The coronavirus (COVID‐19) pandemic is evolving very quickly and has affected healthcare systems worldwide. Many uncertainties remain about transplantation from a SARS‐CoV‐2‐positive donor as only a few cases have been reported. Here, we present the successful transplantation of two kidneys from a 52‐year‐old male donor with active (2 weeks of COVID‐19‐like symptoms and positive nasopharyngeal swab SARS‐CoV‐2 PCR on the day of organ recovery) SARS‐CoV‐2 disease. The immediate postoperative course of both recipients was uneventful. This case emphasizes that patients with SARS‐CoV‐2 may be safe organ donors.

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Objective: Malignant hypertension (MH) is a form of hypertensive emergency defined by a severe increase in blood pressure (BP) with multiple organ injuries. One possible pathophysiology of MH is an acute activation of the renin-angiotensin system (RAS) driven by the intense stimulation of renin secretion in the juxtaglomerulosa cells. Considering this mechanism, aliskiren, a direct renin inhibitor (DRI), can be a treatment option for MH. However, there is little information on the efficacy and safety of DRI in controlling MH. We herein report four cases with MH that have been successfully controlled by DRI for a long term.Case description: All of the four cases (three male and one female; 34 to 57 years of age) developed advanced retinopathy (III or IV grade on Keith-Wagener classification) and severe hypertension (> 200/120 mmHg) at presentation, meeting the criteria for MH according to the 2020 ISH global hypertension practice guideline. Mean systolic/diastolic BP was 215 ± 5/148 ± 8 mmHg. All developed acute kidney injury, with the mean serum creatinine (sCr) of 4.47 ± 1.13 mg/dl on admission. The ranges of plasma renin activity (PRA) and plasma aldosterone concentration (PAC, as measured by RIA) were 11-33 ng/mL/hr and 371-1370 pg/mL, respectively. Followed by initial treatment with an intra-venous calcium channel blocker, these patients were prescribed aliskiren, starting at 150 mg/day once daily, after confirmation of the elevated PRA levels. In general, aliskiren was well tolerated and BP was successfully controlled in all of the four cases (at discharge, mean systolic/diastolic BP was 123/74 mmHg and mean sCr was 3.84 mg/dL). Patients continued to receive aliskiren (at a dose of 150 or 300 mg/day) after the discharge and mean systolic/diastolic BP and sCr were 131 ± 4/84 ± 3 mmHg and 2.02 ± 0.16 mg/dl at two years of follow-up, respectively. The ranges of PRA and PAC of four cases have fallen to 0.2-0.8 ng/mL/hr and 105-203 pg/ mL, respectively.Literature review: The voltage-dependent K(+) channel responsible for activating delayed K(+) current is composed of pore-forming KCNQ1 and regulatory KCNE1/3 subunits which loss of function predispose to sustained torsade de pointes. Animal models demonstrate that KCNQ1 and KCNE1 mRNAs are expressed in the zona glomerulosa of adrenal glands where potassium channels directly participate in the control of aldosterone production. Although KCNE3 is not expressed in mouse adrenals, its deletion is thought to cause activation of lymphocytes targeting adrenal glands, leading to hyperaldosteronism. Furthermore, administration of spironolactone to KCNE3 knockout mice ameliorates their QT

