Ukrainian Journal of Nephrology and Dialysis

Post-traumatic intravesical clot retention causing recurrent post-renal acute kidney injury in a pregnant woman: A case report

2026-09-14T16:26:39+03:00

Intravesical blood clot obstruction is a recognized cause of postrenal acute kidney injury (AKI), but recurrent obstruction after apparent renal recovery may be difficult to recognize. We report a 30-year-old pregnant woman at approximately 27 weeks’ gestation who developed severe AKI after a motor vehicle accident with gross hematuria. At the first admission, serum creatinine was 8.210 mg/dL, and ultrasonography showed bilateral pelvicalyceal ectasia without a definite obstructing lesion. After bladder drainage, renal function rapidly improved, with serum creatinine decreasing to 1.130 mg/dL without hemodialysis. Ten days later, the patient was readmitted with recurrent gross hematuria, anuria, hyperkalemia, metabolic acidosis, and recurrent AKI. Repeat ultrasonography demonstrated a large intravesical blood clot, supporting clot-related obstruction as the most likely mechanism. Repeat bladder drainage and one emergency hemodialysis session were followed by marked renal recovery. The subsequent course was complicated by fetal loss, postpartum hemorrhage, puerperal sepsis, multiorgan dysfunction, and death.

The clinical importance of this case lies in the recurrence of severe postrenal AKI after near-complete renal recovery. In patients with trauma-associated gross hematuria, rapid improvement after bladder drainage does not exclude persistent or recurrent clot-related obstruction. Repeat urinary tract imaging should be considered when hematuria, anuria, or kidney dysfunction recurs, particularly when initial imaging shows upper urinary tract dilatation without a clear cause.

Enavogliflozin attenuates early sepsis-associated acute kidney injury in a murine cecal ligation and puncture model

2026-09-14T19:04:44+03:00

Sepsis is often complicated by the onset of acute kidney injury (AKI) through processes involving inflammation, oxidative stress, tubular damage, and cell death. In this study, we investigated whether enavogliflozin might mitigate acute renal damage following Cecal Ligation and Puncture (CLP)-induced sepsis.

Methods. Twenty-four male mice were allocated to the following four experimental groups: sham operation (Sham), CLP, CLP plus dimethyl sulfoxide (DMSO), and CLP plus enavogliflozin. Enavogliflozin was administered intraperitoneally at 1mg/kg, 1h before CLP surgery. At 24 hours after surgery, blood and kidney tissue samples were collected. Serum creatinine was measured to assess kidney function, while renal tissue levels of kidney injury molecule-1 (KIM-1), nuclear factor kappa B (NF-κB), malondialdehyde (MDA), caspase-3, and nuclear factor erythroid 2-related factor 2 (Nrf2) were measured using an enzyme-linked immunosorbent assay (ELISA). We also performed a kidney histopathological assessment using Hematoxylin & Eosin staining and a score assigned for renal damage.

Results. Serum creatinine was significantly elevated in mice undergoing CLP compared to sham controls (2.240 ± 0.2546 mg/dL vs 0.4307 ± 0.05516 mg/dL; P < 0.0001). Administration of enavogliflozin in CLP animals resulted in a decrease in serum creatinine levels (1.117 ± 0.1276 mg/dL vs 2.240 ± 0.2546 mg/dL; P < 0.01). Compared with the CLP group, enavogliflozin significantly reduced renal tissue levels of the tubular injury marker KIM-1 (359.3 ± 12.30 vs. 461.4 ± 18.32 pg/mL; P < 0.001), the inflammatory mediator NF-κB (844.7 ± 20.09 vs. 1429 ± 11.38 pg/mL; P < 0.0001), the oxidative stress marker MDA (204.5 ± 18.79 vs. 320.6 ± 23.51 ng/mL; P < 0.01), and the apoptosis-related protein caspase-3 (7.726 ± 0.4581 vs. 10.21 ± 0.5911 ng/mL; P < 0.05). In contrast, renal Nrf2 levels were significantly higher in enavogliflozin-treated mice than in the CLP group (4383 ± 123.6 vs. 3210 ± 117.6 pg/mL; P < 0.0001), indicating enhancement of the antioxidant response. Histologically, renal tissue of enavogliflozin-treated mice showed ameliorated injury scores compared to the CLP controls [0.0 (0.0–1.0) vs 3.5 (3.0–4.0); P < 0.05].

