Unclogging the effects of the Angiojet® thrombectomy system on kidney function: a case report

Background AngioJet® is an increasingly used method of percutaneous mechanical thrombectomy for the treatment of patients with arterial and venous thromboses. AngioJet® has been shown to cause intravascular haemoylsis universally. We report the case of a 29 year old patient who underwent AngioJet® thrombectomy and post-procedure developed a stage 3 Acute kidney injury (AKI.) requiring renal replacement therapy (RRT), secondary to intravascular haemolysis. We aim to explore the mechanism and potential risk factors associated with developing AKI in these patients and suggest steps to optimise patient management. Case presentation A 29 year old Caucasian male who developed a stage 3 AKI, requiring RRT, following AngioJet® thrombectomy for an occluded femoral vein stent. Urine and laboratory investigations showed evidence of intravascular haemolysis, which was the likely cause of AKI. Following a brief period of RRT he completely recovered renal function. Conclusions AKI is an increasingly recognised complication following AngioJet® thrombectomy, but remains underappreciated in clinical practice. AKI results from intravascular haemolysis caused by the device. Up to 13% of patients require RRT, but overall short-term prognosis is good. Pre-procedural risk factors for the development of AKI include recent major surgery. Sodium bicarbonate should be administered to those who develop renal impairment. Renal biopsy is high risk and does not add to management. Increased clinician awareness and vigilance for AKI post-procedure can allow for early recognition and referral to nephrology services for ongoing management.

How to use Donath-Landsteiner test to diagnose paroxysmal cold haemoglobinuria (PCH)

Paroxysmal cold haemoglobinuria (PCH) accounts for around a third of cases of autoimmune haemolytic anaemia in children. PCH is caused by an autoantibody that fixes complement to red cells at low temperatures and dissociates at warmer temperatures (a biphasic haemolysin), triggering complement-mediated intravascular haemolysis. Named the Donath-Landsteiner (D-L) antibody after its discoverers, it is usually formed in response to infection and demonstrates specificity for the ubiquitous red cell P-antigen. A D-L test can be used to detect the presence of the D-L autoantibody in the patients’ serum. Here we discuss the use of the D-L test in identifying PCH in a 2-year-old boy who presented with haemolytic anaemia. A summary of the key information can be found in the infographic.

Immune-mediated Coombs negative intravascular haemolysis in systemic lupus erythematosus (SLE)

A 27-year-old woman presented with a history of excessive hair loss, loss of appetite, loss of weight, amenorrhoea and loss of axillary and pubic hair for 6 months followed by fever and vomiting for 5 months and abdominal pain for 1 month. During the course of her illness, the patient developed intravascular haemolysis as evidenced by a drop in haemoglobin, indirect hyperbilirubinaemia, raised lactate dehydrogenase (LDH) and haemoglobinuria. Examination revealed severe pallor, mild icterus, elevated jugular venous pressure, generalised lymphadenopathy and hyperpigmentation. Investigations revealed severe anaemia, indirect hyperbilirubinaemia, raised LDH and negative Coombs test. Antinuclear antibody and anti-dsDNA, anti-Sm and anti-SS-A/Ro antibodies were positive and complement C3 was low. The patient was diagnosed to have systemic lupus erythematosus and immune-mediated intravascular haemolysis and was treated with prednisolone and hydroxychloroquine. Haemolysis resolved following steroid therapy, and during follow-up, there were no further episodes of haemolysis.

Intravascular haemolysis after transcatheter aortic valve implantation with self-expandable prosthesis: incidence, severity, and impact on long-term mortality

