Mickevičius, Lukas

Introduction Kidney transplantation is the preferred treatment for patients with advanced chronic kidney disease, including those with CKD stages G4–G5 [1]. Donor-origin urolithiasis is a rare complication, described as stones that are already present in the donor kidney. As the number of transplants increases, awareness of potential complications is crucial [2]. Case Presentation A 58-year-old man with end-stage renal disease due to biopsy-confirmed IgA nephropathy, underwent deceased-donor kidney transplantation on 22–23 March 2022. The early postoperative course was unremarkable, serum creatinine decreased by 50% on day 2 after transplantation, and he no longer required hemodialysis. Ultrasound evaluation of the transplanted kidney showed no dilatation of the collecting system. The patient was discharged home on postoperative day 14. In September 2022, during a routine follow-up visit, progressive hydronephrosis of the graft was noted. The patient was asymptomatic. Due to the increasing hydronephrosis of Tx kidney on ultrasound, a CT scan was performed and revealed a radiopaque calculus at the pelviureteric junction of the transplanted kidney, consistent with a donor-derived stone that had gone unrecognized at the time of transplantation. A minipercutaneous nephrolithotomy (mini-PCNL) was performed with complete stone removal. Postoperatively, graft function remained stable. Discussion Post-operative urolithiasis after kidney transplantation is relatively uncommon, with reported incidence of 0.1% to 6.3% [3]. Stones may be donor-derived or form de novo [3-6]. In general, donors with recurrent stone disease or metabolic abnormalities are excluded, although stones less than 4 mm could be left in situ [4]. Most of the time, there is no common colic pain because of the denervation of the kidney and ureter graft [5]. Typically it is diagnosed accidentally 12 months or more post-transplant. Lithiasis has different treatment options, namely active surveillance, ureteroscopy, percutaneous/combined approach, or open surgery [3]. Conclusions Regular follow-up of kidney transplant recipients is essential, as graft complications may develop silently. Early detection through routine imaging allows timely intervention and preserves function of kidney transplants.

Nutukimas - viena aktualiausių dabartinės visuomenės problemų, neigiamai veikianti daugelį organizmo sistemų ir trikdanti sergančiojo šia liga gyvenimo kokybę, darbingumą bei trumpinanti gyvenimą. Tai - metaboliškai aktyvi ir recidyvuojanti liga, kurios metu kūno masė didėja riebalinio audinio sąskaita. Nutukimą kaip ligą Amerikos medicinos asociacija oficialiai pripažino 2013 metais. Nutukimas pastaruoju metu yra labiausiai aptarinėjama tema tiek medicinos, tiek plačiojoje visuomenėje. Kalbant apie nutukimą, dažnai ši būklė siejama su asmeniniu kaltės priskyrimu: „reikia tik noro“, „reikia suimti save į rankas“ ir t. t. Įvairiais istoriniais laikotarpiais požiūris į žmogaus kūno formas keitėsi nuo Rubenso tipo moterų iki anoreksinių mados manekenių formų. Menamų kūno formų standartų neatitinkantis žmogus gali būti pavadintas putliu, stambiu, apkūniu, didelio dydžio ar net storuliu ar apsileidusiu. Medicinos bendruomenėje vyrauja terminai: antsvoris, hipotalaminis, pilvinis, centrinio tipo, kušingoidinis, morbidinis nutukimas ir kt. Nutukimas turi kompleksines pasekmes - skatina lėtines ligas, galinčias sutrumpinti žmogaus amžių 10-15 metų. Per pastaruosius 5 dešimtmečius nutukimo paplitimas pasaulyje padidėjo daugiau nei 3 kartus, ir dabar tai įvardijama kaip nutukimo pandemija. Klinikinėje praktikoje nustatomos įvairiausios nutukimo priežastys - nuo genetinių (Prader-Willi sindromas, Aistrom sindromas, LEPR (leptino receptoriaus) ar LEP (leptino) geno mutacijos ir kt.), endokrininių (hipotirozė, hiperkorticizmas, hipogonadizmas ir kt.) iki valgymo priklausomybių. Skirtingos yra ir nutukusių kūno formos bei kūno kompozicija. Todėl kūno masės indeksas (KMI) klinikiniu požiūriu jau nebetenka prasmės. KMI tikslinga naudoti populiaciniams, palyginamiesiems tyrimams. Statistiniais duomenimis (HIS Lietuva, Eurostat, 2019-2022 m.), pagal KMI nutukusių suaugusių Lietuvoje buvo 21-23 proc. Skaičiuojama, kad apie 60 proc. suaugusiųjų Lietuvoje turi antsvorio ar yra nutukę. Tai - tik statistika, neatspindinti konkrečios individo būklės. 2025 m. pasaulio 58 ekspertų grupė, atstovaujanti įvairioms medicinos specialybėms ir šalims, išanalizavo turimus įrodymus ir, pritarus 75 medikų ir pacientų organizacijoms, rekomendavo klasifikaciją, kurioje išskiriamas ikiklinikinis ir klinikinis nutukimas. Pagal epidemiologinius ir klinikinius duomenis, nutukimas susijęs su daugiau nei 200 skirtingų ligų ir sveikatos sutrikimų. [...]