Conclusions. Treatment with enavogliflozin attenuates acute CLP-induced renal injury by ameliorating tubular damage, suppressing inflammation and oxidative stress, and promoting an antioxidative cellular response. Further studies are warranted to elucidate the mechanism of action and establish the clinical utility of enavogliflozin administration following sepsis.

Metabolic-associated fatty liver disease in patients undergoing hemodialysis: A cross-sectional study of prevalence and diagnostic accuracy of the triglyceride–glucose index

2026-09-14T16:26:39+03:00

Metabolic dysfunction-associated fatty liver disease (MAFLD) is increasingly recognized in patients with metabolic and renal disorders; however, data in hemodialysis populations remain limited. This study assessed the prevalence of MAFLD in patients receiving maintenance HD and identified factors associated with its presence.

Methods. A total of 95 patients with end-stage kidney disease (ESKD) receiving maintenance HD were included in this cross-sectional study conducted at Ain Shams University Hospital from January to September 2024. Clinical assessment, abdominal ultrasonography, and laboratory investigations were performed. The triglyceride-glucose (TyG) index, non-alcoholic fatty liver disease (NAFLD) fibrosis score, and fibrosis-4 (FIB-4) score were calculated.

Results. MAFLD was identified in 21 of 95 patients (22.1%). Compared with patients without MAFLD, those with MAFLD had significantly higher body mass index (35.14 ± 3.09 vs. 25.51 ± 4.74 kg/m²), WC (116.95 ± 6.74 vs. 100.24 ± 9.56 cm), CRP (20.38 ± 5.24 vs. 4.59 ± 2.49 mg/L), ALT, AST, TC, LDL-C, triglycerides, TyG index (9.20 ± 0.34 vs. 8.63 ± 0.27), NAFLD fibrosis score, and FIB-4 score (all P < 0.05). Hemoglobin and albumin were substantially lower in the MAFLD group. The TyG index showed high discrimination for MAFLD, with an AUC of 0.906 (95% CI, 0.815–0.998); at a cutoff >8.88, sensitivity was 95.2% and specificity was 82.4%.

Conclusions. MAFLD is common among patients receiving hemodialysis and is associated with metabolic and inflammatory disturbances. The TyG index showed promising discriminative performance for identifying MAFLD in this population. However, the findings are exploratory and require validation in larger, multicenter studies.

Serum glucagon-like peptide-1 and G-protein-coupled receptor levels are associated with albuminuria and kidney function in type 2 diabetes: A cross-sectional study

2026-09-14T16:26:39+03:00

The relationship of serum glucagon-like peptide-1 (GLP-1) and G-protein-coupled receptor (GPCR) with kidney-related outcomes continues to be poorly studied. The purpose of this study was to determine whether serum GLP-1 and GPCR are related to urinary albumin-to-creatinine ratio (uACR), estimated glomerular filtration rate (eGFR), and cystatin C in patients with type 2 diabetes mellitus (T2DM).

Methods. A total of 150 participants were included in this cross-sectional study and divided into three groups: the healthy subjects (Control group), T2DM patients with albuminuria stage A1 (T2DM-A1 group), and T2DM patients with albuminuria stage A2/A3 (T2DM-A2/A3 group). There were 50 subjects in each group. The clinical information was collected: fasting glucose, HbA1c, insulin, urea, creatinine, eGFR, uACR, cystatin C, GLP-1, and GPCR values. Serum GLP-1, GPCR, and cystatin C were measured using sandwich ELISA kits. Groups were compared using non-parametric testing. Analysis of Spearman correlation was utilized in the diabetic cohort. Linear regression adjusted for age, BMI, diabetes duration, and HbA1c was conducted to identify independent associations of GLP-1 and GPCR with uACR and eGFR.

