Eclampsia spectrum disorders are a set of serious complications of pregnancy that commonly present after 20 weeks of gestation. There is an association between molar pregnancy, a gestational trophoblastic disease resulting from abnormal fertilisation and gametogenesis, and eclampsia spectrum disorders which can result in manifestation of pre-eclamptic symptomatology earlier than 20 weeks of gestation. We report a case of a gravida 1 para 0 in her mid 20s at 16-weeks gestation presenting with partial hydatidiform mole who developed eclampsia, haemolysis, elevated liver enzymes and low platelets syndrome and posterior reversible encephalopathy syndrome. Ultrasound findings were consistent with molar pregnancy and pathology confirmed partial molar pregnancy with triploid 69, XYY karyotype. This case highlights the early onset potential of eclampsia spectrum disorders in molar pregnancies while suggesting screening such patients for hypertensive disorders.

BACKGROUND: Intracerebral hemorrhage (ICH) is a major cause of maternal morbidity, but its pathophysiology is poorly characterized. We investigated characteristics of pregnancy-associated ICH (P-ICH), compared with ICH in similar aged nonpregnant adults of both sexes.
RESULTS: We performed a retrospective analysis of 134 adults aged 18 to 44 years admitted to our center with nontraumatic ICH from January 1, 2012, to December 31, 2021. We compared ICH characteristics among 3 groups: those with P-ICH (pregnant or within 12 months of end of pregnancy); nonpregnant women; and men. We categorized ICH pathogenesis according to a modified scheme, SMASH-UP (structural, medications, amyloid angiopathy, systemic, hypertension, undetermined, posterior reversible encephalopathy syndrome/reversible cerebral vasoconstriction syndrome), and calculated odds ratios and 95% CIs for primary (spontaneous small-vessel) ICH versus secondary ICH (structural lesions or coagulopathy related), using nonpregnant women as the reference. We also compared specific ICH pathogenesis by SMASH-UP criteria and functional outcomes between groups. Of 134 young adults with nontraumatic ICH, 25 (19%) had P-ICH, of which 60% occurred postpartum. Those with P-ICH had higher odds of primary ICH compared with nonpregnant women (adjusted odds ratio, 4.5 [95% CI, 1.4-14.7]). The odds of primary ICH did not differ between men and nonpregnant women. SMASH-UP pathogenesis for ICH differed significantly between groups (P<0.001). While the in-hospital mortality rate was lowest in the P-ICH group (4%) compared with nonpregnant women (13%) and men (24%), 1 in 4 patients with P-ICH were bedbound and dependent at the time of discharge.
CONCLUSIONS: In our cohort of young adults with ICH, 1 in 5 was pregnancy related. P-ICH differed in pathogenesis compared with non-pregnancy-related ICH in young adults, suggesting unique pathophysiology.

BACKGROUND: During the past 3 years of the corona virus disease 2019 (COVID-19) pandemic, COVID-19 has been recognized to cause various neurological complications, including rare posterior reversible encephalopathy syndrome (PRES). In previously reported cases of PRES associated with COVID-19, the majority of patients had severe COVID-19 infection and known predisposing factors for PRES, such as uncontrolled hypertension, renal dysfunction, and use of immunosuppressants. It remains unclear whether these risk factors or infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contributes to the development of PRES in these patients. Here we report a special case of PRES associated with COVID-19 without any known risk factors for PRES, indicating the SARS-CoV-2\'s direct role in the pathogenesis of PRES associated with COVID-19.
METHODS: An 18-year-old female patient presented to the emergency department with abdominal pain. Preliminary investigations showed no abnormalities, except for positive results in novel coronavirus nucleic acid tests using oropharyngeal swabs. However, the patient subsequently developed tonic-clonic seizures, headaches, and vomiting on the second day. Extensive investigations have been performed, including brain MRI and lumbar puncture. Brain MRI showed hypointense T1-weighted and hyperintense T2-weighted lesions in the bilateral occipital, frontal, and parietal cortices without enhancement effect. Blood and cerebrospinal fluid analyses yielded negative results. The patient had no hypertension, renal insufficiency, autoimmune disease, or the use of immunosuppressants or cytotoxic drugs.
METHODS: PRES was diagnosed based on the clinical features and typical MRI findings of PRES.
METHODS: Symptomatic treatments such as anticonvulsants were administered to the patients.
RESULTS: The patient fully recovered within 1 week. The initial MRI abnormalities also disappeared completely on a second MR examination performed 11 days later, supporting the diagnosis of PRES. The patient was followed up for 6 months and remained in a normal state.
CONCLUSIONS: The current case had no classical risk factors for PRES, indicating that although the cause of PRES in COVID-19 patients may be multifactorial, the infection of SARS-CoV-2 may play a direct role in the pathogenesis of PRES associated with COVID-19.

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Posterior reversible encephalopathy syndrome (PRES) is a rare clinical disease, which has been seen in patients with systemic lupus erythematosus (SLE). Its main manifestations are seizure, headache and other neurological symptoms. While the condition is reversible, if not treated in time, there can be risks of cerebral haemorrhage. We report here the case of a young patient with SLE who developed PRES after receiving the immunosuppressant, mycophenolate mofetil. Neurological symptoms, signs, or changes in a patient\'s condition that cannot be explained by lupus, should alert physicians to the possibility of the drug causing PRES, and prompt discontinuation should ensue.

