Acute Kidney Injury Resulting From Hemoglobinuria After Pulsed-Field Ablation in Atrial Fibrillation: Is it Preventable?

BACKGROUND: High-voltage pulses can cause hemolysis. OBJECTIVES: The authors evaluated the occurrence of hemoglobinuria after pulsed-field ablation (PFA) and its impact on renal function in patients with atrial fibrillation (AF). METHODS: A consecutive series of patients with AF undergoing PFA were included in this analysis. The initial patients who did not receive postablation hydration immediately after the procedure were classified as group 1 (n = 28), and the rest of the study patients who received planned fluid infusion (0.9% sodium chloride ≥2 L) after the procedure were categorized as group 2 (n = 75). RESULTS: Of the 28 patients in group 1, 21 (75%) experienced hemoglobinuria during the 24 hours after catheter ablation. The mean postablation serum creatinine (S-Cr) was significantly higher than the baseline value in those 21 patients (1.46 ± 0.28 mg/dL vs 0.86 ± 0.24 mg/dL, P < 0.001). Of those 21 patients, 4 (19%) had S-Cr. >2.5 mg/dL (mean: 2.95 ± 0.21 mg/dL). The mean number of PF applications was significantly higher in those 4 patients than in the other 17 patients experiencing hemoglobinuria (94.63 ± 3.20 vs 46.75 ± 9.10, P < 0.001). In group 2 patients, no significant changes in S-Cr were noted. The group 2 patients received significantly higher amounts of fluid infusion after catheter ablation than did those in group 1 (2,082.50 ± 258.08 mL vs 494.01 ± 71.65 mL, P < 0.001). In multivariable analysis, both hydration (R2 = 0.63, P < 0.01) and number of PFA applications (R2 = 0.33, P < 0.01) were independent predictors of postprocedure acute kidney injury. CONCLUSIONS: On the basis of our findings, both the number of PFA applications and postablation hydration were independent predictors of renal insult that could be prevented using planned fluid infusion immediately after the procedure.

March hemoglobinuria progressed to acute kidney injury after kendo practice: a case report.

BACKGROUND: March hemoglobinuria is caused by a hemolytic mechanism due to transient hematuria after physical exercise which, although rare, may lead to acute kidney injury. We report a case of a patient with march hemoglobinuria induced by kendo, which was diagnosed by the presence of Berlin blue iron staining in the proximal tubules through renal biopsy. CASE PRESENTATION: A 15-year-old male complained of fever (37 °C), general malaise, and nausea after hard kendo sessions. Laboratory findings revealed indirect bilirubin dominant hyperbilirubinemia (total bilirubin 3.8 mg/dL), high lactate dehydrogenase (LDH), and acute kidney injury (serum creatinine: 3.11 mg/dL and estimated glomerular filtration rate: 26 mL/min/1.73m2). Urine test was positive for occult blood but without hematuria. Renal biopsy was performed to clarify the cause of renal injury, which showed minor glomerular abnormalities. Meanwhile, hemosiderin deposition was identified in the proximal tubules by Berlin blue iron staining, and lysosomes were observed to contain granular iron. In addition to clinical background of strenuous kendo exercise, renal biopsy led to a definitive diagnosis of march hemoglobinuria. CONCLUSIONS: March hemoglobinuria is a hemolytic disease that can occur after intense exercise, especially kendo. Considering its rarity due to the lack of critical symptoms, it is important to note that occult blood-positive findings may be indicative of march hemoglobinuria if the patient underwent strenuous exercise. Therefore, clinicians should be aware of this possibility to provide timely and appropriate treatment.

Safety and efficacy of microwave versus radiofrequency ablation for large hepatic hemangioma: a multicenter retrospective study with propensity score matching.

