OBJECTIVES: Fabry disease (FD) is a rare disease associated with sphingolipid accumulation. Sphingolipids are components of plasma membranes that are important in podocyte function and accumulate in various glomerular diseases such as focal segmental glomerulosclerosis (FSGS). Both FD and FSGS can cause podocyte damage and are classified as podocytopathies. In this respect, FD and FSGS share the same pathophysiologic pathways. Previous screening studies have shown that a significant proportion of end-stage renal disease (ESRD) patients receiving hemodialysis (HD) have unsuspected [...] OBJECTIVES: Fabry disease (FD) is a rare disease associated with sphingolipid accumulation. Sphingolipids are components of plasma membranes that are important in podocyte function and accumulate in various glomerular diseases such as focal segmental glomerulosclerosis (FSGS). Both FD and FSGS can cause podocyte damage and are classified as podocytopathies. In this respect, FD and FSGS share the same pathophysiologic pathways. Previous screening studies have shown that a significant proportion of end-stage renal disease (ESRD) patients receiving hemodialysis (HD) have unsuspected

The Medical Bulletin of Sisli Etfal Hospital

Background and Objectives: Donor acute kidney injury (AKI) is increasingly recognized in deceased-donor kidney transplantation. However, its independent association with long-term graft outcomes remains controversial. We investigated whether donor AKI predicts death-censored graft failure (DCGF) after adjusting for confounding factors and competing risks. Materials and Methods: We conducted a retrospective cohort study of 285 deceased-donor kidney transplant recipients (146 with AKI donors, 139 with non-AKI donors). Propensity score matching (1:1 matching, caliper = 0.2 SD) created 110 matched pairs. The matched pair structure was accounted for in the competing risk regression by specifying robust variance estimation with clustering on matched pairs' IDs. The primary outcome was DCGF, analyzed using competing risk regression (Fine-Gray model) with patient death as a competing event. Secondary outcomes included delayed graft function (DGF), acute rejection, and patient survival. Results: After matching, baseline characteristics were well-balanced (all SMD 14 days (sHR 2.15, p=0.001), acute rejection (sHR 2.45, p<0.001), and expanded criteria donor status (sHR 1.98, p=0.005) were independent predictors of DCGF, while donor AKI severity showed no dose-dependent effect (p=0.586). Conclusions: Donor AKI does not independently predict long-term graft failure when confounding is minimized through propensity score matching and competing risks are appropriately modeled. Post-transplant factors, particularly DGF duration and acute rejection, are the dominant determinants of graft survival. These findings support the selective use of AKI donor kidneys in appropriate recipients and emphasize the importance of post-transplant management strategies, especially monitoring DGF duration.

Background: Early postoperative changes in creatinine-based estimated glomerular filtration rate (eGFR) after bariatric surgery can be misread as a kidney injury. During rapid weight loss, indexing eGFR to a fixed body surface area (BSA) of 1.73 m² may alter apparent trajectories. We compared absolute (mL/min) and BSA-indexed (mL/min/1.73 m²) eGFR changes after sleeve gastrectomy, stratified by baseline glomerular hyperfiltration (GH). Methods: In this retrospective cohort of 145 adults undergoing laparoscopic sleeve gastrectomy, serum creatinine was obtained at baseline (≤30 days pre-op) and 3 months (post-op days 75–105). Indexed eGFR was calculated with the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) 2021 creatinine equation; BSA with the Mosteller formula; and absolute eGFR as indexed eGFR × (BSA/1.73). GH was defined as indexed eGFR ≥ 120 mL/min/1.73 m². A REML mixed-effects model (Group, Time, Group × Time) with patient-cluster bootstrap inference was used. An age-adjusted sensitivity model including Age and Age × Time was also fitted. Results: Fifty-four participants (37%) met the GH criteria. Absolute eGFR declined by −26.6 mL/min in GH versus −17.3 mL/min in non-GH (difference-in-differences [DiD] −9.3 mL/min; 95% CI −13.9 to −4.7; p < 0.001). The indexed eGFR changes were smaller (−4.2 vs. −0.5 mL/min/1.73 m²; DiD −3.7; 95% CI −7.3 to −0.03; p = 0.048; bootstrap p_sign = 0.052). In the age-adjusted sensitivity model, the Group × Time interaction for absolute eGFR attenuated but remained statistically significant (−6.57 mL/min; 95% CI, −13.09 to −0.06; p = 0.048), whereas the corresponding interaction for indexed eGFR was attenuated and no longer statistically significant (−3.99 mL/min/1.73 m²; 95% CI −9.15 to 1.16; p = 0.129). Conclusions: Within three months after sleeve gastrectomy, participants with higher baseline indexed filtration showed a larger decline in absolute eGFR but only a small change in indexed eGFR. These results show that early postoperative creatinine-based eGFR trajectories are scale dependent and should be interpreted cautiously during rapid weight loss. Because postoperative acute kidney injury (AKI) was not adjudicated and direct kidney function markers were unavailable, this study does not distinguish physiological hemodynamic change from structural kidney injury. Reporting both absolute and indexed eGFR may improve early postoperative interpretation and help align dosing decisions with rapid changes in body size.