Results. GLP-1 and GPCR concentrations were gradually increasing from Сontrol group to group T2DM-A1 and group T2DM-A2/A3. Within the diabetic cohort, GLP-1 and GPCR were positively correlated with uACR and cystatin C and negatively correlated with eGFR. After adjustment for covariates, GLP-1 was associated with higher log-transformed uACR (standardized = 0.529, p < 0.001) and lower eGFR (standardized = -0.415, p < 0.001). Similarly, GPCR also showed a positive correlation with log-transformed uACR (standardized = 0.319, p = 0.002) and a negative correlation with eGFR (standardized = -0.365, p = 0.002).

Conclusions. Circulating GLP-1 and GPCR levels were associated with higher albuminuria and lower eGFR in T2DM. GLP-1 demonstrated a stronger association with albuminuria, while GPCR displayed a comparable negative association with kidney function. The study’s findings offer evidence for a cross-sectional GLP-1-GPCR kidney-related biomarker profile that characterizes the albuminuric T2DM phenotype and call for longitudinal studies to confirm the clinical utility of these markers.

A composite score of neutrophil gelatinase-associated lipocalin and fibroblast growth factor-23 is associated with survival in multiple myeloma: A retrospective study

2026-09-14T16:49:45+03:00

Multiple myeloma (MM) is frequently complicated by renal impairment, but traditional markers like the estimated glomerular filtration rate (eGFR) are inherently late indicators that fail to capture early structural damage. We aimed to evaluate the combined prognostic value of neutrophil gelatinase-associated lipocalin (NGAL), a marker of tubular injury, and fibroblast growth factor-23 (FGF-23), a reflection of bone-mineral dysregulation and tumor burden, independently of eGFR and disease stage.

Methods. This retrospective cohort study included 95 adult patients with a confirmed diagnosis of MM. Baseline serum NGAL and FGF-23 concentrations were quantified using enzyme-linked immunosorbent assays (ELISA). Optimal prognostic cutoffs were determined using maximally selected rank statistics. A composite risk score was constructed to compare patients with concurrent biomarker elevations (score 2) against those with zero or one elevated marker (score 0–1). Overall survival was assessed using Kaplan-Meier analysis and multivariable Cox proportional hazards regression models adjusted for eGFR and International Staging System (ISS) stage.

Results. The optimal prognostic cutoffs were identified as 153.8 ng/mL for NGAL and 36.4 pg/mL for FGF-23. Patients with a composite score of 2 experienced significantly lower overall survival probabilities (log-rank p = 0.0071). In multivariable analysis, the composite risk score remained a potential independent prognostic marker for mortality after adjustment for baseline eGFR (adjusted HR = 6.32, 95% CI: 1.25–31.88, p = 0.025) and ISS stage (p = 0.0057).

Conclusions. The combined assessment of serum NGAL and FGF-23 provides additional prognostic insight over standard eGFR evaluations. Due to the critically low number of events, these findings are strictly hypothesis-generating. This exploratory composite score may aid in identifying a highly vulnerable patient subgroup, independent of baseline filtration status and global tumor burden, but requires validation in larger cohorts.

Phenotypic ESBL and AmpC in community-acquired urinary tract infections in Babylon, Iraq: Empirical therapy mismatch and clinical outcomes

2026-09-14T16:26:40+03:00

Community-acquired urinary tract infections (UTI) are commonly treated empirically before culture and susceptibility results are available. The rising prevalence of extended-spectrum beta-lactamase (ESBL) and AmpC beta-lactamase phenotypes in uropathogens could lead to decreased effectiveness of empiric treatment and higher incidence of treatment failure and recurrence. The present study was carried out to investigate the prevalence of phenotypic ESBL and AmpC-producing community-acquired UTIs caused by E. Coli and K. Pneumoniae in Babylon, Iraq, and to determine their association with empirical therapy mismatch and clinical outcomes.

