Bilateral Renal Vein Thrombosis Research Articles

A Case of NELL-1-Positive Membranous Nephropathy With Acute Kidney Injury Due to Bilateral Renal Vein Thrombosis

A Case of NELL-1-Positive Membranous Nephropathy With Acute Kidney Injury Due to Bilateral Renal Vein Thrombosis

PB0298 Catheter-Directed Thrombolysis and Systemic Anticoagulation for IVC and Bilateral Renal Vein Thrombosis in a Septic Neonate

PB0298 Catheter-Directed Thrombolysis and Systemic Anticoagulation for IVC and Bilateral Renal Vein Thrombosis in a Septic Neonate

Double trouble - management of perinephric hematoma and renal vein thrombosis post percutaneous renal biopsy

BackgroundPerforming percutaneous renal biopsy procedures in lupus nephritis (LN) and nephrotic syndrome presents a unique challenge to the nephrologist because of the risk of bleeding from the procedure and the hypercoagulable state in hypoalbuminemia. The management of a patient with venous thrombosis with perinephric hematoma post renal biopsy can be difficult if occurred.Case presentationWe are presenting a case of perinephric hematoma following percutaneous renal biopsy in a 23-year-old man with lupus nephritis, nephrotic syndrome, and lower limbs deep vein thrombosis (DVT). The patient developed persistent frank haematuria, flank pain and acute urinary retention post-procedure. We have withheld his oral warfarin three days before the procedure, and no anticoagulation was given subsequently. Initial CT Angiography (CTA) renal showing stable hematoma and no visible evidence of vascular injury. Three weeks later, the patient still has persistent frank haematuria and a repeated CTA renal revealed new bilateral renal vein thrombosis. Considering the high risk of worsening symptomatic venous thrombosis, we gave subcutaneous enoxaparin sodium and restart oral warfarin despite ongoing haematuria. The frank haematuria resolved within two days of anticoagulation with no radiological evidence of worsening of the perinephric hematoma. The follow-up ultrasonography a month later showed resolution of the hematoma and renal vein thrombosis with no adverse effect.ConclusionOur experience, in this case, highlighted the importance of case selection for percutaneous renal biopsy among high-risk patients. Additionally, a prolonged frank haematuria in post-renal biopsy with nephrotic syndrome warranted a reassessment, as a clinical presentation of post-procedure perinephric hematoma and renal vein thrombosis can overlap. We also demonstrated that restarting anticoagulation earlier than four weeks in a patient with renal vein thrombosis and post-renal biopsy perinephric hematoma can be safe in the selective case.

The value of repeat kidney biopsy during an atypical course of membranous nephropathy

BackgroundThe clinical trajectory for patients with primary membranous nephropathy ranges widely from spontaneous remission to a rapid decline in kidney function. Etiologies for rapid progression with membranous nephropathy include concurrent bilateral renal vein thrombosis, malignant hypertension, and crescentic membranous nephropathy. Given the wide heterogeneity in prognosis, timing of immunosuppressive therapy is often challenging and centers around an individual patient’s perceived risk for rapidly progressive disease.Case presentationHerein, we describe the clinical course of a young patient who initially developed a typical presentation of membranous nephropathy with consistent kidney biopsy findings. Given clinical stability, a six month observation period was undertaken prior to initiating immunosuppression. Within this observation window, the patient developed community acquired pneumonia followed several weeks later by a sudden, rapid decline in kidney function requiring dialysis. Repeat kidney biopsy revealed post-infectious glomerulonephritis superimposed upon a background of membranous nephropathy. Immunosuppressive therapy resulted in a favorable long-term outcome with normalization of kidney function and remission of nephrotic syndrome. To our knowledge, this is the first report of the simultaneous occurrence of these two glomerular disease processes.ConclusionThis case illustrates the value of repeat kidney biopsy during an atypical course of membranous nephropathy. Superimposed glomerular disease processes should be considered during a course of rapidly progressive membranous nephropathy.