Background: Parvovirus B19 (B19V) has a well-established tropism for erythroid progenitor cells and is a recognized cause of anemia in immunocompromised individuals. Patients with end-stage renal disease (ESRD) receiving maintenance hemodialysis are predisposed to anemia due to multiple mechanisms and are frequently exposed to healthcare settings, raising concern that prior B19V infection may contribute to anemia severity or resistance to erythropoiesis-stimulating agents (ESAs). However, data regarding the clinical relevance of B19V seroprevalence in hemodialysis patients remain limited. Methods: We conducted a single-center, observational cross-sectional study including 131 adult patients on maintenance hemodialysis and 50 healthy controls. Parvovirus B19 IgG serostatus was assessed by enzyme-linked immunosorbent assay (ELISA) and used exclusively as a marker of prior (past) exposure rather than active infection; our aim was to determine whether IgG-defined prior exposure leaves a measurable long-term imprint on erythropoiesis. None of the participants had clinical features suggestive of acute parvovirus infection or an unexplained aplastic episode at enrollment. Demographic data, comorbidities, dialysis characteristics, ESA use, and laboratory parameters (hemoglobin, hematocrit, mean corpuscular volume, inflammatory markers, and albumin) were collected. Between-group and within-cohort comparisons used non-parametric tests, and multivariable logistic and linear regression models were used to adjust for age, sex, and other relevant covariates. Results: Parvovirus B19 IgG seropositivity was common in both groups (64.9% of hemodialysis patients vs. 48% of controls; crude odds ratio [OR] 2.00, 95% confidence interval [CI] 1.03–3.88, p = 0.043). However, hemodialysis patients were substantially older and more often male; after adjustment for age and sex, dialysis status was no longer independently associated with seropositivity (adjusted OR 1.4, 95% CI 0.8–2.3, p = 0.20), and within the hemodialysis cohort seropositivity was not associated with age or sex. Hemodialysis patients exhibited significantly lower hemoglobin and hematocrit and higher inflammatory markers than controls, consistent with ESRD-related anemia. Within the hemodialysis cohort, B19 IgG-positive and IgG-negative patients did not differ in hemoglobin, hematocrit, mean corpuscular volume, C-reactive protein, albumin, or ESA use, and IgG serostatus remained unrelated to hemoglobin in a multivariable model adjusting for age, sex, inflammation, nutrition, dialysis vintage, and ESA use (adjusted β = −0.20 g/dL, 95% CI −0.68 to 0.28, p = 0.42). Past Parvovirus B19 exposure was therefore not associated with anemia severity or treatment requirements. Conclusions: In this cohort of stable maintenance hemodialysis patients, prior Parvovirus B19 exposure, as indicated by IgG seropositivity, was not associated with increased anemia severity, inflammation, or ESA use, and the higher crude seroprevalence in dialysis patients was attributable to their older age rather than to dialysis itself. Because IgG reflects past exposure only and IgM and viral DNA were not assessed, these findings apply strictly to past (IgG-defined) exposure and cannot address active or persistent B19V infection. They suggest that routine Parvovirus B19 IgG screening in asymptomatic hemodialysis patients is unlikely to be useful for anemia management, whereas active or persistent infection—detectable only by molecular testing—remains the more plausible contributor to unexplained or refractory anemia and merits study in selected patients.

Subarachnoid hemorrhage (SAH) induces a sympathetic surge and systemic inflammation that may impair renal perfusion and glomerular integrity. Although the vagus nerve is central to autonomic and anti-inflammatory regulation, its relationship to renal structural injury in severe SAH is unclear. This study evaluated whether electrophysiological vagal CAP amplitude correlates with glomerular integrity in an experimental SAH model. Nineteen rabbits were assigned to control (n = 5), sham (n = 5), and SAH groups (n = 9). SAH was induced by daily cisterna magna injections of autologous blood for three days, and animals were followed for 14 days; those that did not survive to the 14-day endpoint formed the SAH-Nonsurvivor subgroup (n = 4). Vagal compound action potential (CAP) amplitude (mV) was recorded electrophysiologically and used as the principal physiologic readout of vagal nerve integrity. Renal tissue and perirenal parasympathetic ganglia were analyzed histologically and stereologically to quantify degenerated neurons and atrophic glomeruli (per mm³). Vagal CAP amplitude decreased from 1.42 ± 0.36 mV in controls to 0.34 ± 0.11 mV in the SAH-Nonsurvivor subgroup (p < 0.001), while atrophic glomeruli increased from 4 ± 1 to 98 ± 11 per mm³. Degenerated neuronal density peaked in the SAH-Nonsurvivor subgroup (98 ± 19 per mm³). Vagal CAP amplitude was inversely correlated with glomerular injury (Spearman ρ = –0.89, p < 0.001). In this small exploratory study, reduced vagal CAP amplitude was associated with greater glomerular injury after severe SAH. These hypothesis-generating findings warrant confirmation in larger, adequately powered studies before any physiologic or translational interpretation can be made.