Normal Complement Research Articles

Headless hemagglutinin-containing influenza viral particles direct immune responses toward more conserved epitopes.

Seasonal influenza vaccines provide mostly strain-specific protection due to the elicitation of antibody responses focused on evolutionarily plastic antigenic sites in the hemagglutinin head domain. To direct the humoral response toward more conserved epitopes, we generated an influenza virus particle where the full-length hemagglutinin protein was replaced with a membrane-anchored, "headless" variant while retaining the normal complement of other viral structural proteins such as the neuraminidase as well as viral RNAs. We found that a single administration of a headless virus particle-based vaccine elicited high titers of antibodies that recognized more conserved epitopes on the major viral glycoproteins. Furthermore, the vaccine could elicit these responses even in the presence of pre-existing, hemagglutinin (HA) head-focused influenza immunity. Importantly, these antibody responses mediated protective, but non-neutralizing functions such as neuraminidase inhibition and antibody-dependent cellular cytotoxicity. Additionally, we show the vaccine can provide protection from homologous and heterologous challenges in mouse models of severe influenza without any measurable HA head-directed antibody responses. Thus, headless hemagglutinin containing viral particles may represent a tool to drive the types of antibody responses predicted to increase influenza vaccine breadth and durability.IMPORTANCECurrent seasonal influenza vaccines provide incomplete protection from disease. This is partially the result of the antibody response being directed toward parts of the virus that are tolerant of mutations. Redirecting the immune response to more conserved regions of the virus has been a central strategy of next-generation vaccine designs and approaches. Here, we develop and test a vaccine based on a modified influenza virus particle that expresses a partially deleted hemagglutinin protein along with the other viral structural proteins. We demonstrate this vaccine elicits antibodies that recognize the more conserved viral epitopes of the hemagglutinin stalk and neuraminidase protein to facilitate protection against influenza viruses despite a lack of classical viral neutralization activity.

A Case of Idiopathic Multicentric Castleman Disease Developing in a Patient with a History of Biopsy Proven Membranous Nephropathy

Abstract Introduction/Objective Idiopathic multicentric Castleman disease (iMCD) is a lymphoproliferative disorder involving two or more lymph node sites. It is usually associated with systemic inflammatory symptoms and organ dysfunction related to hypercytokinemia. Renal involvement in iMCD has only been described in a limited number of studies and case reports. Of note, only one previous case report has described results from renal biopsies taken prior to the development of iMCD. Methods/Case Report Our patient is a 43 year old female who was first diagnosed with membranous nephropathy in early 2020. She had PLA2 R negative and Exostosin-2 positive disease. Age appropriate screening for malignancy was unremarkable. She had positive ANA titres and normal complement levels but did not meet criteria for SLE per rheumatology. Her proteinuria was improved and maintained on Lisinopril for 3 years. In October 2023, her proteinuria suddenly increased. Repeat renal biopsy was unchanged from the initial biopsy. This time, she also noticed acute swelling over her subpectoral region. PET-CT scan revealed multiple areas of avid lymphadenopathy on either sides of the diaphragm but the highest yield PET- avidity was in the subpectoral region. Biopsy of the right subpectoral lymph node was performed. According to the WHO Classification, 5th edition, diagnostic criteria for iMCD-NOS was met with the histological features displaying grade 3 plasmacytosis, grade 2 regressed germinal centers, follicular dendritic cell prominence, increased hyperplastic follicles and increased vascularity. Immunohistochemical staining for CD138 highlighted abundant plasma cells, CD21 highlighted follicular dendritic cell prominence. Vascular proliferation was seen by CD34 staining. Kappa and Lambda- ISH demonstrated polytypic staining pattern and HHV-8 was negative. Results (if a Case Study enter NA) NA Conclusion There is a significant clinical, histologic and immunologic overlap between iMCD, autoimmune or infectious disorders and malignancy. HHV-8 negative/iMCD is less well understood and has no specific biomarkers. It is important to follow the available clinicopathologic diagnostic criteria for early diagnosis, follow up and treatment. Timely recognition can help prevent multiple organ system dysfunction, systemic inflammatory symptoms, cytopenias and polyclonal lymphoproliferation. Although the pathophysiology maybe unclear, this case may also suggest that in patients with a previously diagnosed membranous nephropathy, iMCD may play a role in recurrence and worsening of the disease.