POS-100 THE VALUE OF REPEAT KIDNEY BIOPSY WHEN THE COURSE OF MEMBRANOUS NEPHROPATHY IS ATYPICAL

The clinical trajectory for patients with primary membranous nephropathy ranges widely from spontaneous remission to rapid declining kidney function. Etiologies for rapid progression with membranous nephropathy include concurrent bilateral renal vein thrombosis, malignant hypertension, and crescentic membranous nephropathy. Given the wide heterogeneity in prognosis, timing of immunosuppressive therapy is often challenging and centers around an individual patient’s perceived risk for rapidly progressive disease.

Case of COVID-19 and Acute Pancreatitis: A Case Report

Background: Respiratory symptoms, including cough, shortness of breath, and fever, have been reported to be the most common symptoms of Coronavirus disease (COVID-19). However, extra respiratory symptoms, such as gastrointestinal manifestations, have also been reported. Case Presentation: In our paper, we report a case of a 32-year-old African female patient with no previous medical history who presented to the emergency department with altered mental status for one day. The patient had a history of fever, epigastric pain, decreased oral intake, vomiting, and diarrhea. Initial laboratory findings revealed elevated blood glucose, amylase, lipase, blood urea nitrogen, and creatinine levels. Urine ketones were also positive, and blood gases demonstrated severe metabolic acidosis. The patient was admitted to the intensive care unit as a case of diabetic ketoacidosis, acute kidney injury and acute pancreatitis that was later confirmed by computed tomography imaging, where it revealed bilateral renal vein thrombosis with left kidney infarction. Additionally, reverse transcriptasepolymerase chain reaction (RT‒PCR) confirmed COVID-19. The patient improved significantly following conservative management and anticoagulation and was discharged home. Conclusion: Our case demonstrates the importance of considering COVID-19 as a possible cause of acute pancreatitis and that acute kidney infarctions should be part of the differential diagnosis of acute kidney injury in patients who are COVID-19 positive.

MO322VENOUS THROMBOEMBOLISM AND NEPHROTIC SYDROME: A FAMOUS BUT STILL SURPRISING COUPLE

Abstract Background Venous thromboembolism (VTE) is a multifactorial disorder, accounting for high morbidity and mortality rates, due to a complex interplay of several variables classifiable as inherited (mutated Leiden V factor, prothrombin, protein C, protein S and antithrombin) and acquired (lupus anticoagulants, pregnancy, major surgery procedures, cancer and inflammatory diseases) risk factors. The association of VTE with the nephrotic syndrome, particularly deep vein and renal vein thrombosis (DVT and RVT, respectively) is tightly established. This risk is particularly high in patients with idiopathic membranous nephropathy. In fact, thromboembolic events occur with a frequency between <10% and 45% in this disease. The reason(s) underlying the hypercoagulable status in nephrotic patients are not clearly understood. Multiple hemostatic abnormalities have been described, including decreased levels of antithrombin and plasminogen (due to urinary losses), increased platelet activation, reduced plasminogen activation, overproduction of fibrinogen and factors V and VIII as a compensatory response to hypoalbuminemia. The risk of thrombosis seems to be related to the severity and duration of the nephrotic status and seems to be particularly increased with serum albumin concentrations ≤2.0 g/dl (20 g/L). Case report We report the case of a 28 year-old male with nephrotic syndrome due to membranous nephropathy positive for serum anti-phospholipase-A2 receptor antibody. The patient was asymptomatic for VTE, but abdominal ultrasound showed endoluminal obstruction of both renal veins. Abdominal Computer Tomography confirmed the extensive bilateral renal vein thrombosis and also revealed an extension of the thrombosis to the inferior cava vein and the left common iliac vein. He was treated with low-molecular weight heparin for six months. According to our internal protocol, a complete Thrombophilia Molecular Study was performed and showed a normal Leiden V factor, but a rare homozygous mutation of the G20210A gene encoding for prothrombin. The prevalence of this is less than 5% in the general population, but is highly variable with ethnicity. The G20210A mutation confers a mildly increased thrombotic risk that is amplified by the presence of other risk factors, such as nephrotic syndrome. Conclusions In our case report, the association of a nephrotic syndrome secondary to a primitive membranous glomerulonephritis and the mutation in homozygous of the G20210A prothrombin, a rare mutation associated with a high thrombotic risk, led to a severe VTE in an still asymptomatic 28-year-old patient. Based on this experience, we would highlight the importance of the genetic screening for polymorphisms associated with inherited thrombophilia in nephrotic patients complicated with VTE.

