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The aim of this study is to describe a case of haemoglobinuria in a cat after near-drowning. A 6-year-old male neutered domestic short hair cat weighing 6.5 kg with a pre-existing seizure disorder presented to an emergency hospital after near-drowning in a swimming pool during a seizure episode. On presentation, the patient was obtunded, dyspnoeic, bradycardic and hypothermic. Imaging revealed evidence of severe bilateral pulmonary infiltrates. Treatment with intravenous diazepam, amoxicillin, fluid therapy, active warming and oxygen therapy was administered. The cat developed haemoglobinuria approximately 6 h after nearly drowning. Despite improvements in mentation, pulse quality and heart rate, respiratory compromise and poor oxygen saturation persisted, prompting euthanasia approximately 10 h after admission. To the author's knowledge, this is the first reported clinical case of haemoglobinuria following near-drowning in veterinary medicine., (© 2024 The Authors. Veterinary Medicine and Science published by John Wiley & Sons Ltd.)

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 (R 2  = 0.63, P < 0.01) and number of PFA applications (R 2  = 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., Competing Interests: Funding Support and Author Disclosures Dr. Chierchia has received compensation for teaching purposes and proctoring from Medtronic, Abbott, Biotronik, Boston Scientific, and Acutus Medical. Dr. Burkhardt is a consultant for Biosense Webster and Stereotaxis. Dr. Di Biase is a consultant for Biosense Webster, Boston Scientific, Stereotaxis, and St. Jude Medical and has received speaker honoraria from Medtronic, Atricure, EPiEP, and Biotronik. Dr. de Asmundis has received research grants on behalf of the center from Biotronik, Medtronic, Abbott, LivaNova, Boston Scientific, AtriCure, Philips, and Acutus and compensation for teaching purposes and proctoring from Medtronic, Abbott, Biotronik, Livanova, Boston Scientific, Atricure, Acutus Medical, and Daiichi Sankyo. Dr. Dello Russo is a consultant for Abbott Medical. Dr, Natale is a consultant for Abbott, Biosense Webster, Biotronik, Boston Scientific, and iRhythm. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

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., Competing Interests: K. Nath reports being a scientific advisor or member of the Journal of the American Society of Nephrology and Mayo Clinic Proceedings. N. Leung reports consultancy agreements with AbbVie, Lilly, and Omeros; reports having an ownership interest in Checkpoint Therapeutics; and reports receiving research funding from Alnylam and Omeros; reports being a scientific advisor or member of the Journal of Nephrology. All remaining authors have nothing to disclose., (Copyright © 2021 by the American Society of Nephrology.)

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 01 st July-31 st 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 » (86.8%), pallor (63.2%), hepatomegaly (50%). Glomerular filtration flow was less than 80 mL/min/1.73m 2 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)., Competing Interests: Les auteurs ne déclarent aucun conflit d’intérêts., (© Hamidou Savadogo et al.)

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 cm 2 , 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., (Copyright © 2019 European Society for Vascular Surgery. Published by Elsevier B.V. All rights reserved.)

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., (Copyright © 2018 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.)

Competing Interests: Competing interests We have read and understood The BMJ policy on declaration of interests and declare that we have no competing interests.

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., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Ltd (unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

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.

A 25-year-old man developed macroscopic haemoglobinuria after a persistent dry cough. Although chest radiograph findings were normal, since the serum antibody for Mycoplasma pneumoniae was significantly elevated, a diagnosis infection with this organism was made. Despite the absence of apparent anaemia, a marked increase in serum haemolytic markers and positive result for urine haemoglobin indicated the haemolysis of red blood cells, which was likely to have occurred secondarily to M. pneumoniae infection. Shortly after the initiation of a macrolide antibiotic, clarithromycin, the patient's haemoglobinuria completely disappeared together with a complete resolution of his respiratory symptoms. In this case, due to the lymphocyte-stimulatory nature of M. pneumoniae, an enhanced immune response, such as the production of cold agglutinins, was likely to be involved in the pathogenesis of erythrocyte haemolysis. The immunomodulatory property of clarithromycin was thought to repress the increased immunological reaction and thus enable the resolution of the urine abnormality.