Extracellular traps in peripheral blood mononuclear cell fraction in childhood-onset systemic lupus erythematosus.

Although the role of low-density granulocytes (LDGs), neutrophils in the peripheral blood mononuclear cell (PBMC) fraction, and neutrophil extracellular traps (NETs) in assessing lupus disease severity is acknowledged, data specific to childhood-onset lupus remains scarce. This study analyzed 46 patients with childhood-onset systemic lupus erythematosus (82.6% females, mean age 14.5 ± 0.3 years), including 26 cases with normal complement levels and 20 with low complement levels, along with 20 healthy adult volunteers. Key parameters that distinguished healthy volunteers from lupus patients and differentiated between lupus patients with low and normal complement were serum interferon (IFN)-α, serum citrullinated histone 3 (CitH3), and extracellular traps (ETs) in LDGs. However, NETs (assessed by nuclear staining morphology), LDG abundance, and other parameters (such as endotoxemia, cytokines, and double-stranded (ds) DNA) did not show such differentiation. When lipopolysaccharide (LPS) was administered to LDGs in the PBMC fraction, it induced ETs in both low and normal complement groups, indicating the inducible nature of ETs. In adult healthy volunteers, activation by recombinant IFN-α or dsDNA in isolated neutrophils induced LDGs and NETs (identified using immunofluorescent staining for CitH3, myeloperoxidase, and neutrophil elastase) at 45min and 3h post-stimulation, respectively. Additionally, approximately half of the LDGs underwent late apoptosis at 3h post-stimulation, as determined by flow cytometry analysis. Activation by IFN-α or dsDNA in LDGs also led to a more pronounced expression of CD66b, an adhesion molecule, compared to regular-density neutrophils, suggesting higher activity in LDGs. In conclusion, IFN-α and/or dsDNA in serum may transform regular-density neutrophils into LDGs before progressing to NETosis and apoptosis, potentially exacerbating lupus severity through cell death-induced self-antigens. Therefore, LDGs and ETs in LDGs could provide deeper insights into the pathophysiology of childhood-onset lupus.

12333 46 XX/XY Chimerism - Positive NIPT And Post-natal Karyotype Is It Real?

Abstract Disclosure: K.L. Del Rosario: None. N. Sheriden: None. N. Vijayakanthi: None. Introduction: Non-Invasive Prenatal Testing(NIPT) using cell free fetal DNA in plasma of pregnant women has become a routine part of prenatal care in screening for fetal aneuploidies including sex chromosome abnormalities in most regions around the world. False positive results are increasingly imposing challenges in pre-natal as well as post-natal care. Case Discussion: We report a neonate born at 32+2 weeks gestation to a 42-year-old G2 P2 mother. Pregnancy was complicated by insulin dependent maternal type 2 diabetes mellitus, maternal chronic hypertension and a positive NIPT for high-risk monosomy X. Prenatal ultrasound showed male anatomy. Interestingly on physical exam after birth, the neonate had typical male external genitalia with bilateral normal male gonads. Chromosome analysis done immediately after birth revealed the presence of two cell lines: 40 of the 50 cells (80%) had a normal female 46 XX karyotype and 10 of the 50 cells (20%) had a normal male 46 XY karyotype. These findings could be due to reabsorbed twin, Klinefelter syndrome with two trisomy rescue events, maternal cell contamination or true chimerism. In addition, fluorescence in situ hybridization (FISH) analysis for X and Y probes revealed the presence of two cell lines. The first cell line (70% of the cells) had two hybridization signals for chromosome X and the second cell line (∼25% of the cells) had one hybridization signal for chromosome X and one for chromosome Y. Postnatal ultrasound showed normal testicles with no evidence of Mullerian structures. Newborn screening was negative for congenital adrenal hyperplasia (CAH). Genetics was consulted and recommended repeat chromosomal analysis, parental testing to determine sex chromosome segregation, and follow-up with pediatric endocrinology. Repeat cytogenetic testing at 2 weeks of life resulted in a normal male chromosome complement of 46,XY. Previous abnormal cytogenetics were thought to be due to maternal cell contamination. Further endocrine labs showed LH(1.16 uIU/ml) and testosterone levels ( 87 ng/dL), appropriate levels for age indicating normal Hypothalamic Pituitary Gonadal (HPG) axis and testicular Leydig cell function. Since the family was previously counseled regarding the concept of maternal cell contamination, they expressed understanding and were happy with the update of the normal karyotype result. Conclusion: False-positive results concerning for rare chimerism on NIPT can occur and should prompt a thorough history, physical exam, ultrasound studies and repeat testing to confirm its presence. Careful consideration should be taken when counseling family about the implications of these results, especially communication about gender assignment of the infant. Presentation: 6/3/2024

