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Nephritis is a frequent and severe complication of Systemic Lupus Erythematous (SLE). The clinical course of lupus nephritis (LN) is usually characterized by alternating phases of remission and exacerbation. Flares of LN can lead to deterioration of kidney function, necessitating timely diagnosis and therapy. The presence of autoantibodies against C1q (anti-C1qAb) in the sera of SLE patients has been reported in various studies. Some research suggests that the presence and changes in the titer of anti-C1qAb may be associated with the development of LN, as well as with LN activity and renal flares. However, the exact role of anti-C1qAb in LN remains a subject of debate. Despite variability in the results of published studies, anti-C1qAb hold promise as noninvasive markers for assessing LN activity in SLE patients. Measuring anti-C1qAb levels could aid in diagnosing and managing LN during periods of both inactive disease and renal flares. Nevertheless, larger controlled trials with standardized laboratory assays are necessary to further establish the utility of anti-C1qAb in predicting the reactivation and remission of LN and guiding treatment strategies.

Dense deposit disease (DDD) and C3 glomerulonephritis (C3GN) are types of membranoproliferative glomerulonephritis classified as C3 glomerulopathies. These conditions are characterized by an increased number of intraglomerular cells and diffuse thickening of the glomerular capillary walls, along with the deposition of C3 and minimal or absent immunoglobulin deposits. The underlying cause of both DDD and C3Gn is an abnormal activation of the alternative complement pathway, which can result from acquired or genetic alteration. In acquired forms of DDD and C3GN, the dysregulation of the alternative pathway is commonly induced by the presence of C3 nephritic factors (C3NeFs), which are autoantibodies that stabilize C3 convertase. Both DDD and C3GN can affect individuals of any age, but DDD is primarily diagnosed in children, whereas C3GN tends to be diagnosed at a significantly higher age. The presenting features of these diseases are variable and may include proteinuria, hematuria, hypertension, or kidney failure. A common finding in these diseases is low serum C3 levels with normal serum C4 levels. Chronic deterioration of renal function is commonly observed in DDD and C3GN, often leading to end-stage renal disease (ESRD), especially in DDD. Kidney transplantation outcomes in patients with these conditions are characterized by histological recurrence, which may contribute to higher rates of allograft failure.

Introduction:Solanum aethiopicum L., commonly known as scarlet eggplant (Solanaceae family) is one of the most traditionally cultivated vegetables in Basilicata, a southern region of Italy. Although multiple uses have been given to this vegetable, data about its anti-obesogenic activity are still limited.Methods: This study focuses on testing two different extracts obtained either from the peel or from the whole fruit of the Lucanian Solanum aethiopicum. Their ability to inhibit certain enzymatic activities was tested in vitro and then, the one that showed the better outcomes was tested on an experimental model of High-Fat Diet (HFD) induced obesity.Results: Spectrophotometric assays demonstrated that the peel extract possessed the highest ability to inhibit the selected enzymatic activities and so, its phytochemical profile was obtained through LC-MS chromatography. The oral administration of this extract (25 mg/kg) to HFD-fed mice reduced body weight gain and improved glucose and lipid metabolism. Similarly, the extract ameliorated the obesity-induced inflammatory status by reducing the expression of pro-inflammatory cytokines in both adipose and hepatic tissues. Interestingly, these effects were associated with the improvement of vascular dysfunction.Discussion: Lucanian Solanum aethiopicum extract may represent a new strategic approach for managing obesity and its associated diseases.

Sarcoidosis is a systemic inflammatory disease of unknown etiology. Kidney involvement in sarcoidosis may be present in up 25–30% of cases. An early diagnosis and prompt treatment with corticosteroids can improve the prognosis but rarely renal sarcoidosis can lead to kidney failure needing renal replacement therapy (RRT). Acute kidney injury (AKI) in sarcoidosis may be caused by granulomatous interstitial nephritis (GIN) or hypercalcemia. These disorders are usually clinically silent and may lead end stage renal disease (ESKD) if not diagnosed or detected too late. In patients with ESKD, dialysis and renal transplantation can offer results comparable to those observed in patients with other causes of kidney failure. Based on a review of literature, we present an overview of RRT in patients with AKI or chronic kidney disease (CKD) caused by sarcoidosis.

