Seminars in Dialysis最新文献

This report describes a novel and effective salvage strategy for managing perigraft seroma complicated by a small-caliber expanded polytetrafluoroethylene arteriovenous graft (AVG). Our patient developed a persistent seroma near the arterial anastomosis following AVG placement. The patient underwent successful seroma removal and delayed graft recanalization after 1 week of spontaneous graft thrombosis, which permitted partial tissue incorporation. The treatment was successful, achieving complete resolution of the seroma and restoration of graft function. The patient has remained free of recurrence for 40 months of follow-up. This approach represents an effective strategy for treating perigraft seromas of hemodialysis grafts.

Background: Renal replacement therapy (RRT) is crucial for end-stage renal disease, yet its pulmonary effects remain unclear. Fractional exhaled nitric oxide (FeNO) serves as a biomarker for airway inflammation. This study evaluates FeNO levels in hemodialysis (HD) and peritoneal dialysis (PD) patients and their relationship with pulmonary function.

Methods: RRT patients aged 18-65, followed for at least 2 years in our nephrology clinic, were included. FeNO tests were performed after routine blood sampling. The study comprised 110 patients: 50 HD, 30 PD, and 30 controls.

Results: FeNO levels before and after dialysis were statistically significantly higher in HD patients compared to PD patients (p = < 0.001 for both). Exhaled NO levels measured in the control group were 7.6 ± 5.2 ppb and were statistically significantly lower compared to HD patients before and after dialysis (p = < 0.001 for both). A negative correlation was observed between FeNO and FEV1 and FVC percent (R = -0.807, p = 0.01; R = -0.801, p = 0.01, respectively). A positive correlation was observed between exhaled NO levels before and after dialysis and ΔFVC, ΔFEV1, and ΔPEF25-75 (R = 0.74, p = 0.01; R = 0.74, p = 0.01; R = 0.89, p = 0.01, respectively).

Conclusion: This study showed that FeNO levels were significantly higher in HD patients before and after RRT compared to PD and healthy controls, suggesting a greater impact of HD on airway inflammation. FeNO measurement may serve as a biomarker for monitoring pulmonary health in RRT patients.

Background: Intradialytic hypotension (IDH) is a common and clinically significant complication in patients undergoing chronic hemodialysis. The application of low-temperature dialysate has been proposed as a potential intervention to mitigate this condition; however, its effectiveness requires further evaluation through systematic reviews and meta-analyses.

Methods: A comprehensive literature search of articles published up to April 10, 2025, systematically searched electronic databases (PubMed, Embase, CINAHL, and Cochrane Library). Quality assessment was performed using the Cochrane Risk of Bias 2 tool for randomized crossover trials.

Result: Low dialysate temperature significantly decreases the incidence of IDH (OR = 0.35, 95% CI: [0.28, 0.46], p < 0.001), increases mean arterial pressure (SMD = 0.67, 95% CI: [0.38, 0.96], p < 0.001), and mean systolic blood pressure (SMD = 0.54, 95% CI: [0.30, 0.79], p < 0.001). Additionally, low dialysate temperature improves urea clearance dialysis adequacy (SMD = 0.25, 95% CI: [0.03, 0.47], p = 0.029) and urea reduction rate (SMD = 0.24, 95% CI: [0.02, 0.47], p = 0.035), while decreasing intradialytic mean body temperature (SMD = -0.68, 95% CI: [-0.99, -0.37], p < 0.001). The subgroup analysis revealed that dialysate temperatures between 34.5°C and 35.0°C were more effective in improving these related outcomes compared to temperatures ranging from 35.1°C to 36.0°C.

Conclusions: Maintaining low dialysate temperatures between 34.5°C and 36.0°C is recommended to reduce the incidence of IDH and improve dialysis adequacy in chronic hemodialysis patients. The specific low dialysate temperature should be individualized to minimize IDH risk, enhance patient comfort, and optimize treatment outcomes.

Background: Knowledge of residual kidney function is potentially useful in patients receiving hemodialysis for risk stratification, adjusting the dialysis prescription, and early identification of renal function recovery. However, periodic urine collection is problematic. We examined the potential of predicting residual kidney creatinine (water) clearance (KrCrW) without urine collection using a creatinine kinetic model, which allows KrCrW to be estimated based on previously measured or anthropometrically estimated creatinine generation rate (GCr), volume of distribution (VdCr), and measured predialysis serum creatinine.

Methods: Studies were done in 12 patients receiving once weekly hemodialysis and 12 other patients being dialyzed twice a week in whom KrCrW was measured by collection of urine. GCr and VdCr were taken either from the modeling outputs or were estimated from anthropometric values.