HIV-Associated Immune Complex Kidney Disease in a Patient with Normal Complement Levels

HIV-Associated Immune Complex Kidney Disease in a Patient with Normal Complement Levels

Surgical Management of Palatally Impacted Mesiodens in a Pediatric Patient: A Case Report

Supernumerary teeth are additional teeth or tooth-like structures that can develop either erupted or unerupted, beyond the normal complement of 20 primary teeth and 32 permanent teeth. A mesiodens is a specific type of supernumerary tooth located in the midline between the two central incisors. The presence of these extra teeth can lead to various clinical complications. This paper presents a case involving a palatally positioned, impacted mesiodens that was associated with an unerupted permanent left maxillary central incisor. Surgical removal of the mesiodens was performed, resulting in the successful eruption of the permanent incisor.

Complement system activation: bridging physiology, pathophysiology, and therapy.

The complement system is a set of over 50 proteins that constitutes an essential part of the innate immune system. Complement system activation involves an organized proteolytic cascade. Overactivation of complement system activation is the main pathogenic mechanism of several diseases and contributes to the manifestations of many other conditions. This review describes the normal complement system and the role for complement dysregulation in critical illnesses, notably sepsis and acute respiratory distress syndrome. Complement activation is involved in the immune system response to pathogens but, when excessive, can contribute to tissue damage, runaway inflammation, and capillary leakage syndrome. Complement overactivation may play a key role in severe forms of coronavirus disease 2019 (COVID-19). Two diseases whose manifestations are mainly caused by complement overactivation, namely, atypical hemolytic and uremic syndrome (aHUS) and myasthenia gravis, are discussed. A diagnostic algorithm for aHUS is provided. Early complement-inhibiting therapy has been proven effective. When renal transplantation is required, complement-inhibiting drugs can be used prophylactically to prevent aHUS recurrence. Similarly, acetylcholine-receptor autoantibody-positive generalized myasthenia gravis involves complement system overactivation and responds to complement inhibition. The two main complement inhibitors used in to date routine are eculizumab and ravulizumab. The main adverse event is Neisseria infection, which is rare and preventable, but can be fatal. The complement system is crucial to health but, when overactivated, can cause or contribute to disease. Effective complement inhibitors are now available, although additional data are required to determine optimal regimens. Further research is also needed to better understand the complement system, develop advanced diagnostic tools, and identify markers that allow the personalization of treatment strategies.

Low serum complements in idiopathic inflammatory myositis: clinical features and impact on the prognosis

This study investigated the clinical features and prognostic relevance of decreased serum complement levels in patients with idiopathic inflammatory myositis (IIM). The clinical information of IIM patients with less than normal serum complement levels (L-Com) and that of those with normal serum complement levels (N-Com) was compared. In patients with interstitial lung disease (ILD), regression analyses were used to investigate the implication of L-Com in their PaO2/FiO2 (P/F) ratio. Prognostic outcomes of ILD were evaluated using the log-rank test. Of 94 IIM patients, 26 with L-Com (median age, 56.0 years) and 68 with N-Com (56.5 years) were included. The prevalence of women was significantly higher in patients with L-Com (92.3%) than in those with N-Com (67.6%). ILD was observed in 17 (65.4%) patients with L-Com and in 46 (67.6%) with N-Com. Among patients with ILD, the P/F ratio was significantly lower in those with L-Com than in those with N-Com. Serum C3 levels were correlated with decreased P/F ratio. Inferior prognosis of ILD was significantly demonstrated in patients with L-Com, especially in those positive for anti-melanoma differentiation-associated protein 5 antibody. L-Com may be implicated in reduced arterial oxygen levels and a poorer prognosis in patients with IIM-related ILD.