BackgroundCoronary access after transcatheter aortic valve implantation (TAVI) with supra-annular self-expandable valves may be challenging or un-feasible. There is little data concerning coronary access following transcatheter aortic valve-in-valve implantation (ViV-TAVI) for degenerated surgical bioprosthesis.AimsTo evaluate the feasibility and challenge of coronary access after ViV-TAVI with the supra-annular self-expandable ACURATE neo valve.Materials and methodsSixteen patients underwent ViV-TAVI with the ACURATE neo valve. Post-procedural computed tomography (CT) was used to create 3D-printed life-sized patient-specific models for bench-testing of coronary cannulation. Primary endpoint was feasibility of diagnostic angiography and PCI. Secondary endpoints included incidence of challenging cannulation for both diagnostic catheters (DC) and guiding catheters (GC). The association between challenging cannulations with aortic and transcatheter/surgical valve geometry was evaluated using pre and post-procedural CT scans.ResultsDiagnostic angiography and PCI were feasible for 97 and 95% of models respectively. All non-feasible procedures occurred in ostia that underwent prophylactic “chimney” stenting. DC cannulation was challenging in 17% of models and was associated with a narrower SoV width (30 vs. 35 mm, p < 0.01), STJ width (28 vs. 32 mm, p < 0.05) and shorter STJ height (15 vs. 17 mm, p < 0.05). GC cannulation was challenging in 23% of models and was associated with narrower STJ width (28 vs. 32 mm, p < 0.05), smaller transcatheter-to-coronary distance (5 vs. 9.2 mm, p < 0.05) and a worse coronary-commissural overlap angle (14.3° vs. 25.6o, p < 0.01). Advanced techniques to achieve GC cannulation were required in 22/64 (34%) of cases.ConclusionIn this exploratory bench analysis, diagnostic angiography and PCI was feasible in almost all cases following ViV-TAVI with the ACURATE neo valve. Prophylactic coronary stenting, higher implantation, narrower aortic sinus dimensions and commissural misalignment were associated with an increased challenge of coronary cannulation.

Primary Membranous Nephropathy (PMN) is the most frequent cause of nephrotic syndrome in adults. If untreated, PMN can lead to end-stage renal disease; moreover, affected patients are at increased risk of complications typical of nephrotic syndrome such as fluid overload, deep vein thrombosis and infection. The association of PMN with HLA-DQA1 and the identification in around 70% of cases of circulating autoantibodies, mainly directed towards the phospholipase A2 receptor, supports the autoimmune nature of the disease. In patients not achieving spontaneous remission or in the ones with deteriorating kidney function and severe nephrotic syndrome, immunosuppression is required to increase the chances of achieving remission. The aim of this review is to discuss the evidence base for the different immunosuppressive regimens used for PMN in studies published so far; the manuscript also includes a section where the authors propose, based upon current evidence, their recommendations regarding immunosuppression in the disease, while highlighting the still significant knowledge gaps and uncertainties.

The entire skin surface of octopus embryos, hatchlings and juveniles bears scattered tufts of tiny chitinous setae within small pockets, from which they can be everted and retracted. Known as Kölliker’s organs (KO), they disappear before the subadult stage. The function of these structures during the early life of the octopus is unknown, despite having been first described nearly two centuries ago. To investigate these organs further, general trends in size of KO distribution and density were analyzed in hatchlings and juveniles of 17 octopod species from all oceans, representing holobenthic, holopelagic and meropelagic modes of life. The size of the KO is fairly constant across species, unrelated to mode of life or hatchling size. The density of KO is similar on ventral and dorsal body surfaces, but hatchlings of smaller size tend to have a higher density of KO on the aboral surface of the arms. Analysis of a series of post-hatching Octopus vulgaris shows KO size to be constant throughout ontogeny; it is therefore a consistent structure during the octopus early life from planktonic hatchling to benthic juvenile. New KO are generated on the skin of the arm tips during the planktonic period and initial benthic lives of juveniles. Their density, on both the mantle and arms, gradually decreases as the octopus grows. In older benthic juveniles, the KO degrades, losing its setae and the base of its follicle becomes exposed as a nearly circular stump of muscle. It is estimated that fully everted KO increase the body surface area by around two-thirds compared to when the KO are retracted. This modular mechanism of body surface extension and roughness probably influences flow-related forces such as drag and propulsion of the moving surface of the young octopus while it is of small size with a relatively large surface area. In addition, the distribution of these organs on the aboral surface of the arms of the octopus and their birefringent properties suggest a role in camouflage. Further research is needed to test these hypotheses of KO function in live animals.

Membranous nephropathy (MN) is a common cause of proteinuria and nephrotic syndrome all over the world. It can be subdivided into primary and secondary forms. Primary form is an autoimmune disease clinically characterized by nephrotic syndrome and slow progression. It accounts for ~70% cases of MN. In the remaining cases MN may be secondary to well-defined causes, including infections, drugs, cancer, or autoimmune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), urticarial vasculitis, sarcoidosis, thyroiditis, Sjogren syndrome, systemic sclerosis, or ankylosing spondylitis. The clinical presentation is similar in primary and secondary MN. However, the outcome may be different, being often related to that of the original disease in secondary MN. Also, the treatment may be different, being targeted to the etiologic cause in secondary MN. Thus, the differential diagnosis between primary and secondary MN is critical and should be based not only on history and clinical features of the patient but also on immunofluorescence and electron microscopy analysis of renal biopsy as well as on the research of circulating antibodies. The identification of the pathologic events underlying a secondary MN is of paramount importance, since the eradication of the etiologic factors may be followed by remission or definitive cure of MN. In this review we report the main diseases and drugs responsible of secondary MN, the outcome and the pathogenesis of renal disease in different settings and the possible treatments.