Background and Aim. Acute kidney injury (AKI) is a potentially reversible process, but its episodes can lead to chronic kidney disease (CKD) - in about 15% of patients (1, 2, 3, 4). There is currently no effective or timely treatment to stop the progression of the disease (5, 6). Human placenta-derived mesenchymal stromal cells (hpMSCs) are a promising new remedy in regenerative medicine and pharmacology. HpMSCs may be a promising source for cells therapy due to their extensive sources and low immunogenicity (7). Our aim was to compare evolution of histological biomarkers during AKI emergence and conversion towards CKD. [...].

Acute kidney injury (AKI) is widely recognized as a precursor to the onset or rapid progression of chronic kidney disease (CKD). However, there is currently no effective treatment available for AKI, underscoring the urgent need for the development of new strategies to improve kidney function. Human placental mesenchymal stromal cells (hpMSCs) were isolated from donor placentas, cultured, and characterized with regard to yield, viability, flow cytometry, and potency. To mimic AKI and its progression to CKD in a rat model, a dedicated sensitive non-clinical bilateral kidney ischemia-reperfusion injury (IRI) model was utilized. The experimental group received 3 × 105 hpMSCs into each kidney, while the control group received IRI and saline and the untreated group received IRI only. Urine, serum, and kidney tissue samples were collected over a period of 28 days. The hpMSCs exhibited consistent yields, viability, and expression of mesenchymal lineage markers, and were also shown to suppress T cell proliferation in a dose-dependent manner. To ensure optimal donor selection, manufacturing optimization, and rigorous quality control, the rigorous Good Manufacturing Practice (GMP) conditions were utilized. The results indicated that hpMSCs increased rat survival rates and improved kidney function by decreasing serum creatinine, urea, potassium, and fractionated potassium levels. Furthermore, the study demonstrated that hpMSCs can prevent the initial stages of kidney structural fibrosis and improve kidney function in the early stages by mitigating late interstitial fibrosis and tubular atrophy. Additionally, a robust manufacturing process with consistent technical parameters was established.

Introduction: Acute kidney injury (AKI) is a dangerous condition. Its episodes can lead to chronic kidney disease (CKD). There is no effective and timely treatment. Therefore, it is very important to develop a new strategy for maintaining and improving the kidney function. Currently, regenerative medicine, especially human placental mesenchymal stem cells (hPSCs), is the most promising area. Methods: Human placental amniotic and chorionic cells have been isolated. hPSCs have been cultivated and characterized by yield, viability, flow cytometry and potency in vitro. Rats underwent preclinical ischemia-reperfusion injury (IRI). Experimental group received 3x105 of hPSCS in each kidney, control group - phosphate buffer solution (PBS), untreated group - only induced IRI. Urine, blood serum samples and kidneys for histological analysis collected. Results: hPSCs had a consistent yield, viability, mesenchymal stem cell markers expression and suppressed proliferation of T cells in a dose-dependent fashion. hPSCs increased survival and kidneys function by decreased creatinine, urea in serum in compare with surviving rats in control groups. Cells decreased renal injury scores and prevented chronic injury by reduced kidneys structural damage compare with control groups. Conclusion: Although hPSCs are not use widely in preclinical and clinical trial yet, however, in the present study, we demonstrated that hPSCs have the potential to prevent initial kidney fibrosis cascade through ameliorating initial kidney damage and improving kidney function.