Lack of causative mutation in the AMH and AMHR2 genes in a cat (38,XY) with persistent Mullerian duct syndrome (PMDS).

A 1-year-old European shorthair male cat with a normally developed penis was subjected to genetic, endocrinological and histological studies due to unilateral cryptorchidism. The blood testosterone level was typical for males, while the level of anti-Mullerian hormone (AMH) was very low. Surgical removal of internal reproductive organs was followed by a histological study, which revealed inactive testicles with neoplastic changes and derivatives of Mullerian ducts. Cytogenetic analysis showed a normal XY sex chromosome complement and molecular analysis confirmed the presence of Y-linked genes (SRY and ZFY). Although the level of AMH was low, two normal copies of the AMH gene were found using droplet digital PCR (ddPCR). Analysis of the coding sequences of two candidate genes (AMH and AMHR2) for persistent Mullerian duct syndrome (PMDS) in the affected cat and in control male cats (n = 24) was performed using the Sanger sequencing method. In the affected cat, homozygosity was found for three novel missense variants in Exon 1 (one SNP) and Exon 5 (two SNPs) of AMH, but the same homozygous genotypes were also observed in one and two control cats, respectively, whose sex development was not examined. Three known synonymous variants with homozygous status were found in AMHR2. We conclude that the DNA variants identified in AMH and AMHR2 are not responsible for PMDS in the affected cat.

#1976 Non-IgA mesangial proliferative glomerulonephritis in a patient with IgA deficiency, a case report

Abstract Background and Aims IgA deficiency (IgAD) is the most common primary immunoglobulin deficiency in western countries. This entity is associated with increased risk of other autoimmune diseases. Mesangial proliferative glomerulonephritis (MesPGN) is a histological pattern defined by mesangial cell proliferation and expansion of the extracellular matrix within the mesangium. The clinical presentation can vary, from nephrotic syndrome to isolated hematuria. 30-40% of MesPGN cases are associated with IgA nephropathy. Other common diagnostic entities that present with this pattern include IgM nephropathy, C1q nephropathy or lupus nephritis, as well as Hepatitis B or C virus infection; idiopathic MesPGN is poorly described in the literature. To the best of our knowledge, this is the first report of idiopathic MesPGN associated with IgAD. Results A 17-year old woman with a background of IgAD and occasional episodes of bronchitis in her childhood presented in January 2022 with nonspecific abdominal pain and macroscopic hematuria. She had been suffering these symptoms for the last few weeks, usually after physical exercise. She was normotensive and showed no fever, skin rashes or other symptoms. Laboratory tests revealed normal renal function (serum creatinine 0.65 mg/dL), urinary albumin-to-creatinine ratio of 23.9 mg/g, a 24-h protein excretion ranging from 40 to 240 mg and non-dysmorphic hematuria of up to 51-150 erythrocytes/field. Additional laboratory tests repeatedly showed only low IgA serum levels, with normal ANA, ANCA or complement levels. Renal ultrasound showed both kidneys with normal size and cortical thickness. A CT urogram observed multiple, bilateral, non-obstructive small-sized kidney stones and a persistent nephrogram. Genetic tests were negative for Alport syndrome-related mutations. Additional workup included occult blood in the stool, stool culture, rectal biopsy and colonoscopy, which were all negative. Symptoms persisted during the following 12 months. A kidney biopsy was performed, finding 40 glomeruli with normal optical appearance, none of them sclerosed. Discrete mesangial expansion and cell proliferation was observed, with capillary lumens with occasional congestion but without thrombi or fibrinoid necrosis. Tubules and interstitium showed no sign of sclerosis or fibrosis, with conserved basement membranes and brush borders. In vessels, subintimal fibrosis, hyalinosis or concentric arteriolar hyperplasia or endarteritis were ruled out. Immunofluorescence showed low-intensity, discrete granular C3 mesangial deposits and no deposition of IgA, IgG, IgM, fibrinogen, C4, C1q or albumin. A diagnosis of non-IgA MesPGN was reached. The patient stopped performing intense physical exercise on a regular basis. This translated in hematuria and abdominal pain of much lower intensity. The patient is currently receiving only supportive therapy and maintains a normal renal function, with persistence of microscopic non-dysmorphic hematuria and occasional, low-grade proteinuria as described. Conclusion MesPGN is the most diagnosed form of glomerulonephritis worldwide. However, most cases are associated with granular IgA deposition in the mesangium, which was absent in this case. Idiopathic, non-IgA MesPGN is a much rarer condition that has been considered by some authors as a form focal segmental glomerulosclerosis or minimal change disease, although others believe it to be a separate condition. IgAD has been previously associated with Crohn's disease, which could explain this patient's symptoms. Crohn's disease has also been associated with non-IgA MesPGN in a low number of patients. Nevertheless, no findings in the patient workup were suggestive of Crohn's disease. A capsule endoscopy study will be performed to clearly rule out such diagnosis.