Atypical hemolytic uremic syndrome (aHUS) is a life-threatening thrombotic microangiopathy, and as many as 70% of patients with aHUS have mutations in the genes encoding complement regulatory proteins. Eculizumab, a humanized recombinant monoclonal antibody targeting C5, has been used successfully in patients with aHUS since 2009. The standard maintenance treatment requires life-long eculizumab therapy, but the possibility of discontinuation has not yet been tested systematically. We report the safety of discontinuing eculizumab treatment in 10 patients who stopped treatment with the aim of minimizing the risk of adverse reactions, reducing the risk of meningitis, and improving quality of life while also reducing the considerable treatment costs. Disease activity was monitored closely at home by means of urine dipstick testing for hemoglobin. During the cumulative observation period of 95 months, 3 of the 10 patients experienced relapse within 6 weeks of discontinuation, but then immediately resumed treatment and completely recovered. Our experience supports the possibility of discontinuing eculizumab therapy with strict home monitoring for early signs of relapse in patients with aHUS who achieve stable remission., (Copyright © 2014 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Hemolysis and consequent hemoglobinuria is a well-known cause of acute kidney injury (AKI). Hemolysis has been associated with malpositioned prosthetic valves, but other prosthetic devices may rarely be associated with red cell shear stress. We report a case of a 56-year-old man who presented with hemolysis, AKI, and anemia. During workup, he was found to have anti-phospholipid antibodies, leading to a presumptive diagnosis of catastrophic anti-phospholipid antibody syndrome. However, further investigation revealed the cause of hemolysis to be from aortic root graft dysfunction. Following replacement of the prosthesis, there was complete resolution of his hemolysis and recovery of renal function. This case underscores the need to consider cardiac prosthetic devices in patients presenting with hemoglobinuric AKI.

Microwave assisted liver resection is a useful technique, especially when haemostasis could be difficult to achieve with conventional methods. However, prolonged administration of microwaves can be responsible for intraoperative haemoglobinuria. We describe the first case of acute haemolysis secondary to microwave assisted liver resection.

To evaluate the association between haemoglobinuria and chronic kidney disease (CKD) in sickle cell anaemia (SCA), we analysed 356 adult haemoglobin SS or Sβ(o) thalassaemia patients from the University of Illinois at Chicago (UIC) and 439 from the multi-centre Walk-Treatment of Pulmonary Hypertension and Sickle Cell Disease with Sildenafil Therapy (Walk-PHaSST) cohort. CKD was classified according to National Kidney Foundation Kidney Disease Outcomes Quality Initiatives guidelines. Haemoglobinuria, defined as positive haem on urine dipstick with absent red blood cells on microscopy, was confirmed by enzyme-linked immunosorbent assay in a subset of patients. The prevalence of CKD was 58% in the UIC cohort and 54% in the Walk-PHaSST cohort, and haemoglobinuria was observed in 36% and 20% of the patients, respectively. Pathway analysis in both cohorts indicated an independent association of lactate dehydrogenase with haemoglobinuria and, in turn, independent associations of haemoglobinuria and age with CKD (P < 0·0001). After a median of 32 months of follow-up in the UIC cohort, haemoglobinuria was associated with progression of CKD [halving of estimated glomerular filtration rate or requirement for dialysis; Hazard ratio (HR) 13·9, 95% confidence interval (CI) 1·7-113·2, P = 0·0012] and increasing albuminuria (HR 3·1, 95% CI: 1·3-7·7; logrank P = 0·0035). In conclusion haemoglobinuria is common in SCA and is associated with CKD, consistent with a role for intravascular haemolysis in the pathogenesis of renal dysfunction in SCA., (© 2013 John Wiley & Sons Ltd.)

Objective: The purpose of this article is to study the incidence, risk factors, and treatment of gross hemoglobinuria and oliguria following sclerotherapy for venous malformations., Materials and Methods: The clinical records and imaging studies of 131 patients with venous malformations (57 male and 74 female patients; age range, 2-58 years) who underwent sclerotherapy at our institution between July 1993 and August 2007 were reviewed. Demographic data, the location and estimated size of the malformation, the type and dose of the sclerosing agents, development of postprocedural hemoglobinuria and oliguria, and the treatment given were documented and analyzed., Results: Four hundred seventy-five sclerotherapy procedures were performed on 131 patients, with the number of procedures per patient ranging from 1 to 21 (mean, 3.6 procedures). Sodium tetradecyl sulfate was used in 47% of the procedures, ethanol in 27%, and both agents in 26%. Transient hemoglobinuria occurred after 34% of the sclerotherapy procedures, and 57% of these were associated with transient oliguria, with increased risk with higher adjusted doses (sclerosant volume/weight of patient) for both agents. Resolution of the hemoglobinuria and oliguria with hydration, alkalinization, and diuretics occurred in all patients. The risk of hemoglobinuria increased with higher adjusted dose (sclerosant volume/weight of patient) for both agents and with sclerotherapy of venous malformations affecting the lower extremities and multiple locations., Conclusion: Transient hemoglobinuria and oliguria are common complications of sclerotherapy for venous malformation. Nevertheless, with proper fluid management, all the patients promptly recovered. The risk correlates with the volume of sclerosant (adjusted to patient's weight) and is higher for lower extremity and multiple locations.