Spontaneous neonatal renal vein thrombosis, a known pathology without clear management guidelines: An overview.

Renal vein thrombosis (RVT) was first described in 1837 by Rayer. Although tremendous progress has been achieved in the comprehension of its pathophysiology, its management remains controversial over 20 decades later. Therapeutic modalities vary from supportive measures alone to the utilization of thrombolytic agents whose protocols are derived from adult medicine. This review aims to show how difficult the treatment of RVT still is, especially with regard to the prognosis. The majority of affected neonates end with various renal complications (renal atrophy, dysfunction, hypertension, etc.).Like others, we suggest that simple unilateral RVT be managed conservatively, while thrombolytic agents may be attempted in unilateral RVT with extension to VCI and in bilateral RVT. Further studies are needed to reach appropriate consensual guidelines.

CATHETER DIRECTED THROMBOLYSIS OF THE INFERIOR VENA CAVA AND BILATERAL RENAL VEIN THROMBOSIS

Thrombus formation is a significant complication of unretrievable inferior vena cava filters. This case recognizes the role of catheter directed thrombolysis (CDT) of the Inferior Vena Cava (IVC) and bilateral renal vein thrombosis (RVT) in setting of acute pulmonary embolism (PE) and renal failure

Bilateral Renal Vein Thrombosis with Inutero Onset in a Preterm Newborn: A Case Report

Bilateral Renal Vein Thrombosis with Inutero Onset in a Preterm Newborn: A Case Report

Spontaneous neonatal renal vein thromboses: Should we treat them all? A report of five cases and a literature review

A retrospective study of the medical records of children managed between January 1990 and December 2013, and whose final diagnosis was RVT. The diagnosis was initially clinical and subsequently confirmed by the abdominal ultrasonography (AUS) and Doppler imaging if necessary. The abdominal CT scan was performed when the AUS finding led to the suspicion of RVT extension to the inferior vena cava (IVC). Each patient's birth parameters (birth weight [BW], birth length [BL], and head circumference [HC]) and modalities were recorded. The treatment modalities, the outcome at follow-up along with results of etiological screening were also recorded. Five newborn infants were diagnosed as having unilateral RVT at the mean postnatal age of 3.8 days (range, 1-11 days). All presented with a classical triad associated nephromegaly, thrombocytopenia, and gross hematuria. Two patients had genetic thrombophilic risk factors (1 heterozygous Leiden factor V mutation in case 4, and Activated Protein C resistance in case 5). Two infants were managed conservatively, and the other three received antithrombotic treatment (recombinant tissue plasminogen activator and heparin). All five patients had a similar course, leading to non-functioning renal atrophy, despite aggressive thrombolytic therapy or conservative treatment. We suggest that simple unilateral RVT be managed conservatively, while antithrombotic therapy may be attempted for unilateral RVT extending into the inferior vena cava and for bilateral RVT.

PNH: A Rare Hematological Disease with Profound Implications for a Gastroenterologist