#2000 Analysis between site-specific N-glycosylation of monoclonal immunoglobulin and complement system activation

Abstract Background and Aims Monoclonal immunoglobulin produced by clonal plasma cells is the main cause in multiple myeloma (MM) and monoclonal gammopathy of renal significance (MGRS). Hypocomplementemia and deposition of complement components in the kidney is observed in some patients with MM or MGRS. Previous studies have suggested that glycosylation of the immunoglobulin was associated with complement-mediated-effector activities. Whereas, site-specific N-glycosylation characterization for monoclonal immunoglobulin in MM or MGRS and its effects on complement system activation still remains unclear. Method We separated plasma monoclonal IgG1 and IgA immunoglobulin from patients with MM and human plasma immunoglobulin from healthy controls (HC). Purified IgG and IgA molecules were digested by trypsin. Tryptic peptides without enrichment of intact N-glycopeptides were analyzed using a combination of electron-transfer/higher-energy collisional dissociation (EThcD) and stepped collision energy/higher-energy collisional dissociation (sceHCD) mass spectrometry (EThcD-sceHCD-MS/MS). N-glycosylation characterization was compared between monoclonal immunoglobulin from MM patients and healthy controls and its association with complement level was evaluated. Results A total of 46 IgG1 digestion samples (HC, n = 16; MM, n = 30) and 38 IgA1 digestion samples (HC, n = 16; MM, n = 22) were analyzed using the EThcDsceHCD-MS/MS. On average, 34 and 37 unique N-glycopeptides of IgG1, 19 unique N-glycans per IgG were identified from HC and MM. The relative abundance of fucosylated N-glycans of IgG1 in MM was significantly higher than HC (94.7% vs 88.8%, p = 0.002). Other types of N-glycans including sialylated, hybrid and complex were similar between the two groups. The types of N-glycans including fucosylated, sialylated, hybrid and complex were similar between patients with hypocomplementemia and normal complement levels. Regarding IgA1, on average, 63 and 52 unique N-glycopeptides of IgA1, 40 and 35 unique N-glycans per IgA were identified from HC and MM. The relative abundance of fucosylated (41.0% vs 26.4%, p < 0.001), sialylated (61.0% vs 45.6%, p = 0.003), mannose (2.44% vs 0.28%, p < 0.001) N-glycans of IgA1 in MM was significantly higher than HC. In MM, the relative abundance of mannose N-glycans of IgA1 in patients with hypocomplementemia was significantly lower than patients with normal complement levels (1.69% vs 7.52%, p < 0.001). The relative abundance of fucosylated and sialylated N-glycans were similar between patients with hypocomplementemia and normal complement levels. Conclusion Site-specific N-glycosylation characterization of monoclonal IgG1 and IgA1 in MM patients were differentially expressed from healthy controls. Certain specific N-glycan types were associated with complement levels. These findings laid a foundation for future investigations of their biological effects.