Introduction: Acute kidney injury is affecting about 20% of surgically treated patients.1,2,3 Placental mesenchymal stem cells (PSCs) have been shown to possess anti-inflammatory and immunomodulatory properties.4 Methods: After the removal of maternal decidua basalis, placental amniotic and chorionic cells have been isolated, cultivated for four weeks and characterized by yield, viability, flow cytometry and potency in vitro. Wistar rats underwent kidneys ischemia-reperfusion injury. Index group received 3x105 PSCs and Control group – vehicle in the corticomedullar region of each kidney. Survival was analyzed. Urine and blood serum samples were collected on days 0, 3 and 7. Histological kidney analysis – days 3 and 7. Results: PSCs had a consistent yield, viability, MSCs markers expression and suppressed proliferation of T cells in a numerical fashion. Survival rate improved – 100% (Index) vs. 80% (Control). Creatinine clearance in Index group was comparable to healthy control on day 7. Normal serum creatinine, urea and Na+ was retained in Index group up to day 7. Extensive acute tubular necrosis (ATN) with broad coagulative tubular epithelial necrosis was evident after 3 days in the Control. A clear tendency for a lower ATN area, loss of brush border and tubular dilatation and ATN without significant coagulative necrosis was evident in Index group up to day 7. Conclusion: PSCs have the potential to prevent initial kidney fibrosis cascade through ameliorating initial kidney damage. A superior 100% survival rate of treated animal group exhibits the potential of characterized PSCs to be used in a larger scale preclinical study.

Introduction and Aim Acute kidney injury can lead to a chronic kidney disease.1,2,3,4 Placental mesenchymal stem cells (PSCs) have been shown to possess anti-inflammatory and immunomodulatory properties.5 Methods Human placental amniotic and chorionic cells have been isolated. 8-12 wk. Wistar female and male rats (at least 3 per end point) underwent preclinical ischemia-reperfusion injury (IRI). Treated group (Index group) received 3x105 PSCs, Control group received phosphate buffer solution (PBS) in the corticomedullar region into each kidney. Both groups were compared to Untreated group. Urine and blood serum samples collected on days 0, 3, 7, and 21 to 28. Histological kidney analysis – days 3, 7, 21 to 28. Survival was calculated based on histological censoring. Kidney specimens were stained with haematoxylin and eosin and periodic acid–Schiff for histological analysis. Results PSCs had a consistent yield, viability, mesenchymal stem cell markers expression and suppressed proliferation of T cells in a dose-dependent fashion. Survival rate improved – 100% (Index) vs. 63% and 72% in Control and Untreated groups, respectively. Numerical normalization of mean creatinine levels observed at Day 3 in Index group and was 2 times lower than Control and Untreated group. Unlike Control and Untreated groups, serum creatinine and urea levels normalized at day 7 and 28 in Index group. Serum K+ and Na+ remains without essential dynamics in Index group. Extensive acute tubular necrosis (ATN) with broad coagulative tubular epithelial necrosis was evident after 3 days in the Untreated group. A clear tendency for a lower ATN area, loss of brush border and tubular dilatation and ATN without significant coagulative necrosis was observed in Index group up to day 7. Only minor features of acute tubular damage and no interstitial fibrosis or tubular atrophy were observed in the Index group at day 21, compared to the residua[...].