OBJECTIVES: To compare the safety and efficacy of microwave ablation (MWA) and radiofrequency ablation (RFA) for such hemangiomas (5-9.9 cm in diameter). METHODS: This multicenter retrospective cohort study investigated the differences in technical success, ablation time, complete ablation, complications, hospital stay, and clinical response between MWA and RFA. A total of 452 patients with hepatic hemangiomas were screened. Propensity score matching was performed. Univariable and multivariate regression analyses were used. RESULTS: Among the 452 patients, 394 met the eligibility criteria and completed the follow-up. After the propensity score matching analysis, 72 pairs of patients were created. No technical failures were found. The RFA group had a longer ablation time (48.63 ± 18.11 min versus [vs.] 37.18 ± 15.86 min, p < 0.001), higher morbidity of hemoglobinuria (77.78% vs. 50.00%, p < 0.001), and longer hospital stay (5.01 ± 1.56 days vs. 4.34 ± 1.42 days, p < 0.05) than the MWA group. The treatment methods (p = 0.032, OR = 0.105, 95% CI = 0.013-0.821), size of the hemangioma (p = 0.021, OR = 5.243, 95% CI = 1.285-21.391), and time of ablation (p = 0.031, OR = 1.145, 95% CI = 1.013-1.294) were significant independent risk factors associated with hemoglobinuria. No recurrence or delayed complications were observed. There were no differences in complete ablation, clinical response, and health-related quality of life between the groups. CONCLUSIONS: MWA and RFA appear to be effective treatments for large hepatic hemangiomas. However, MWA had a shorter ablation time than RFA, and MWA was associated with fewer hemolysis-related complications and shorter hospital stays. KEY POINTS: • MWA and RFA appear to be effective treatments for large hepatic hemangiomas. • MWA had a shorter ablation time than RFA. • MWA was associated with fewer hemolysis-related complications and shorter hospital stays.

Hemoglobinuria in the Early Poststem-Cell-Transplant Period: Risk Factors and Association with Outcomes.

Background: Information on risk factors of hemoglobinuria after hematopoietic stem-cell transplant (HSCT) and its association with AKI, mortality, and engraftment is limited. Methods: We conducted a retrospective cohort study on all consecutive adults that underwent HSCT from January 6, 1999, to November 6, 2017. The study included 6039 patients that underwent bone marrow transplantation (BMT), umbilical cord blood, and peripheral blood stem-cell transplantation (PBSCT). Results: Early post-HSCT, AKI occurred in 393 (7%) patients, and 52 (0.9%) patients had post-HSCT hemoglobinuria. Post-HSCT hemoglobinuria was associated with graft type (BMT+Cord), underlying disease (lymphoma, acute leukemia), and fludarabine-based conditioning regimen. Post-HSCT hemoglobinuria was associated with early (48-72 hours) post-HSCT AKI. Graft type (BMT+Cord) was associated with AKI among patients with hemoglobinuria. AKI in patients with hemoglobinuria was associated with delayed platelet engraftment and delayed WBC engraftment but not 100-day mortality. Conclusion: Close monitoring is recommended in this patient group to facilitate a good engraftment outcome.

Haemolytic anaemia: a consequence of COVID-19.

A man in his early 50s presented with jaundice, mild shortness of breath on exertion and dark urine. He had had coryzal symptoms 2 weeks prior to admission. Medical history included obstructive sleep apnoea and hypertension. His initial blood tests showed a mild hyperbilirubinaemia and acute kidney injury stage 1. Chest X-ray and CT pulmonary angiogram were negative for features suggestive of COVID-19. He later developed a drop in haemoglobin and repeat bloods showed markedly raised lactate dehydrogenase and positive direct antiglobulin test. These results were felt to be consistent with a haemolytic anaemia. A nasopharyngeal swab came back positive for COVID-19. We suspect the cause of his symptoms was an autoimmune haemolytic anaemia secondary to COVID-19 which has recently been described in European cohorts.

Case Report: Spherocytic Hemolytic Anemia after Envenomation by Long-Nosed Viper (Vipera ammodytes).

Snakebite envenoming is a major health issue in many parts of the world, especially in rural areas. Vipera ammodytes is the commonest cause of snakebite in Greece. We report our experience with a patient bitten by such a snake, who developed massive intravascular hemolysis characterized by a spherocytic rather than microangiopathic hemolytic picture. This case illustrates the potential of snakebite envenoming to cause spherocytic hemolytic anemia associated with hemoglobinuria and acute renal failure, and represents the first report of V. ammodytes in this context. Another important point is that antivenom was rapidly effective in reversing spherocytic hemolytic anemia, even though several hours had elapsed since the bite.

Risk Factors for Macroscopic Haemoglobinuria After Sclerotherapy Using Ethanolamine Oleate for Venous Malformations.