#2989 Superposition of atypical hemolytic syndrome and tubulointerstitial nephritis, a case report

Abstract Background and Aims Hemolytic uremic syndrome is a heterogeneous group of diseases that have in common the development of thrombotic microangiopathy with diffuse endothelial damage, resulting in the classic triad composed of microangiopathic hemolytic anemia, thrombocytopenia and acute kidney injury, on the other hand, tubulointerstitial nephritis is characterized by the presence of inflammatory infiltrates and edema and of the interstitial compartment that causes deterioration of renal function. Method The following is the case of a patient with acute kidney injury of etiology composed of thrombotic microangiopathy and tubulointerstitial nephritis. Results 27-year-old female patient without significant history, began 3 weeks prior to admission with fever, chills, asthenia, nausea and vomiting of food content, approximately 5 episodes per day for 3 days, presenting intermittent episodes of jaundice of the mucous membranes and conjunctivae, with progressive increase of the symptoms to the point of preventing daily activities, she was admitted for study, detecting hemolytic anemia, thrombocytopenia and severe acute kidney injury, so she was referred to our center was decided for evaluation by Nephrology and Hematology. In our institution, urinary sediment with dysmorphic erythrocytes was documented, peripheral blood smear without the presence of schistocytes, positive Coombs 4 crosses, renal ultrasound with data compatible with acute kidney injury, and supportive management with hemodialysis was initiated. Due to suspicion of autoimmune glomerulopathy, an autoantibody panel was indicated with negative antinuclear antibodies, anti-double-stranded DNA, anti-Sm, anti-B2 glycoproteins, and lupus anticoagulant, with normal complement values, stool culture, and negative stool Shiga protein assay, angiotomography of the abdomen where the integrity of renal circulation is verified, so renal biopsy with immunohistochemical study is performed, finding data compatible with thrombotic microangiopathy and acute tubulointerstitial nephritis. The patient is maintained with supportive care, steroids and hemodialysis as required with progressive recovery of renal function until renal replacement therapy is weaned, she is discharged with a steroid regimen and clinical nephrology and hematology follow-up. Conclusion Acute kidney injury is a complex and multifactorial entity, which requires a comprehensive approach in order to identify the best therapeutic option and to offer a better outcome in the renal function of these patients. The case of our patient presented a sudden deterioration of renal injury composed of two entities with different pathophysiology, demonstrating that, although the approach to these two entities converge in certain etiologies, it is imperative that the clinician does not forget the wide variety of factors that contribute to the development of renal injury.

#314 Systemic lupus erythematous (SLE) and isolated multiple sclerosis: analysis of BAFF—VAR variant on gene TNSF13B

Abstract Background and Aims We report a case of young a woman (33 years old) affected by SLE since 2007. In this year, a renal biopsy showed class IV lupus nephritis and the patient received corticosteroids and immunosuppressant for 3 years. The patient remained thereafter in disease remission with normal renal function, no proteinuria and normal complement levels. In 2013 the patient performed brain MRI for sudden hearing loss. The MRI showed a pattern compatible with isolated multiple sclerosis (RIS), confirmed on subsequent radiographic checks. In 2023, due to the initial onset of renal failure, a new re-staging biopsy showed microscopic aspects compatible with class I/II lupus nephritis (INS/RPS Classification 2004, 2018); the activity index calculated with SLEDAI—2K was +4. A new brain MRI carried out without onset of new symptoms showed a new hyperintense region at the level of the head of the right caudate nucleus and enlargement of the intrasellar CSF content as per the condition of a “partially empty” sella. A genetic variant of the TNFSF13B gene was therefore suspected, since it is involved in encoding the cytochine and drug target B-cell activating factor (BAFF), associated with multiple sclerosis as well as SLE. We searched for the genetic variant in order to undertake target therapy early in our patient. Method We performed PCR amplification and direct sequencing of all coding exons plus all the intron-exon junctions of the analyzed gene, by automatic sequencer with SeqStudio Genetic Analyzer (analytical sensitivity and specificity >99%). Results We found the heterozygous presence of the BAFF-var variant in the 3' UTR region of the TNFSF13B gene (Heterozygous genotype for BAFF-var). This variant involves an insertion/deletion (GCTGT>A) at the level of the 3' UTR region with consequent production of an alternative polyadenylation site (APA). This APA leads to the formation of a shorter transcript (BAFF-var mRNA) which causes greater production of the encoded protein compared to the wild-type transcript (BAFF-WT mRNA). Conclusion The molecular analysis conducted highlighted the presence of the BAFF-var variant in heterozygosis which leads to increased levels of soluble BAFF in the serum, with consequent up-regulation of humoral immunity. It is reported in the literature1 that this variant is associated with both Multiple Sclerosis and SLE and may represent a valid therapeutic target being treatable with the monoclonal antibody Belimumab.