Paroxysmal Nocturnal Hemoglobinuria (PNH) is a rare thrombophilic and hematopoietic stem cell disorder with an annual incidence rate of as low as 1-2 cases per million. About 16% of these patients present with visceral vein thrombosis which is the most common cause of mortality. We here present an extremely rare case of a young man presenting with extensive thrombosis of multiple visceral veins from PNH. A 36-year-old Hispanic man with no significant medical history presented to the emergency department with diffuse abdominal pain of four days duration. The patient also reported weight loss of 5lbs over the preceding one month. Initial laboratory tests revealed transaminitis; and pancytopenia with reticulocytosis, increased serum lactate dehydrogenase (LDH) and decreased serum haptoglobin levels. The patient was found to have elevated urobilinogen in urine pointing towards intravascular hemolysis. A computerized tomography (CT) scan (Figure-1) of the abdomen demonstrated extensive portal vein thrombosis (PVT), superior mesenteric vein thrombosis and bilateral renal vein thrombosis. Flow cytometry and bone marrow biopsy (Figure-2) confirmed the diagnosis of PNH. The patient underwent esophagogastroduodenoscopy for screening esophageal varices. No varices were found. The patient was started on anticoagulation and Eculizumab.Figure 1Figure 2PNH caused by mutation of the PIG-A gene, is characterized by uncontrolled complement activity with decreased CD-55 and 59 levels leading to- intravascular hemolysis, thrombosis, and bone marrow failure. Patients with PNH often present with hemoglobinuria, abdominal pain, fever, headache, and fatigue. While hepatic and cerebral veins are the most common sites of thrombosis, PVT is extremely rare with only about 12 cases reported in the literature. Sparing of hepatic vein with involvement of portal vein and mesenteric veins makes this case highly unusual. A gastroenterologist must be keenly aware and consider the diagnosis of PNH in any young patient presenting with abdominal pain and hemolysis with abdominal visceral vein thrombosis, especially in the absence of underlying cirrhosis. It is imperative that these patients are started on anticoagulation at the earliest given the high mortality. Eculizumab is a monoclonal antibody used in the secondary prevention of disease known to act by inhibiting the activation of complement cascade system. Allogeneic hemopoietic stem cell transplantation is considered for refractory cases.

Antenatal Bilateral Renal Vein Thrombosis with Combined Protein S and C Deficiency

In neonates, renal vein thrombosis (RVT) is the second most common thrombosis.We report a case of antenatal bilateral RVT and we review the optimal therapeutic approaches. I, a male newborn was admitted in the Neonatal Intensive Care Unit of the Center for Maternity and Neonatology of Tunis (CMNT) for respiratory distress and gross hematuria. Initial laboratory work demonstrated renal impairment and Doppler renal ultrasound confirmed the diagnosis of bilateral RVT. Thrombophilia evaluation found a combined protein C and S deficiency. Thrombolysis was started with tissue plasminogen factor in association to anticoagulation with unfractionated heparin. Renal vein thrombosis in neonates is a rare condition with a high morbidity rate. Thrombotic conditions may be associated with more severe clinical presentations. Currently, there is a lack of consensus concerning the management of RVT.

Neonatal renal venous and arterial thrombosis

Renal vein thrombosis (RVT) is one of the more common forms of neonatal thrombosis accounting for 15-20% of systemic thromboembolism[1,2]. A median age at presentation of 2-3 days have been reported [1,3], with unilateral and bilateral involvement of renal vein in 89-72% and 28-11% of cases, respectively[4,5]. The clinical presentation of RVT consists of increased kidney size, macroor microhematuria, reduced urine output with some degree of renal failure and thrombocytopenia. RVT in neonates is a multifactorial disease and it was associated with coagulopathy, maternal diabetes, birth asphyxia, sepsis, placement of central venous lines (CVL) and hereditary thrombophilic factors[5,6]. In specific, FV 1691G>A mutation and elevated Lp(a) concentrations are independent risk factors for the development of RVT in neonates. In non-CVL-related RVT, thrombus formation occurs in the small vessels of the kidney and may extend into the renal vein and inferior vena cava. In the neonates with CVL-related RVT, the thrombus most likely formed first in the vessel adjacent to the CVL and then extended into the kidney[4]. Renal ultrasonography shows unior bilateral kidney enlargement with loss of cortico-medullary differentiation and reduced or absent flow in renal vein[7]. Long-term functional complications include renal insufficiency, renal tubular dysfunction and hypertension in up to 30% of patients[1,8]. Controlled data on appropriate clinical management of neonatal RVT are lacking and recommendations of its treatment are based on low quality evidence. Current guidelines suggest for unilateral RVT in the absence of renal impairment or extension into the inferior vena cava, either 1) supportive care with radiologic monitoring for extension of thrombosis or 2) anticoagulation with unfractionated heparin (UFH)/ low-molecolar-weight heparin (LMWH) in therapeutic doses rather than no therapy[9]. For unilateral RVT that extends into the inferior vena cava, anticoagulation with UFH/LMWH for a total duration of between 6 weeks and 3 months is suggested[9]. For bilateral RVT with evidence of renal impairment, anticoagulation with UFH/LMWH or initial thrombolytic therapy with tissue plasminogen activator followed by anticoagulation with UFH/LMWH is suggested[9]. Renal artery thrombosis (RAT) in the neonate is far less common than RVT, and there is little information about its incidence. It is associated with umbilical catheters, patent ductus arteriosus and hereditary thrombophilia [10,11]. The clinical presentation is rather silent and renal ultrasound findings can be minimal unless Doppler imaging is used. The outcome of the affected kidneys is poor with common global atrophy. For neonates with a peripheral arterial catheter-related thrombosis, immediate removal of the catheter and UFH anticoagulation with or without thrombolysis or surgical thrombectomy and microvascular repair with subsequent heparin therapy are suggested[9].