OBJECTIVES: Sclerotherapy is an essential component of the treatment for venous malformations, and ethanolamine oleate (EO) is known as a useful sclerosing agent. However, macroscopic haemoglobinuria (MH) and subsequent renal impairment are severe complications after sclerotherapy using EO. The present study aimed to clarify the MH risk factors for better peri-operative management of venous malformations. METHODS: Data collected during 130 procedures involving 94 patients who were undergoing sclerotherapy using EO for venous malformation were retrospectively analysed. Pre-operative and operative variables, including sex, age, pre-operative body mass index, location, depth, type of lesion, size, number of procedures, type of drainage vein, ratio of sclerosant to air, and injected total dose of 5% EO per body weight (BW), were examined. Univariable analysis and multivariable logistic regression were performed to determine the possible risk factors for MH. RESULTS: Following sclerotherapy, MH occurred in 27.7% of patients, but no patient developed post-operative renal impairment because of aggressive hydration and haptoglobin administration. On univariable analysis, diffuse lesion, lesion size ≥50 cm2, and total injected dose of 5% EO ≥ 0.18 mL/kg were found to be the MH risk factors. Multivariable logistic regression analysis identified a total injected dose of 5% EO ≥ 0.18 mL/kg as the significant independent factor contributing to MH risk. CONCLUSIONS: Macroscopic haemoglobinuria is a reversible complication if immediate and appropriate interventions with aggressive hydration and haptoglobin administration are performed; therefore, it should be closely monitored following sclerotherapy, especially when using 5% EO ≥ 0.18 mL/kg.

[Hemoglobinuria in children hospitalized in Ouagadougou: short term inpatient care and prognosis]. / Hémoglobinurie chez l'enfant à Ouagadougou: prise en charge hospitalière et pronostic à court terme.

INTRODUCTION: The purpose of this study was to analyze the epidemiological, diagnostic, therapeutic and evolutionary features of hemoglobinuria in children hospitalized in the Pediatric University Hospital Charles de Gaulle, Ouagadougou. METHODS: We conducted a cross-sectional descriptive study over the period 01st July-31st December 2014. All children aged 0-15 years hospitalized in the Department of Medical Pediatrics of the Pediatric University Hospital Charles de Gaulle and diagnosed with macroscopic hemoglobinuria during the study period were enrolled. RESULTS: Thirty-eight patients were included in the study. Hospitalization rate for hemoglobinuria was 1.9%. The average age of patients was 80.8 ± 44.1 months (ranging from 21 to 168). The study involved 23 boys (60.5%) and 15 girls (39.5%). The major clinical signs were: fever (86.8%), dark urines like « coca cola ¼ (86.8%), pallor (63.2%), hepatomegaly (50%). Glomerular filtration flow was less than 80 mL/min/1.73m2 in 23 patients (69.7%); 21 patients had Glucose-6-phosphate dehydrogenase (G6PD) deficiency. The main suspected causes of hemoglobinuria were: severe malaria, bacterial and viral infections, G6PD deficiency, biliary haemoglobinuric fever. Treatments included: artemisinin derivatives, antibiotics and antipyretics. One patient underwent dialysis. CONCLUSION: Hemoglobinuria is a symptom mainly causing diagnostic problems in our context. It is a severe disorder which can result in acute renal failure (ARF).

Risk factors of haemoglobinuria after microwave ablation of liver tumours.

AIM: To explore the risk factors predicting haemoglobinuria after ultrasound-guided percutaneous microwave ablation (MWA) of liver tumours and discuss the treatments and outcomes. MATERIALS AND METHODS: The present study comprised 2,829 patients admitted for liver tumours treated with MWA from Jan 2011 to April 2017. Ethics committee approval was waived and informed consent for treatment procedures were obtained from the patients. Haemoglobinuria after MWA was found in 149 patients. The influence of 19 risk factors was assessed. Binary logistic regression and receiver operating characteristic (ROC) curve analysis were used for statistical analysis. The treatments and outcomes of patients with haemoglobinuria were summarised. RESULTS: By univariate analysis, histopathology, liver cirrhosis, MWA volume, MWA energy, and MWA duration were significant risk factors. By multivariate analysis and ROC curve, MWA energy, duration, and volume were identified as predictors of haemoglobinuria after MWA. Drug treatments including kidney protection, adequate hydration, alkalisation of urine, and diuresis were administrated to the patients with haemoglobinuria. One patient progressed to acute kidney injury (AKI) while others had good clinical outcomes. CONCLUSION: Haemoglobinuria is a controllable side effect after MWA of liver tumours, which is related to high MWA energy, long MWA duration, and great MWA volume. It usually caused few side effects on renal function with correct treatment.