Background & Aim Acute kidney injury (AKI) is a life-threatening postoperative complication, affecting 10-30% of treated patients and characterized by the damage to the proximal tubular cells, thereby markedly impairing renal function.1,2,3 15% of patients develop chronic kidney disease (CKD) and fibrosis, eventually managed by hemodialysis and kidney transplantation.4 Mesenchymal stem cells have been shown to possess anti-inflammatory and immunomodulatory properties and be able to aid in tissue repair.5 A link between AKI and CKD has been established and the optimal treatment approach to reduce the high unmet medical need and an economical burden is still being researched.6 Placenta-derived mesenchymal stem cells (PSCs) may be a viable approach to treat AKI and prevent subsequent CKD development. Methods, Results & Conclusion M.: PSCs have been isolated using GMP grade materials, cultivated for three weeks and characterized by yield, viability, flow cytometry and potency in vitro. Wistar rats (8-12 wk) underwent preclinical ischemia-reperfusion injury (IRI). Two experimental groups received treatment. Experimental group (Index) received 3×105 of PSCs in the corticomedullar region of each kidney. Control group (Control) received PBS vehicle solution. Survival analysis was carried out till day 7. Urine and blood serum samples were collected on day 0, 3 and 7 and analysed for urine volume/24hrs., protein, creatinine, urea, Na+ and K+. Histological kidney analysis on days 3 and 7 for evaluation of tubular necrosis. R. PSCs had a consistent yield, viability, MSCs markers expression and suppressed proliferation of T cells. Survival rate improved – 100% (Index) vs. 75% (Control). Serum urea and K+ was reduced in index group on day 7 (p<0.05). Serum creatinine was 1.9 and 1.6 times lower in index group on days 3 and 7, respectively. Na+ was similarly lower after 7 days after PSCs injection. Extensive acute [...].

Introduction & Objectives: Our aim was to evaluate patients with prostate cancer (PCa) from our active surveillance (AS) study whose parameters are out of European Association of Urology (EAU) guidelines and to find out their further changes after second biopsy. Materials & Methods: We conducted our PCa AS chart review which consists of 248 patients and picked out 114 patients which do not match EAU guidelines for AS by one or more of following criteria: PSA value >9, 5 ng/ml, Gleason score 7, percentage of cancer in one bioptate > 50%, positive cores in prostate biopsy ≥ 4 and PSA density > 0,15 ng/ml/g. Results: From all 114 patients 3 of them had all of mentioned criteria, four of them had 4, eleven of them had 3, twenty three of them had 2 and seventy three of them had 1 mentioned criteria. After second biopsy 33 patients were out of AS criteria. During the initial biopsy the Gleason score of 7(3+4) was in 32 patients and Gleason 7(4+3) was in 1 patient and after second biopsy Gleason score of 7(3+4) was in 13 patients and Gleason 7(4+3) was in 2 patients. PSA value of more than 9, 5 ng/ml after initial biopsy was in 12 patients and after second biopsy was in 2 patients. By number of positive cores after initial biopsy that is or overcomes number 4 was in 30 patients and after second biopsy was in 6 patients. More than 50% of cancer in one of the bioptate after initial biopsy was in 20 patients and after second biopsy was in 3 patients. PSA density of more than 0.15 ng/ml/g after initial biopsy was in 88 patients and after second biopsy was in 7 patients. Conclusions: Our study showed that there was no evident progression of PCa parameters after second biopsy.. [...].

Duration of ischemia is very important factor which influences postoperative kidney function. The aim of this study was to test effect of renal ischemia in vivo on mitochondrial functions. Results: Ischemia/reperfusion (20 min/30 min) did not affect oxygen consumption in rat kidney mitochondria but slightly increased permeability of inner mitochondrial membrane. Acivity of mitochondria respiratory chain complex I after this time of ischemia/reperfusion was decreassed by 30%, however activity of SDH and complex II+III remained unchanged. Ischemia/reperfusion longer than 20 minutes induced r enal mitochondria injury: mitochondrial respiration rate in state 3 with glutamate + malate and the respiratory control index (RCI) were decreased by 38% and 68% after 30 and 40 min of ischemia and 30 min of reperfusion, respectively. Succinate oxidation was also affected. After 40 min of ischemia respiration rate was decreased by about 50%. Complex I activity after 30 and 40 min ischemia and 30 min of reperfusion was decreased by 56% and 62%, respectively. SDH activity was not affected after 30 min of ischemia and 30 min reperfusion but increased by 66% after 40 min ischemia and 30 min of reperfusion. Ischemia (20,30 and 40 min) and reperfusion did not affect complex II+III activity. .