Intravascular hemolysis is a rare but potentially life threatening cause of red urine characterized by brisk hemolysis and release of large amounts of hemoglobin into the urine. We present an unusual case of red urine in a 20-year-old male who was subsequently diagnosed with intravascular hemolysis due to an aorto-atrial fistula. Fistula formation was likely secondary to a recently implanted atrial septal occluder, which is a reported but exceedingly rare complication of the device. We discuss the diagnostic approach to hemolytic anemia and conclude with a literature review of other cases of device associated fistula formation and hemolysis.

A 54-year-old woman was scheduled for the total hip replacement. She was anesthetized with continuous epidural blockade combined with general anesthesia using oxygen, sevoflurane, and propofol. When she received her autologous blood transfusion, we noticed the obstruction of the venous line, and pushed 30 ml of blood with 10 ml syringe. However, it was difficult to return her blood through the venous line. At that time, a sudden onset of red urine without any special symptom occurred. We investigated the cause of the red urine, whether this urine is attributable to hemoglobinuria, myoglobinuria, or porphyria. According to the patient's symptoms during and after the operation, and blood as well as urine examination, a microfilter in the venous line might have led to red blood cell destruction. The filter-induced hemolysis can be life-threatening especially in a child. We conclude that the early recognition and management of reactions associated with blood transfusion is essential during the operation.

A 57-year-old man with lung tumor was scheduled for right middle lobectomy under general anesthesia. The patient received glycerin enema 2 hours before anesthesia. Anesthesia was induced with propofol, fentanyl, ketamine and vecuronium. After the induction, urine of dark-red color was drained through the urinary catheter. Massive (3+) occult blood and few erythrocytes in the urine sediment were observed. Furthermore, blood analysis showed hemolysis with mild renal dysfunction (Cr 1.3 mg x dl(-1)). Although serum CPK and myoglobin increased, there was no apparent symptom that supported the onset of rhabdomyolysis induced by anesthetics, acute myocardial infarction or malignant hyperthermia. At this time, we noticed that blood sample taken before the induction had been hemolysed. With all the above information in mind, we suspected that the main cause of the hemoglobinuria could be the enema and the surgery was canceled. The patient made a good progress with laboratory data normalized on the 4th postanesthesia day. However, rectal ulcer developed as a possible late complication of the enema. Although it is well-known that glycerin enema could cause hemolysis, renal failure and rectal ulcer, the increase of CPK and myoglobin in serum made the diagnosis difficult from other conditions leading to rhabdomyolysis in this case.

A 56-year-old man underwent replacement of the ascending aorta with a sutureless intraluminal graft, for a Stanford type A aortic dissection. Eight years after the operation, he developed gross hemoglobinuria, associated with an intravascular hemolytic anemia. Due to numerous schistocytes in the peripheral blood, the hemolysis was attributed to mechanical injury of the red blood cells at the site of the vascular graft. The patient's course was complicated by an infection of the aortic graft, which led to an urgent graft replacement. The hemolytic anemia resolved completely shortly after the reoperation. Physicians should consider this etiology in the differential diagnosis of fragmentation hemolytic anemia.

Radiofrequency ablation is a safe and effective treatment for small primary or secondary liver tumors. Development of new probes has allowed the use of radiofrequency ablation for ablation of tumors > 5 cm in the liver. We present a case of acute intravascular hemolysis and hemoglobinuria during radiofrequency ablation of a large 8-cm hepatocellular carcinoma via laparotomy. The hemolysis was recognized during the operation by change of urine color, and prompt management was initiated to prevent acute renal failure. Literature search revealed that radiofrequency ablation can induce hemolysis in experimental setting, but this is the first clinical report of acute hemolysis during radiofrequency ablation for liver tumors.