Results: The mean modeled GCr was 1091 ± 377 (SD) mg/day, similar to the value predicted by an anthropometric equation suggested by Ix et al. (1198 ± 304). The mean kinetically modeled VdCr was 22.7 ± 2.4 L, somewhat lower than expected. The KrCrW from urine collection was 7.43 ± 4.07 mL/min. Predicted KrCrW from modeled GCr, modeled VdCr, and measured predialysis serum creatinine was similar (7.35 ± 4.01, r² = 0.987) with an average error less than 1%. When anthropometric estimates of GCr and VdCr were used as inputs, the mean modeled KrCrW was somewhat higher (8.66 ± 4.27, y = 1.09x, R² = 0.585) and the mean error was 1.23 ± 2.6 mL/min.

Conclusions: Residual kidney creatinine clearance (KrCrW) can be estimated in patients receiving one or two dialysis treatments weekly based on creatinine kinetic modeling. Using anthropometric estimates of GCr and VdCr in the modeling equations yields similar values of KrCrW to those when modeled GCr and VdCr inputs are used, but with a substantial error. A strategy of using a baseline modeled values of GCr and VdCr for future KrCrW change prediction may be promising, but the stability of GCr over time needs to be confirmed.

Background: In hyponatremic patients, concurrent dialysate flow during hemodialysis may be an ideal option to mitigate complications such as osmotic demyelination syndrome (ODS).

Methods: Present randomized controlled trial enrolled dialysis-requiring chronic kidney disease (CKD) and acute kidney injury (AKI) patients with serum sodium levels < 125 mEq/L during January 2020 over 16 months. Hemodynamically unstable patients, as well as those with a history of seizures and neurological conditions, were excluded. All were randomized to concurrent and countercurrent dialysate flow groups during two-h dialysis session. Hydration status was evaluated by Body Composition Monitor BCMTM and hourly sodium was estimated to guide ultrafiltration. Comparative analysis of sodium correction rates (meq/L/h) during dialysis, neurological deterioration via Mini-Mental State Examination (MMSE) scores, and ODS during 1 week and 1 month in both groups was done. Two-way repeated measures ANOVA was used to compare sodium correction trends.

Results: A total of 44 hyponatremic patients of AKI (17.39%), CKD (56.52%) and acute on CKD (26.09%) were randomized to concurrent (n = 23) and countercurrent (n = 21) dialysate groups. Postdialysis sodium correction rate was nonsignificantly slower in the concurrent group (45.45%) vs. the countercurrent group (36.36% group, p = 0.44). Neurological deterioration, measured via MMSE scores, and ODS incidence were absent in both groups. The concurrent group exhibited a higher proportion of patients without neurological deterioration (73.91%) compared to the countercurrent group (57.14%, p = 0.241). Comparable survival between the two groups was seen at 10, 20, and 30 days. No significant risk factors for mortality were identified in either group.

Conclusion: Concurrent dialysate flow demonstrates a slower but nonsignificant rate of sodium correction, making it a safer alternative for managing severe hyponatremia during hemodialysis by reducing the risk of rapid neurological shifts.

Background: Previous studies suggested adjusting insulin doses during hemodialysis to reduce intra- and post-hemodialysis hypoglycemia. However, the impact of insulin adjustment on cardiovascular morbidity and mortality in diabetic patients with end-stage renal disease (ESRD) remains unclear. Although reducing hypoglycemia is a well-documented benefit of insulin dose modification in this population, the broader metabolic and inflammatory consequences-particularly those related to cardiovascular risk-are not well understood. This study aimed to investigate the effects of a 25% reduction in total daily insulin dose on hemodialysis days in T2DM patients with ESRD, focusing on daily blood glucose profiles, glycated albumin, IL-6, and TNF-α.

Methods: A multicenter study with clinical trials was designed in five hemodialysis centers. It was a 4-week clinical trial involving 17 eligible type 2 diabetic patients with ESRD on insulin therapy and regular hemodialysis. Self-monitoring blood glucose was performed seven times a day before, during, and 1 month after the intervention. Blood samples were collected before and after the intervention. The Wilcoxon test was used to assess differences in daily glucose profiles, glycated albumin, IL-6, and TNF-α before and after insulin dose adjustment.

Results: After 1 month of adjusting total daily insulin dose during hemodialysis, no statistically significant difference was observed in daily blood glucose, IL-6, and TNF-α levels. However, glycated albumin levels increased both before and after the insulin dosage modification.

Conclusions: Reducing the total daily insulin dose by 25% during hemodialysis day effectively reduces hypoglycemia incidence intra- and post-hemodialysis in T2DM patients with ESRD without impacting pro-inflammatory factors IL-6 and TNF-α, which are associated with increased cardiovascular morbidity and mortality risk.

Objective: We investigated the clinical characteristics and treatment outcomes of heparin-induced thrombocytopenia (HIT) following therapeutic plasma exchange (TPE) with heparin anticoagulation in patients with neurological autoimmune diseases.

