuria, serum creatinine of 0.69 mg/dl, urea 34 mg/dl, serum albumin of 2.4 g/dl, hemoglobin 10.9 g/dl, platelets 292,000/mm3, leukocytes 4950/mm3, lymphocytes 594/mm3 and neutrophils 3910/mm3. The hemolysis tests were negative and serum iron was low. Analysis of glicemia and serum lipids levels were normal as well as serum complement and imunoglobulins, except for an IgM level of 283 mg/dl (normal values 40 to 230 mg/dl) and undetectable IgE. Serologies for Syphilis, HIV, hepatitis B, C and antibodies for autoimmune diseases were negative. 

Granulomatosis with polyangiitis (GPA), a form of ANCA-associated vasculitis (AAV), is a rare disease with an often-occult presentation. It is more common in 4th and 5th decades of life but can be seen in all ages. This case report details a 76-year-old female presenting with abdominal pain, generalized weakness, and malaise, who was found to have pulmonary nodules on chest imaging. Biopsy of the lung nodule showed organizing pneumonia. Initially, antibiotics were used to treat the patient. However, she developed acute renal failure a few days after presentation and found to have positive serum C-ANCA as well as elevated ANCA-PR3 serologies. A subsequent kidney biopsy demonstrated pauci-immune necrotizing and crescentic glomerulonephritis that was consistent with GPA and the patient was started immediately on combination immunosuppressive therapy, plasmapheresis, and hemodialysis. GPA’s clinical and radiological presentation can mimic other common conditions such as pneumonia, malignancy, bacterial sinusitis, pulmonary tuberculosis, sarcoidosis, and urinary tract infection. Because of this, a high level of suspicion is required for early diagnosis and treatment to alter the high mortality rate in this disease entity. All forms of ANCA-associated vasculitis (AAV) should be in the differential diagnosis for all patients presenting with multiorgan system involvement particularly in individuals with pulmonary and renal manifesations.

Acute renal injury is a rare complication of idiopathic nephrotic syndrome with mesPGN. Here we present a 2-year-old male patient with 4 days history of anuria, generalized edema and hypervolemia. Any evidence other than proteinuria and renal failure could not be identified with laboratory tests and doppler ultrasonography. Anuric presentation was thought to be related with rapidly progressive glomerulonephritis, diffuse mesangial sclerosis or acute tubular necrosis. However, renal biopsy revealed mesangial proliferative glomerulonephritis (mesPGN). Prednisolone 2 mg/kg/day was prescribed. Diuresis was started gradually and on the 10th day of disease, anuria was resolved and acute renal injury recovered without any sequel. This case is presented because of the incompatibility between clinical findings and histopathologic diagnosis. It is concluded that although rare, anuria and acute renal injury could be the presenting symptom of idiopathic nephrotic syndrome in childhood.