Methods. This multicenter observational cohort study included 150 episodes of symptomatic community-acquired UTIs caused by E. coli or K. pneumoniae. ESBL and AmpC production were detected phenotypically. Empirical therapy mismatch was defined as initial antibiotic therapy that was inactive against the isolated organism according to susceptibility testing. Outcomes included treatment failure within 14 days and recurrence within 30 and 90 days. Logistic regression was used to assess predictors of empirical therapy mismatch and treatment failure.

Results. ESBL production was detected in 44 isolates (29.3%), AmpC production in 16 isolates (10.7%), and ESBL and/or AmpC positivity in 54 isolates (36.0%). Six isolates were positive for both ESBL and AmpC phenotypes. Multidrug resistance was detected in 48 isolates (32.0%). Empirical therapy mismatch occurred in 42 episodes (28.0%). In multivariable logistic regression, ESBL phenotype was independently associated with empirical therapy mismatch (aOR 4.10, 95% CI 1.90–8.90; p < 0.001), as was prior antibiotic exposure within 90 days (aOR 2.05, 95% CI 1.00–4.20; p = 0.049). Empirical therapy mismatch was independently associated with treatment failure within 14 days (aOR 3.02, 95% CI 1.20–7.60; p = 0.019). ESBL/AmpC-positive infections also showed higher rates of treatment failure, antibiotic escalation, and recurrence.

Conclusions. Phenotypic ESBL and AmpC production were common among community-acquired E. coli and K. pneumoniae urinary isolates in Babylon, Iraq. Empirical therapy mismatch occurred in more than one-quarter of cases and was associated with poorer short-term outcomes. Our findings support local antibiogram-guided, risk-stratified empirical therapy with early culture-directed adjustment.

Association of serum galectin-3 levels and LGALS3 gene expression across albuminuria categories in patients with type 2 diabetes mellitus: A cross-sectional study

2026-09-14T16:26:40+03:00

Diabetic kidney disease (DKD) remains the leading cause of end-stage kidney disease worldwide because conventional markers, such as urinary albumin and the estimated glomerular filtration rate, are not sensitive enough to detect renal stress until significant damage has occurred. Galectin-3 (Gal-3), a β-galactoside-binding lectin encoded by the galectin-3 (LGALS3) gene, is implicated in renal fibrosis, macrophage-driven inflammation, and advanced glycation end-product signaling, making it a biologically plausible candidate biomarker.Methods. This cross-sectional study enrolled 90 adults with type 2 diabetes mellitus (T2DM), stratified by urinary albumin-to-creatinine ratio (UACR) into A1 (UACR < 30 mg/g), A2 (UACR 30–300 mg/g), and A3 (UACR > 300 mg/g) categories (n = 30 each), along with 30 age- and sex-matched healthy controls. Serum Gal-3 was measured by sandwich enzyme-linked immunosorbent assay (ELISA), and LGALS3 messenger RNA expression in peripheral blood mononuclear cells (PBMCs) was quantified by reverse transcription quantitative polymerase chain reaction. Discriminative performance was assessed using receiver operating characteristic (ROC) analysis, and the independent statistical association of Gal-3 was evaluated using multivariate logistic regression.Results. Serum Gal-3 was significantly elevated in normoalbuminuric T2DM patients compared to that in healthy controls (21.2 ± 3.6 vs 17.6 ± 3.8 ng/mL; p = 0.003) and rose progressively across albuminuria categories (A1 to A3; one-way analysis of variance [ANOVA] p < 0.001). The LGALS3 mRNA expression increased simultaneously. Serum Gal-3 showed good cross-sectional discriminative ability for any category of albuminuria A2/A3 vs A1; area under the curve 0.84, 95% CI 0.77–0.91, and remained independently associated with albuminuria after multivariate adjustment (odds ratio 1.42 per ng/mL; 95% CI 1.18–1.71; p < 0.001).Conclusion. Serum Gal-3 and LGALS3 expression levels are significantly associated with albuminuria in T2DM and may serve as complementary markers. However, future longitudinal validation studies are required to establish whether Gal-3 has a predictive value for the progression of diabetic kidney disease.