Efectos adversos de la acumulación renal de hemoproteínas. Nuevas herramientas terapéuticas / Adverse effects of the renal accumulation of haem proteins. Novel therapeutic approaches

La hemoglobina y la mioglobina son hemoproteínas que juegan un papel fundamental en el organismo ya que participan en el transporte de oxígeno. Sin embargo, debido a su estructura química, estas moléculas pueden ejercer efectos deletéreos cuando se liberan al torrente sanguíneo de forma masiva, como sucede en determinadas condiciones patológicas asociadas a rabdomiólisis o hemólisis intravascular. Una vez en el plasma, estas hemoproteínas se pueden filtrar y acumular en el riñón, donde resultan citotóxicas, principalmente para el epitelio tubular, e inducen fracaso renal agudo y enfermedad renal crónica. En la presente revisión analizaremos los distintos contextos patológicos que provocan la acumulación renal de estas hemoproteínas, su relación con la pérdida de función renal a corto y largo plazo, los mecanismos fisiopatólogicos responsables de sus efectos adversos y los sistemas de defensa que contrarrestan tales acciones. Por último, describiremos los distintos tratamientos utilizados actualmente y mostraremos nuevas opciones terapéuticas basadas en la identificación de nuevas dianas celulares y moleculares, prestando especial atención a los diversos ensayos clínicos que se encuentran en marcha en la actualidad (AU)

Haemoglobin and myoglobin are haem proteins that play a key role as they help transport oxygen around the body. However, because of their chemical structure, these molecules can exert harmful effects when they are released massively into the bloodstream, as reported in certain pathological conditions associated with rhabdomyolysis or intravascular haemolysis. Once in the plasma, these haem proteins can be filtered and can accumulate in the kidney, where they become cytotoxic, particularly for the tubular epithelium, inducing acute kidney failure and chronic kidney disease. In this review, we will analyse the different pathological contexts that lead to the renal accumulation of these haem proteins, their relation to both acute and chronic loss of renal function, the pathophysiological mechanisms that cause adverse effects and the defence systems that counteract such actions. Finally, we will describe the different treatments currently used and present new therapeutic options based on the identification of new cellular and molecular targets, with particular emphasis on the numerous clinical trials that are currently ongoing (AU)

Mistaken identity: haemoglobinuria secondary to paravalvular leak masking as haematuria.

Haemolytic anaemia caused by a paravalvular leak presenting as progressively worsening red urine. Haemoglobinuria was easily mistaken for gross haematuria, resulting in extensive invasive urological investigation that proved to be futile. Further investigation following an emergency admission led to the realisation that intravascular haemolysis secondary to a paravalvular leakâ€"presenting 43 years following metallic valve insertionâ€"was the cause of discoloured urine and newly presenting symptomatic anaemia. This case highlights that there remains other causes of what often appears to be haematuria, and further exploration of alternative causes should be considered when no urological cause is found.

Hemoglobinuria-related acute kidney injury is driven by intrarenal oxidative reactions triggering a heme toxicity response.

Intravascular hemolysis can result in hemoglobinuria with acute kidney injury. In this study we systematically explored two in vivo animal models and a related cell culture system to identify hemoglobinuria-triggered damage pathways. In models of stored blood transfusion and hemoglobin (Hb) exposure in guinea pigs and beagle dogs we found that hemoglobinuria led to intrarenal conversion of ferrous Hb(Fe(2+)) to ferric Hb(Fe(3+)), accumulation of free heme and Hb-cross-linking products, enhanced 4-hydroxynonenal reactivity in renal tissue, and acute tubule injury. These changes were associated in guinea pigs with activation of a renal cortex gene expression signature indicative of oxidative stress and activation of the unfolded protein response (UPR). Tubule cells of hemolytic animals demonstrated enhanced protein expression of heme oxygenase and heat shock protein and enhanced expression of acute kidney injury-related neutrophil gelatinase-associated lipocalin. These adverse changes were completely prevented by haptoglobin treatment. The in vivo findings were extrapolated to a MS-based proteome analysis of SILAC-labeled renal epithelial cells that were exposed to free heme within a concentration range estimate of renal tubule heme exposure. These experiments confirmed that free heme is a likely trigger of tubule barrier deregulation and oxidative cell damage and reinforced the hypothesis that uncontrolled free heme could trigger the UPR as an important pathway of renal injury during hemoglobinuria.

Red Kidney: Kidney Transplant From a Deceased Donor Who Received Massive Blood Transfusion During Cardiopulmonary Bypass.

Here, we present a case of a deceased-donor kidney transplant. The brain-dead donor had received a massive blood transfusion during cardiopulmonary bypass, which lead to hemolysis, hemoglobinuria, acute kidney injury, and renal replacement therapy. The kidney appeared red after in situ flush. Postoperatively, the recipient developed delayed graft function. Protocol biopsy during the postoperative period revealed the widespread deposition of heme pigment in the renal tubules. Massive blood transfusion and cardiopulmonary bypass surgery are associated with hemolysis and heme pigment deposition in the renal tubules, which subsequently lead to acute kidney injury. Kidneys from such donors appear red and, while this does not preclude transplant, are likely to develop delayed graft function.