Cytological Studies in the Genus <i>Amaryllis</i>

One species and eight horticultural varieties of Amaryllis show a basic number of x=11, which is the predominant basic number of the family. In both Amaryllis belladonna and Amaryllis-Mrs. Garfield the normal somatic number is 2n=22. All the seven colour varieties of Amaryllis-Giant Dutch have 2n=44 chromosomes. These varieties differ from one another in the minor alterations of the chromosome types suggesting the role of minor structural alterations in evolution. In addition to the normal somatic complement a number of variant nuclei with altered karyotypes have been recorded.

Complement C3 Levels in Membranoproliferative and Post-infectious Glomerulonephritides

Objectives − Post infectious glomerulonephritis (PIGN) is the most common type of nephritis in children. Presentation is variable, and most cases initially have low serum complement C3. Membranoproliferative glomerulonephritis (MPGN) is a chronic nephritis less frequently seen in children and is also associated with low serum C3. While management of PIGN is predominantly supportive, MPGN usually requires immunosuppressive therapy. Differentiating PIGN from MPGN at presentation is difficult. Early diagnosis can help inform evaluation and treatment decisions.Materials and Methods − This is a retrospective study of all children 1-21 years of age diagnosed with PIGN and MPGN, treated by nephrologists at Nationwide Children’s Hospital between January 2014 and December 2019. Clinical data, results of kidney function, complement levels, urine testing and biopsy were collected. Children with other types of glomerulonephritis were excluded.Results − Fifty-seven children were included (43 with PIGN and 14 with MPGN). PIGN children were younger at presentation (median age: 7 vs 9.5 years, P=0.0159) and more likely to have a C3 level <40 mg/dl compared to MPGN children (P=0.0031). Most children with PIGN (74.42%) had normal complement levels within 12 weeks after diagnosis compared to 35.71% of children with MPGN. More children with MPGN had evidence of chronic kidney disease as compared to PIGN children, who were more likely to have a full kidney recovery. Conclusions − Younger children with more significant hypocomplementemia at presentation were more likely to have PIGN than MPGN. We recommend earlier evaluation for MPGN in adolescents with milder degrees of hypocomplementemia (>40 mg/dl).

The unit group of the group ring over ℤn

Let ℤ n be the ring of integers modulo n. Let Ct , Em , and F r , s respectively denote the cyclic group of order t, the elementary abelian 2-group of order 2 m , and the abelian group of exponent 4 with order 2 r 4 s . In this article, we find the structure and generators of the unit group V ( ℤ n C 2 ) . We also solve the normal complement problem in V ( ℤ n C 2 ) . Additionally, we provide a normal complement of Em in V ( ℤ 2 n E m ) . At the end, we determine the structure of V ( ℤ p n F r , s ) for an odd prime p and establish that F r , s does not have a normal complement in V ( ℤ p n F r , s ) .

32 Atypical case of Staphylococcus aureus bacteremia related IRGN with normal complement levels

32 Atypical case of Staphylococcus aureus bacteremia related IRGN with normal complement levels

372 A case of diffuse class 4 lupus nephritis with normal complement levels

372 A case of diffuse class 4 lupus nephritis with normal complement levels

A note on the normal complement problem in semisimple group algebras

A note on the normal complement problem in semisimple group algebras

On normal complements

Although the theory of completion has a long history, there are not many results related to completing operator matrices to a normal operator. In this paper, we consider the problem of completion of the upper-triangular operator matrix [A?0B⁎] to normality, where A∈B(H) and B∈B(K) are called normal complements. We give different characterizations of normal complements and explore their joint spectral properties. We also investigate the similarity between A, B, and MC with respect to some essential properties such as regularity, Fredholmness, and others. Finally, we consider the self-duality property of Aluthge and Duggal transforms of hyponormal and semi-hyponormal operators.