Hereditary renal hypouricemia (RHUC) is a heterogenous disorder characterized by defective uric acid (UA) reabsorption resulting in hypouricemia and increased fractional excretion of UA. RHUC is an important cause of exercise-induced acute kidney injury (EIAKI), nephrolithiasis and posterior reversible encephalopathy syndrome (PRES). We present here an unusual case of a patient with RHUC who presented with recurrent EIAKI and had two heterozygous mutations in the SLC2A9 gene.
A 43-year old man was admitted to our clinic because of bilateral loin pain, nausea and sleeplessness for 3 days after strenuous exercise. The laboratory results revealed increased levels of blood urea nitrogen (BUN) (15 mmol/l) and serum creatinine (Scr) (450 μmol/l), while the UA level was extremely low at 0.54 mg/dl, and his fractional excretion of urate (FE-UA) was 108%. The patient had an episode of acute kidney injury after playing soccer approximately 20 years ago, and on routine physical examination, his UA was less than 0.50 mg/dl. In view of the marked hypouricemia and high FE-UA, a diagnosis of RHUC was suspected, which led us to perform mutational screening of the SLC22A12 and SLC2A9 genes. DNA sequencing revealed no mutation in SLC22A12 gene, but two heterozygous mutations in the SLC2A9 gene.
This is a rare report of a patient with RHUC2 due to the mutation of SLC2A9. And this unique symptom of EIAKI and decreased or normal serum concentrations of UA warrant more attention as an early cue of RHUC.

Posterior reversible encephalopathy syndrome (PRES) is characterised by encephalopathy, visual disturbances and seizures, accompanied by radiological parieto-occipital oedema. Immunosuppressive and immunomodulatory drugs are risk factors. While capecitabine-induced PRES cases are rare, this report details a young woman with advanced gastric adenocarcinoma on capecitabine. She exhibited symptoms of nausea, vomiting and abdominal pain before developing hypertension, drowsiness and a seizure. Brain MRI revealed parieto-occipital hyperintense areas indicative of PRES. Suspending capecitabine led to a gradually improved mental state. Prompt recognition and treatment of PRES offer reversibility, often achievable through dose reduction or discontinuation of the causative drug.

Posterior reversible encephalopathy syndrome (PRES) is an uncommon transient neuroradiological phenomenon that develops vasogenic cerebral edema and could be caused by some pharmacological agents, such as molecular-specific target agents. Lenvatinib belongs to the tyrosine kinase inhibitors and was approved in 2015 for progressive locally advanced or metastatic thyroid cancer refractory to radioactive iodine (I-131) treatment. Herein, we present the case of a 65-year-old woman who, while receiving treatment with lenvatinib for radioiodine-refractory metastatic papillary thyroid carcinoma, developed PRES without hypertension at the initial evaluation. Her clinical and radiological findings improved after withdrawing from the mentioned therapy, and later it was possible to re-incorporate lower doses of the medication, as described in the other three case reports found in the worldwide medical literature. The recognition of this entity is essential to timely suspend the drug and avoid greater comorbidity. This is the first paper reporting this kind of adverse event using lenvatinib in a Hispanic population.

BACKGROUND: Rapidly progressive glomerulonephritis (RPGN) is clinically manifestations as a rapidly progressive renal failure and pathologically as crescentic and necrotizing lesions with infiltration of inflammatory cells in the glomeruli. Uremic encephalopathy (UE) usually develops in patients who are suffering from acute or chronic renal failure.
OBJECTIVE: The purpose of this article is to provide reference for clinical diagnosis and treatment of renal disease complicated with seizures. Patients Two cases of anti-glomerular basement membrane type rapidly progressive glomerulonephritis complicated with seizures were reported.
METHODS: In case 1, a 40-year-old woman was hospitalized for the treatment of nausea, anorexia, and fever. On admission, she presented with elevated serum inflammatory indicators, moderate anemia, and advanced acute kidney injury requiring hemodialysis. Her anti-glomerular basement membrane (GBM) antibody in serum and renal tissues was found to be extremely high. She was finally diagnosed with anti-GBM disease. She was treated with a combination of corticosteroid pulse therapy, oral cyclophosphamide and prednisolone, and plasma exchange, while continued to require maintenance hemodialysis for end-stage kidney disease. During treatment, she suddenly suffered blindness, seizure, and consciousness disturbance. She was diagnosed as posterior reversible leukoencephalopathy syndrome by magnetic resonance imaging (MRI). The posterior reversible leukoencephalopathy syndrome subsided quickly after control of her hypertension and reinforcement of immunosuppressive treatment. In case 2, the patient also developed epileptic symptoms on the basis of GBM disease, and was given treatment similar to that of Case 1, so that the epileptic symptoms were controlled.
RESULTS: Reversible posterior leukoencephalopathy syndrome, especially when accompanied by cerebral hemorrhage, may lead to irreversible and lethal neurological abnormalities, and nephrologists should, therefore, be aware of the potential risk of reversible posterior leukoencephalopathy syndrome in patients with anti-GBM disease. We can discuss the current two cases in the light of the previous literature.