Background:Posterior reversible encephalopathy syndrome (PRES) describes a disorder of abrupt onset neurological symptoms due to potentially reversible lesions on brain imaging. Case reports of PRES in PD patients are scarce.Case presentation:A 42-year-old male presented to the emergency department (ED) with two weeks of worsening occipital headaches, nausea, vomiting and dizziness. The patient had a background of end-stage renal disease due to primary focal segmental glomerulosclerosis, and resistant hypertension. He had been receiving peritoneal dialysis (PD) for one month; hypertension was treated with torasemide 100 mg/day, perindopril 10 mg/day, amlodipine 10 mg/day, moxonidine 0.6 mg/day, doxazosin 8–16 mg/day. One week earlier, he was brought into ED due to hypertensive crisis (blood pressure (BP) was 190/120 mmHg); intravenous labetolol 20 mg, oral moxonidine 0.4 mg, doxazosin 8 mg were administered; afterwards he was released for outpatient treatment.On admission, BP was 187/114 mmHg, heart rate - 75 beats/minute, oxygen saturation - 98% on room air, and body temperature - 36.5°C. Laboratory tests revealed severe renal dysfunction (serum creatinine: 1478 mcmol/l, serum urea: 29.1 mmol/l) and normal inflammatory indicators (WBC: 4.51 x 109/l, CRP: 0.65 mg/l) (Table). Head CT showed no obvious intracranial hemorrhage, ischemia, or mass lesion; PRES was suspected. Due to hypervolemia, he was temporarily transferred to hemodialysis. On day 12, fundoscopy revealed flame-shaped hemorrhages, microaneurysms, cotton wool patches in the posterior pole surrounding the optic nerve. On day 14, he was transferred to the intensive care unit (ICU) due to uncontrollable hypertension (BP was 202/129 mmHg) and epileptic seizure; MRI showed bilateral subcortical occipital and frontoparietal hyperintensity with vasogenic edema typical of PRES. BP was decreased to approximately 155/90 mmHg using a combination of anti-hypertensive medication and ultrafiltration. Subsequently he was discharged on day 28. Two months later he underwent cadaveric kidney transplantation. After the transplantation, his BP control improved and he was left with bisoprolol 5 mg/day, amlodipine 10 mg/day, and doxazosine 4 mg/day (office BP one month after the transplantation: 124/90 mmHg, after two months: 135/95 mmHg, after three months: 135/95 mmHg).Conclusions:This is to the best of our knowledge the fifth report of PRES in an adult patient undergoing PD, and the first presenting a PD patient with history of PRES whose hypertension control improved after kidney transplantation. It is likely that the cause of described PRES episode was multifactorial, originating from the complications of ESRD, hypertension and poor compliance with PD.

Reikšminiai žodžiai: inksto transplantacija, nesuderinamos kraujo grupės. Tyrimo tikslas. Apžvelgti pirmąsias gyvo donoro nesuderinamos kraujo grupės (AB0n) inksto transplantacijas Lietuvoje; įvertinti pacientų, kuriems buvo atlikta nesuderinamos kraujo grupės inksto transplantacija, alografto funkcijos rodiklius ir palyginti juos su kontroline grupe pacientų, kuriems atlikta transplantacija iš suderinamos kraujo grupės (AB0s) donoro. Metodika. Atlikta retrospektyvinė paruošimo transplantacijai ir jos rezultatų analizė 10 pacientų, kuriems 2010–2014 m. VUL SK persodintas netapačios kraujo grupės inkstas. Transplantato funkcijos rodiklių dinamika lyginta su kontroline grupe, kurią sudarė 22 asmenys, kuriems per tą patį laikotarpį buvo atliktos tapačios kraujo grupės inksto transplantacijos. Rezultatai. Į analizę įtrauktos 32 inkstų transplantacijos iš gyvo donoro. 9 iš 10 AB0n grupės recipientų buvo pasiektas tikslinis <1:8 IgG titras atliekant antigenui specifiškas imunoadsorbcijas bei dviem iš jų taikytos papildomos plazmaferezės procedūros. Abejose grupėse po vieną transplantatą buvo prarasta ankstyvuoju potransplantaciniu periodu dėl alografto trombozės. Nustatytas AB0n grupei palankesnis statistiškai patikimas skirtumas po Tx praėjus 6 mėn. (pagal CKD-EPI ir MDRD formules atitinkamai p = 0,038 ir p = 0,044). Lyginant transplantato funkcijos rodiklius kitais laikotarpiais, statistiškai patikimo skirtumo nenustatyta (p > 0,05). Vertinant proteinuriją visais periodais, statistiškai reikšmingas skirtumas tarp grupių taip pat nenustatytas (p > 0,05). Išvada. AB0n inksto transplantacija ankstyvuoju potransplantaciniu periodu efektyvumu nenusileidžia AB0s kraujo grupių inksto transplantacijai.