Malignant neoplasms of the kidney in Ukraine: Epidemiological indicators in different regions during 2018-2024

2026-09-14T16:26:40+03:00

The increase in cancer incidence in recent decades is a major problem today, and the need for further improvement in the diagnosis and treatment of patients prompts us to study the dynamics of epidemiological indicators in recent years.

The purpose of the study is to determine the dynamics of malignant neoplasms of the kidney (MNK) incidence and mortality, the number of all persons registered at the end of each year and newly diagnosed, including through medical examinations, with an analysis of the stages of pathology and the index of accumulation of contingents, in different regions of Ukraine in the period 2018-2024 years (ys).

Materials and Methods. The source of data was statistical collections for the analysis of absolute and relative epidemiological indicators of the prevalence and incidence of MNK, patient mortality and others in order to determine trends in the formation of pathology, forecasting and improving the development of onco-urological care. The data obtained was considered both for Ukraine as a whole, including the provinces, and for each of the five regions - Western (West.), Central (Centr.), North-Eastern (North-East.), South-Eastern (South-East.), Southern (South.) - and by their constituent regions, as well as in Kyiv. For statistical processing using the software package "SPSS for Windows. Version 11“ and ”MedStat" software, the chi-square test was used; the proportion of two groups was compared using Fisher's angular transformation (with Yates correction); a difference of p<0.05 was considered significant.

Results. The highest incidence of MNK in 2018–2021 was recorded in the South-East region, while the lowest rates were observed in the North-East and South. In 2022–2024, the West and Central regions had the highest incidence, whereas Kyiv and, during the last three years, the Southern region had the lowest rates. Despite a significant decrease in MNK incidence per 100,000 population from 2018 to 2019, the number of patients registered at the end of each year increased steadily from 2018 to 2024 (p<0.001), including those registered for more than 5 years. This increase was most pronounced in the Western and Central regions, particularly in Kyiv, Mykolaiv, Chernivtsi, and Odesa regions.

The accumulation index increased significantly in 2020 and remained high through 2024. The highest values were observed in the South-East and South regions and in Kyiv in 2022, when the national index also reached its maximum.

The proportion of newly diagnosed patients with stage I–II disease decreased significantly in all regions in 2020 and in Kyiv in 2021–2022, followed by recovery to 2018 levels in 2023–2024. This improvement coincided with an increase in cases detected during medical examinations to 14%, although this indicator had declined almost twofold between 2018 and 2022 (p<0.001). In Kyiv, it decreased from 60% to 52% (p=0.002).

The annual number of deaths from MNK, mortality per 100,000 population, and the proportion of patients who died within 1 year of diagnosis decreased gradually from 2018 to 2021, with a marked decline in 2022 (p<0.001), and remained stable thereafter.

Conclusions. The decline in MNK incidence and in the proportion of newly diagnosed stage I–II cases in 2020–2022 may reflect reduced opportunities for timely screening and preventive care during the COVID-19 pandemic and the beginning of hostilities. The significant decrease in the proportion of MNK cases detected during professional examinations in 2022 compared with 2018 represents an important negative socio-medical trend.

At the same time, the gradual decline in mortality, stabilization in 2023–2024, increasing numbers of patients remaining under follow-up, and the rise in the accumulation index since 2020 may indicate improved survival and continuity of care for patients with MNK in Ukraine.

Kidney graft and recipient survival according to donor type: А retrospective single-centre cohort study

2026-09-14T16:26:40+03:00

Over the past decade, kidney transplant recipient survival has improved due to advances in immunosuppressive therapy protocols, surgical techniques, and post-transplant monitoring. However, chronic kidney transplant dysfunction (graft rejection) and death of recipients with functioning grafts remain among the major clinical challenges in modern transplant nephrology worldwide. The latter is particularly important for Ukraine, where kidney transplantation continues despite the war and its associated challenges.