Focal segmental glomerulosclerosis (FSGS) is a histological term that describes a pathologic renal entity affecting both adults and children, with a wide array of possible underlying etiologies. Podocyte damage with scarring, the hallmark of this condition, leads to altered permeability of the glomerular barrier, which may result in massive proteinuria and relentless renal function deterioration. A definite cause of focal segmental glomerulosclerosis can be confirmed in a minority of cases, while most forms have been traditionally labeled as primary or idiopathic. Despite this definition, increasing evidence indicates that primary forms are a heterogenous group rather than a single disease entity: several circulating factors that may affect glomerular permeability have been proposed as potential culprits, and both humoral and cellular immunity have been implicated in the pathogenesis of the disease. Consistently, immunosuppressive drugs are considered as the cornerstone of treatment for primary focal segmental glomerulosclerosis, but response to these agents and long-term outcomes are highly variable. In this review we provide a summary of historical and recent advances on the pathogenesis of primary focal segmental glomerulosclerosis, focusing on implications for its differential diagnosis and treatment.

Eyes morphologies may differ but those differences are not reflected at the molecular level. Indeed, the ability to perceive light is thought to come from the same conserved gene families: opsins and cryptochromes. Even though cuttlefish (Cephalopoda) are known for their visually guided behaviors, there is a lack of data about the different opsins and cryptochromes orthologs represented in the genome and their expressions. Here we studied the evolutionary history of opsins, cryptochromes but also visual arrestins in molluscs with an emphasis on cephalopods. We identified 6 opsins, 2 cryptochromes and 1 visual arrestin in Sepia officinalis and we showed these families undergo several duplication events in Mollusca: one duplication in the arrestin family and two in the opsin family. In cuttlefish, we studied the temporal expression of these genes in the eyes of embryos from stage 23 to hatching and their expression in two extraocular tissues, skin and central nervous system (CNS = brain + optic lobes). We showed in embryos that some of these genes (Sof_CRY6, Sof_reti-1, Sof_reti-2, Sof_r-opsin1 and Sof_v-arr) are expressed in the eyes and not in the skin or CNS. By looking at a juvenile and an adult S. officinalis, it seems that some of these genes (Sof_r-opsin1 and Sof_reti1) are used for light detection in these extraocular tissues but that they set-up later in development than in the eyes. We also showed that their expression (except for Sof_CRY6) undergoes an increase in the eyes from stage 25 to 28 thus confirming their role in the ability of the cuttlefish embryos to perceive light through the egg capsule. This study raises the question of the role of Sof_CRY6 in the developing eyes in cuttlefish embryos and the role and localization of xenopsins and r-opsin2. Consequently, the diversity of molecular actors involved in light detection both in the eyes and extraocular tissues is higher than previously known. These results open the way for studying new molecules such as those of the signal transduction cascade.

In metazoans, there is a remarkable diversity of photosensitive structures; their shapes, physiology, optical properties, and development are different. To approach the evolution of photosensitive structures and visual function, cephalopods are particularly interesting organisms due to their most highly centralized nervous system and their camerular eyes which constitute a convergence with those of vertebrates. The eye morphogenesis in numerous metazoans is controlled mainly by a conserved Retinal Determination Gene Network (RDGN) including pax, six, eya, and dac playing also key developmental roles in non-retinal structures and tissues of vertebrates and Drosophila. Here we have identified and explored the role of Sof-dac, Sof-six1/2, Sof-eya in eye morphogenesis, and nervous structures controlling the visual function in Sepia officinalis. We compare that with the already shown expressions in eye development of Sof-otx and Sof-pax genes. Rhodopsin is the pigment responsible for light sensitivity in metazoan, which correlate to correlate visual function and eye development. We studied Sof-rhodopsin expression during retina differentiation. By in situ hybridization, we show that (1) all of the RDGN genes, including Sof-pax6, are expressed in the eye area during the early developmental stages but they are not expressed in the retina, unlike Sof-otx, which could have a role in retina differentiation; (2) Sof-rhodopsin is expressed in the retina just before vision gets functional, from stage 23 to hatching. Our results evidence a role of Sof-six1/2, Sof-eya, and Sof-dac in eye development. However, the gene network involved in the retinal photoreceptor differentiation remains to be determined. Moreover, for the first time, Sof-rhodopsin expression is shown in the embryonic retina of cuttlefish suggesting the evolutionary conservation of the role of rhodopsin in visual phototransduction within metazoans. These findings are correlated with the physiological and behavioral observations suggesting that S. officinalis is able to react to light stimuli from stage 25 of organogenesis on, as soon as the first retinal pigments appear.