We aimed to determine the incidence, severity, and long-term impact of intravascular haemolysis after self-expanding transcatheter aortic valve implantation (TAVI). We believe this should be evaluated before extending the indications of TAVI to younger low-risk patients. Prospective, academic, single centre study of 94 consecutive patients treated with supra-annular self-expandable TAVI prosthesis between April 2009 and January 2014. Haemolysis at 1-year post-TAVI was defined per the published criteria based on levels of haemoglobin, reticulocyte and schistocyte count, lactate dehydrogenase (LDH), and haptoglobin. All patients had long-term clinical follow-up (6 years). The incidence of haemolysis at 1-year follow-up varied between 9% and 28%, based on different haemolysis definitions. Haemolysis was mild in all cases, no patient had markedly increased LDH levels. The presence of moderate/severe paravalvular aortic regurgitation was associated with haemolysis (7.7% vs. 23.1%, P = 0.044) and aortic valve area post-TAVI did not differ between groups with or without haemolysis (1.01 vs. 0.92 cm2/m2, P = 0.23) (definition including schistocyte count). The presence of haemolysis did not have any impact on patient prognosis after 6 years with log-rank test P = 0.80. Intravascular haemolysis after TAVI with self-expandable prosthesis is present in 9–28% of patients depending on the definition of haemolysis. The presence of haemolysis is associated with moderate/severe paravalvular aortic regurgitation but not with post-TAVI aortic valve area. Haemolysis is mild with no impact on prognosis.

P. falciparum Malaria induced Renal impairment

Introduction: The involvement of the kidney in falciparum malaria has been known for decades. In 1944, Spitz observed acute renal failure due to falciparum infection in soldiers during World War II. This observation was later supported by other workers who detected oliguria developing in patients with black water fever. The initial clinical pattern is that of reversible renal dysfunction or pre-renal azotemia, which rapidly progresses to acute tubular necrosis if treatment is not started early. Patients with malaria induced renal failure are hypercatabolic with blood urea and serum creatinine levels rising rapidly.Oliguric as well non-oliguric renal failure are observed and duration of oliguric renal failure ranges from a few days to several weeks depending on the severity of renal dysfunction. Acute renal failure in falciparum malaria is usually associated either with acute intravascular haemolysis or heavy parasitemia. Acute renal failure in falciparum malaria is also observed in patients with severe intravascular haemolysis resulting in haemoglobinuria. It may be induced by malarial fever or by anti-malarial drugs in a patient with or without G6-PD deficiency. Materials and Methods: This is a hospital based cross sectional study carried out in a total of 50 cases of acute renal failure who were selected from diagnosed patients of P. falciparum malaria. Cases were confirmed either by P. falciparum antigen test and/or peripheral blood smear test(both thick and thin smear).Malarial ARF (MARF) is diagnosed when serum creatinine level > 3 mg/dl, and/or urine output < 400 ml/24hrs despite adequate rehydration. Result: Out of 174 cases of falciparum malaria 50 patients (28.7%) had acute renal failure in falciparum malaria. 36 (72%) cases were males and 14 (28%) were females, indicating a much higher incidence in males. Approximately 78% of the cases in the present study were below the age of 40 years. The youngest was 15 years old and the oldest was 61 years old (Mean age – 32 ± 11.6 years). All were febrile (100%) and a majority had oliguria or anuria (72%); jaundice was detected in 30 (60%) patients on presentation. Hepatomegaly & Splenomegaly were found in 76% & 66% of the cases respectively. Out of the total 50 cases of malaria induced ARF, 14 cases (28%) had pre-renal ARF while in the majority, 72% the clinical course was that of ATN. The pathogenesis of ATN in the 36 cases was found to be heavy parasitaemia in 40% of the cases, IV hemolysis with haemoglobinuria in 3 (6%) of cases; and cholestatic jaundice in 26% of falciparum patients. Examination of the urinary sediments revealed that albumin was present in urine in 40 cases (80%). Majority of the patients had significant rise in blood urea level with a mean value of 177 mg. S. creatinine levels ranged between 3.2 - 13.6 mg with a mean value of 7.83 mg. The mean creatinine clearance rate was 11.71 ml/min. The overall mortality rate was 26%. Conclusion: AKI is common in Falciparum malaria. The pathogenesis of AKI is largely unknown but may be related to the erythrocyte sequestration and agglutination within the renal microcirculation interfering with flow and metabolism. Clinically and pathologically, this syndrome manifests as Pre-renal azotemia and acute tubular necrosis. Acute renal failure may occur simultaneously with other vital-organ dysfunction (in which case the mortality risk is high) or may progress as other disease manifestations resolve. Early dialysis or hemofiltration considerably enhances the likelihood of a patient’s survival, particularly in acute hypercatabolic renal failure. Severity of oliguria and presence of one or more associated complications like pulmonary oedema, acidosis, and altered sensorium have considerable influence on the outcome of the patients.