The aim of this study was to assess kidney graft and recipient survival according to donor type and to assess the main causes of patient death and graft loss.

Methods. This retrospective cohort study included 168 patients with stage 5 chronic kidney disease who underwent kidney transplantation between January 1, 2021, and September 1, 2024. After applying the inclusion criteria, data from 91 patients who underwent primary kidney transplantation were included in the final analysis. Fifty-three (58,24%) patients were male, and the mean age was 38.69 ± 10,77 years.

During follow-up, all deaths and their causes, as well as all cases of graft loss and their causes, were analyzed. The analysis was performed for the entire cohort and according to donor type: living related donor - Group 1 ( n=45/49,5%) or deceased - Group 2 (n=46/50,5% /).

For the survival analysis, the date of kidney transplantation was used as the starting point. Follow-up continued until death, loss to follow-up, or the end of the study (September 30, 2025), with a minimum follow-up period of 12 months.

Results. Cumulative recipient survival during the first year after transplantation was 84,2% in Group 1 vs 79,7% in Group 2 (P=0,5789), and 3-year survival was 81,4% vs 70,0% (log-rank: χ²= 1,4607; p=0,2268). During the follow-up period, 20 deaths were recorded. Regardless of donation type, the main causes of recipient death were infections (45,0%) and cardiovascular diseases (30,0%).

The overall 1-year graft survival was 80,3 ± 0,04%, and the 3-year - was 68,6 ± 0,06%. Cumulative 1- and 3-year graft survival were 86,2% vs 74,4% (P=0.1599) and 74,6% vs 61,8% (P=0.1926), respectively of kidneys from living and deceased donors (log-rank: χ²=1,0891, df=1, p=0,2967).

Conclusions. No statistically significant differences in recipient or kidney graft survival were found according to donor type.

Magnesium deficiency and cardiovascular calcification in patients with chronic kidney disease: A critical view of the problem

2026-09-14T16:26:40+03:00

Based on current world science data, the potential pathogenetic role of magnesium (Mg) deficiency in cardiovascular calcification processes in chronic kidney disease (CKD) can be confirmed. It has been determined that Mg deficiency can lead to ectopic calcification by affecting the formation of hydroxyapatite crystals, calciprotein particles, and the osteogenic differentiation of vascular smooth muscle cells, and that the direct and indirect effects of Mg are closely associated with endothelial damage/dysfunction. It has been shown that the pathogenetic and integrative significance of Mg deficiency is observed at all stages of the cardiorenal continuum; it takes an active part in the development of arrhythmias, sudden coronary death, manifestations of heart failure, and is one of the key elements in the complex mechanism of cardiac dysfunction and atherosclerosis. It is concluded that large-scale randomized controlled trials are warranted to definitively assess the efficacy and safety of correcting Mg deficiency as a potential tool for slowing the progression of ectopic calcification, reducing cardiovascular risk, and improving prognosis in CKD patients.

Models for screening and prediction of chronic kidney disease progression

2026-09-14T16:26:40+03:00

The course of chronic kidney disease (CKD) in its early stages is typically asymptomatic; therefore, in a significant proportion of patients, the disease is diagnosed incidentally or when clinical manifestations (hypertension, edema, etc.) appear. The current approach to risk stratification, diagnosis, and progression in CKD is based on analyzing the relationship between estimated glomerular filtration rate (eGFR) and albuminuria (primarily the albumin-to-creatinine ratio, ACR) using validated calculators. This study evaluated calculators for determining the probability of developing CKD (SCORED, QKidney, CKD-PC Incident CKD Risk) and its progression (Kidney Failure Risk Equation, KFRE). It was demonstrated that the most clinically useful sequence is as follows: risk-based selection of patients for testing, confirmation of CKD presence based on eGFR and ACR, and assessment of the rate of progression in patients with G3–G5 CKD using KFRE. A practical algorithm for the use of these tools by family physicians and nephrologists is proposed.