Haemoglobinuria and periumbilical discoloration (also known as Cullen's sign) are clinical signs uncommonly reported in veterinary patients. This report describes a case of retroperitoneal haemorrhage in a dog, associated with haemoglobinuria and Cullen's sign. To the authors' knowledge, these clinical signs have not previously been reported singularly or in combination with retroperitoneal haemorrhage in dogs. A neutered male Shetland sheepdog, which was presented for haematuria, also had an abdominal mass, abdominal pain and a large area of periumbilical discoloration. Laboratory studies determined that haemoglobinuria was the cause of the red-coloured urine. Abdominal radiographs suggested a splenic mass and a coeliotomy was performed. During the induction and throughout the anaesthetic period the dog was hypertensive and a large haematoma originating from the right retroperitoneal space was identified at surgery. The cause of the haemorrhage was uncertain but a ruptured phaeochromocytoma was thought possible on the basis of the persistent hypertension and the location of the haemorrhage.

Parturient haemoglobinuria is a disease of economic importance in buffalo rearing countries in general and in India, Pakistan and Egypt in particular. This study reviews the information on aetiology, epidemiology, clinical aspects and treatment of parturient haemoglobinuria in buffaloes. The body of literature reviewed suggests that phosphorus deficiency in the diet of affected animals plays a major role in causing this disease, although the precise mechanism involved is complex. The possible factors involved and their interplay, plus the clinical picture of affected animals and the results of different preventive and therapeutic regimes are discussed. The study also identifies areas for further research.

A 4-month-old, 6.8-kg, castrated male pygmy goat was examined for recurrent episodic fever and red urine of 7 days' duration. A second, 3-month-old, 7-kg, intact female pygmy goat was presented for similar clinical signs. The red discoloration of the urine in each case was determined to be due to hemolysis with subsequent hemoglobinuria. In both cases, hemolysis and hemoglobinuria were closely associated with the goats consuming large volumes of water from a human infant's nipple bottle. A diagnosis of water intoxication-induced hemolysis and hemoglobinuria was made. Episodes of hemoglobinuria in the first case were consistently associated with dilute (specific gravity < 1.010) urine. Water intoxication has been associated with bottle-feeding in human infants and is also widely reported in human psychiatric patients. The small erythrocytes in goats appear to be the most sensitive of the domestic species to hypotonicity-induced hemolysis.

Gross hemoglobinuria following mitral valve replacement can represent a rare form of hemolytic anemia. This condition can masquerade as gross hematuria in the post-valve replacement patient. It is commonly associated with valvular dysfunction, specifically, perivalvular leakage. The leakage may not be apparent on routine echocardiography but it may be documented with trans-esophageal echocardiography.

A 2-year-old spayed female Shetland Sheepdog had recurrent episodes of discolored urine. Treatments administered for presumed urinary tract infection did not prevent recurrence. Episodes of pigmenturia appeared to correlate with stressful situations or excessive activity. Examination of urine sediment consistently revealed that RBC were not evident, despite a positive result for blood on urinalysis. This was suggestive of hemoglobinuria, and diagnostic testing was instituted to determine the underlying cause. Results of alkaline and osmotic fragility tests were useful in determining that an increase in erythrocyte fragility was the underlying cause of the recurrent pigmenturia. Erythrocyte fragility testing should be considered in animals that do not respond to appropriate treatments for pigmenturia.

Between January 1985 and March 1986, in the high altitude area of Kivu, Eastern Zaïre, 38 patients presenting with hemoglobinuria as main manifestation were investigated. Profound glucose-6-phosphate dehydrogenase deficiency was detected in 4 patients, leptospirosis in 2 and Hantaan virus infection in 2. Hemolysis was doubtful (haptoglobin > 40 mg/dl, Hemoglobin > 12 g/dl) in 2 patients. Other potential causes of hemoglobinuria such as hemoglobinopathy, toxic agents, infectious diseases or blood transfusion incompatibility were carefully screened and excluded. The syndrome observed in the remaining 28 cases was strongly suggestive of blackwater fever (BWF) as described in malaria patients by several authors under the french name "fièvre bilieuse hémoglobinurique". Quinine was used as curative treatment of malaria before admission in a significant greater proportion (p < 0.01) of patients with BWF compared to patients with uncomplicated malaria, suggesting that this drug might have played a triggering role in the genesis of BWF. However, quinine was usually administered at inadequate doses to malaria patients non responding to chloroquine and belonging to a population of whom 50% are non immune. It may thus also be hypothesized that BWF in our patients could result from a hyperparasitemic state that remained undetected because of an unusual synchronous lysis of infected erythrocytes. In the latter case BWF would correspond to a major complication of falciparum malaria only coincidentally related to the use of quinine.

