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Chronic kidney disease (CKD) is a global public healthcare concern in the pediatric population, where glomerulopathies represent the second most common cause. Although classification and diagnosis of glomerulopathies still rely mostly on histopathological patterns, patient stratification should complement information supplied by kidney biopsy with clinical data and etiological criteria. Genetic determinants of glomerular injury are particularly relevant in children, with important implications for prognosis and treatment. Targeted therapies addressing the primary cause of the disease are available for a limited number of glomerular diseases. Consequently, in the majority of cases, the treatment of glomerulopathies is actually the treatment of CKD. The efficacy of the currently available strategies is limited, but new prospects evolve. Although the exact mechanisms of action are still under investigation, accumulating data in adults demonstrate the efficacy of sodium-glucose transporter 2 inhibitors (SGLT2i) in slowing the progression of CKD due to diabetic and non-diabetic kidney disease. SGLT2i has proved effective on other comorbidities, such as obesity, glycemic control, and cardiovascular risk that frequently accompany CKD. The use of SGLT2i is not yet approved in children. However, no pathophysiological clues theoretically exclude their application. The hallmark of pediatric CKD is the inevitable imbalance between the metabolic needs of a growing child and the functional capacity of a failing kidney to handle those needs. In this view, developing better strategies to address any modifiable progressor in kidney disease is mandatory, especially considering the long lifespan typical of the pediatric population. By improving the hemodynamic adaptation of the kidney and providing additional beneficial effects on the overall complications of CKD, SGLT2i is a candidate as a potentially innovative drug for the treatment of CKD and glomerular diseases in children.

Spontaneous intracranial hypotension (SIH) results from low cerebrospinal fluid (CSF) volume, typically secondary to a spinal CSF leak. CSF hypovolemia leads to brain sagging, particularly in orthostatic position, and expansion of the intracranial venous compartment. These pathophysiological mechanisms are responsible for the clinical presentation that usually consists of postural headache variably associated with other neurological symptoms. The wide range of clinical manifestations, including the absence of typical headache, may delay diagnosis. Magnetic resonance imaging (MRI) supports diagnosis showing typical findings including subdural fluid collections, pachymeningeal enhancement and brain sagging.

The advent of flow diverter (FD) stents has deeply changed the endovascular treatment of cerebral aneurysms. Endosac- cular devices have been replaced by endoluminal stents and the management of FD-treated patients differs markedly from that of patients treated with metal coils. Whichever technique or devices are used, a thrombus forms within the aneurysmal sac after treatment. The ensuing events are well known: clot formation and inflammation develop in a physiological healing process that takes from months to years These new devices have also given rise to several unpre- dictable complications, including still unexplained fatal case of spontaneous rupture of treated aneurysms The mechanism of post-flow-diversion haemorrhage remains difficult to clearly understand: aneurysm thrombosis, fol lowed by mural inflammation, leading to autolysis and rupture has been described.Nevertheless thrombosis followed by organization and neo-intimal closure of the neck is required for successful occlusion of treated aneurysms, thus there must be further elements to consider for thrombosis leading to rupture rather than occlusion. This report describes the favourable outcome of a focal wall rupture affecting a large carotid-ophthalmic artery aneurysm treated with FD and coils deployment. It displays the potential interaction between thrombosis, inflammation and residual flow in the aneurysm.

The published version of this article unfortunately contained a mistake. Affiliation 2 was presented incorrectly in the original article. The updated affiliation is Neuroradiology Unit, Bellaria Hospital, IRCCS Institute of Neurological Sciences, Bologna, Italy.

Background A diagnosis of idiopathic intracranial hypertension without papilledema (IIHWOP) should be considered in unresponsive chronic daily headache (CDH) patients [1]. A CSF opening pressure (OP) above 200 mm H2O has been detected in chronic migraine patients with conflicting result, ranging from 10% to 86% of patients [1,2]. Moreover, controversies exist regarding the OP cut-off value greater than 200 or 250 mm H2O and the role of transverse sinus stenosis (TSS) [3,4].