Methods: Clinical data were prospectively collected from 158 patients (79 males, 79 females; mean age 37.49 ± 16.95 years) with neurological autoimmune diseases who underwent TPE in the neuro-intensive care unit between January 2016 and June 2024. For patients with continuous platelet decline after TPE, the 4Ts score was determined, and platelet factor 4 (PF4) antibody tests were performed. Their platelet counts, clinical complications (thrombosis and bleeding), treatment plans, outcomes, and prognoses before and after TPE were analyzed.

Results: One hundred thirty-nine patients experienced at least one significant decrease in platelet count during TPE (average decrease 36.75 ± 19.63%), and the average 4Ts score was 3.55 ± 1.87 points. PF4 antibody testing was conducted on 23 patients with continuous platelet decline and 4Ts scores ≥ 4. Four PF4-positive patients were diagnosed with type II HIT and developed deep vein thrombosis. After heparin withdrawal, the platelet count gradually normalized after intravenous immunoglobulin (IVIG), nonheparin TPE, or argatroban/fondaparinux anticoagulant therapy (mean recovery time 8.17 ± 3.54 days). The platelet counts spontaneously recovered for the remaining 116 patients (mean recovery time 3.88 ± 2.66 days).

Conclusion: Platelet counts should be dynamically monitored throughout TPE with heparin anticoagulation. Patients with continually decreasing platelet counts and an intermediate to high 4Ts score should be monitored for HIT. Heparin should be discontinued immediately for patients with type II HIT, and nonheparin anticoagulants, IVIG, or nonheparin TPE may be administered.

The aim of this review is to summarize the literature on the pathophysiology, diagnosis, and etiology of adrenal insufficiency (AI) in dialysis patients. The prevalence of AI in dialysis patients is unknown, and AI appears to be an uncommon complication associated with dialysis. Data in the literature on the impact of chronic kidney disease and dialysis on adrenal function give conflicting results. Patients with end-stage renal disease are at risk of hypercortisolism due to loss of the nychthemeral cortisol cycle. Dialysis itself may lead to a rebound in cortisol synthesis at the end of dialysis session. Nevertheless, it has recently been suggested that dialysis vintage was associated with loss of adrenal function and with the onset of AI, and that among chronically hypotensive dialysis patients, the prevalence of AI may be as high as 20%. In dialysis patients, adrenal function is preserved, and AI is rare. AI is difficult to diagnose and often goes unnoticed, as symptoms are nonspecific and diminish with dialysis, which partially corrects them. Diagnosis is therefore delayed and often occurs during an adrenal crisis. For hemodialysis patients, diagnosis is based on blood cortisol measurements before and after an ACTH stimulation test, which are performed at the start of dialysis, regardless of the dialysis session schedule. Salivary cortisol measurements can be used instead of blood cortisol measurements for peritoneal dialysis patients to avoid venipunctures. Situations suggestive of AI in dialysis patients include history or current low-dose corticosteroid therapy, unexplained chronic arterial hypotension, recurrent hypoglycemia, and unexplained hypercalcemia.

For patients with end-stage renal failure, hemodialysis is a crucial renal replacement therapy, which is meaningful to alleviate patients' symptoms and prolong survival. The principle of hemodialysis is to exchange the substances in the blood and dialysis solution through a semipermeable membrane and to discharge the excess water, metabolic waste, and electrolytes into the dialysis solution, which can balance the water, electrolytes, and acid-base. However, patients on maintenance hemodialysis are at high risk of developing cardiovascular and cerebrovascular diseases. Therefore, the composition of dialysis fluid has been widely studied, and the use of sugar-containing dialysis fluid can reduce the incidence of hypoglycemia, hypotension, and cardiovascular and cerebrovascular complications in hemodialysis patients. This article reviews the effects of current glucose-containing dialysate on cardiovascular and cerebrovascular outcome events in hemodialysis patients.

Objective: Multiple in vitro and in vivo studies indicate that there is a significant amount of dialysis catheter lock leak with tunneled and nontunneled dual lumen hemodialysis (HD) catheters. The impact of heparin 1000 unit/mL HD catheter lock on outcomes in patients on therapeutic heparin has not been previously reported.

Methods: Twenty-nine patients with 42 patient events on HD or continuous renal replacement therapy (CRRT) via double lumen catheters were retrospectively analyzed. Study patients received heparin 1000 unit/mL HD catheter lock while on therapeutic intravenous heparin. All patients had stable activated partial thromboplastin times (PTT) prior to catheter locking and had a PTT drawn within 6 h after administration of the heparin HD catheter lock.

Results: The average prelock PTT was 56 s and postlock PTTs increased on average to 85 s (p < 0.0001). PTTs were significantly higher when drawn closer to the administration time of the heparin catheter lock. Major bleeding occurred in many surgical patients after heparin HD catheter lock administration.

Conclusion: Citrate or saline HD catheter lock may be preferable to heparin HD catheter lock in patients on intravenous heparin infusions, especially in high-bleed-risk surgical patients.