Hemoglobinuria, defined as hemoglobin or hemoglobin subunits in the urine, is an easily monitored, sensitive indicator of renal handling of hemoglobin-based blood substitutes. Hemoglobin tetramer dissociation increases filtration by the kidneys. When the rate of filtration exceeds reabsorption, hemoglobinuria occurs. This study investigates the renal filtration and absorption of polyethylene glycol-modified bovine hemoglobin by monitoring for hemoglobinuria in several model systems.

A 13-year-old boy presented with acute hemolytic anemia a few days after mumps infection. The ensuing hemoglobinuria resulted in acute renal failure in this child, which was corrected with fluid and alkali therapy. We draw attention to this uncommon complication of mumps and the need for careful evaluation.

Severe acute hemoglobinemia and hemoglobinuria developed in a 17-year-old Japanese male with no history of exposure to any oxidizing agents. Examination of erythrocyte enzyme activity revealed that the patient's erythrocyte glutathione peroxidase (GSH-Px) activity was decreased to about a half that in control cells. Serum selenium (Se) concentration was within normal limits. Family studies showed that GSH-Px activity in the erythrocytes of two siblings was similarly decreased. It was suggested that the proband was suffering from a hereditary heterozygous GSH-Px deficiency, which appeared to be associated with acute hemolysis.

The case history is presented of two patients with attacks of cherry-red urine after strenuous exercise. Both had varicosity of the long saphenous veins. Haemoglobinuria disappeared after crossectomy of the long saphenous vein and resection of the convolutes. After one and two years, they have no recurrence.

A case of hemolytic transfusion reaction, accompanied by hypotension and followed by transient renal failure, occurred after the transfusion of 1 unit of previously frozen autologous red cells. Subsequent investigation revealed the probable cause of the hemolysis to be inadequate deglycerolization of the unit. The cause of the associated symptoms is unknown. Possibilities include nephrotoxic effects of hemoglobin or stroma, toxic effects of glycerol, or release of vasoactive or thrombogenic substances from lysed red cells. This case of a hemolytic reaction adds to the known risks of autologous transfusion.

A 2-year-old Suffolk gimmer presented with clinical signs of haemoglobinuria, jaundice, anaemia and acute mastitis. Clinical investigation and bacteriological examination of milk samples revealed Clostridium perfringens type A to be the causal agent.

The authors present two infants with isoimmune hemolytic disease due to ABO incompatibility complicated by massive hemoglobinuria and secondary acute renal failure. This represents an incidence of 0.36% of all neonates with ABO hemolytic disease in the author's newborn population. Only two patients have been reported previously to have similar complications. Analysis of data of these four infants revealed the clinical characteristics of this complication of ABO incompatibility: 1) very low frequency; 2) early onset of hemoglobinuria (first voided urine) and of acute renal failure (first 2 days of life); 3) lack of correlation between the clinical presentation of hemolytic disease and appearance and severity of renal failure; 4) complete recovery of renal functions following intravenous fluid administration; and 5) normal renal radiologic investigations.

Postparturient haemoglobinuria occurred in 11 Holstein-Friesian cows in 8 dairy herds in East Gippsland, Victoria. The affected cows had a wide range of ages, body condition and production level. Seven of 9 cows sampled were hypophosphataemic, 4 of 8 cows examined had Heinz bodies present in erythrocytes and strong ketonuria was present in 6 of 10 urine samples tested. Herdmates having similar calving dates had mostly normal serum phosphorus levels and none had Heinz bodies. There was no evidence for dietary phosphorus (P) deficiency, hypocuprosis or excessive P drain from high production being predisposing factors. There were no cruciferous plants in the diet. Haemolysis persisted in 4 cows despite treatment to raise serum P levels. An hyposthesis is proposed for the sporadic nature and clinical manifestations of the disease. This is based on mechanisms of hypophosphataemia occurring in man and mechanisms of Heinz body formation and haemolysis in other circumstances. We suggest that hypophosphataemia occurs following recovery from preparturient keto-acidosis caused by undernutrition in late pregnancy and then becoming nutritionally replete in the early postparturient period. Circulating oxidants may cause erythrocyte damage which may be predisposed to by hypophosphataemia.

A three-month-old baby with persistent intravascular hemolytic anemia following patch closure of subpulmonic ventricular septal defect was reported. Mechanical hemolysis was diagnosed by the presence of blood cell fragments and schistocytes in peripheral blood smear. It was thought that destruction of red cells developed by turbulent flows and direct contact of red blood cells with bared rough surfaces of the teflon patch at the site of dehiscence. When the cause of severe hemolysis was attributed to inadequate intracardiac repairs, immediate second surgical intervention should be performed.