Large Bladder Clot—An Unusual Presentation of Neonatal Bilateral Renal Vein Thrombosis—Case Report and Review of Literature

A 1-day-old boy born at 37 weeks gestation presented with hematuria, thrombocytopenia, and palpable irregular right flank mass. Renal ultrasound demonstrated large clot within the bladder, bilateral kidney masses with loss of corticomedullary differentiation, and reversal of diastolic flow. The patient was diagnosed with bilateral renal vein thrombosis and was managed conservatively. There was complete resolution of the bladder clot with restoration of corticomedullary differentiation bilaterally. We report the first case of renal vein thrombosis associated with a large bladder clot in a neonate.

2083710 Perinatal Renal Vein Thrombosis; Review of 6 Cases

Renal venous thrombosis (RVT) is the most common form of venous thrombosis in neonates, causing both acute and long term kidney dysfunction. We reviewed 6 cases in which two developed renal vein thrombosis antenatally and four developed it in neonatal period. The purpose of this presentation is to emphasize the typical ultrasound appearance seen in RVT. Neonatal RVT is not a condition associated with a high mortality rate, but it is associated with significant morbidity due to renal impairment. Hence it is important to diagnose it early. Out of 6 cases, 5 neonates presented for ultrasound in first week of life (2 days to 4 days). Three were preterm and two were full term neonates. One case was diagnosed antenatally to have bilateral renal vein thrombosis, IVC thrombosis, unilateral adrenal hematoma when mother was assessed at 37 weeks of pregnancy. All cases were NICU admisssions. Clinical presentation was macroscopic hematuria and thrombocytopenia in 4 neonates. Scanning was done with high frequency linear transducer (L5-12 MHz) Transfontanellar ultrasound to look for cerebral hemorrhage was done in all cases. 5 babies had unilateral RVT and one had bilateral RVT. Typical ultrasound features of renal enlargement, diffuse increase in echogenicity, echogenic medullary streaks were seen in all cases. In 4 neonates IVC and renal vein thrombosis could be seen on first ultrasound itself, in 1 neonate it was demonstrated on follow up scan after 3 days. Calcification of thrombus was visualized in two neonates. In three babies adrenal hematoma was also associated with RVT. Transfontanellar ultrasound was normal in all cases. None of the babied had cerebral hemorrhage. Ultrasound examination is non invasive, portable and can easily be performed on neonates in NICU set up. Typical features of haematuria, palpable mass, and thrombocytopenia may not be seen in all cases of RVT, Also, well defined echogenic IVC or renal vein thrombus may not be visualized at first presentation, hence it is important to understand grey scale ultrasound features to diagnose this condition for timely treatment. It is imortant to remember that though rare, RVT is also seen in fetal life.

Successful surgical thrombectomy for neonatal IVC and bilateral renal vein thrombosis

We propose that renal salvage is possible in neonatal inferior vena cava (IVC) and bilateral renal vein thrombosis utilizing early surgical intervention. Management of bilateral renal vein thrombosis with renal impairment typically includes anti-coagulation and thrombolytic therapy. We report a case of a five day-old premature female, found to have bilateral renal vein thrombosis that had propagated up the IVC, associated with anuric renal failure. Peak BUN/creatinine was 52/4 at day of life 5, with a peak of 90/7.4 at day of life 10. After a failed attempt at intravenous thrombolytic therapy, thrombectomy was performed for the IVC as well as both renal veins. The patient urinated by post-operative day 2. Function improved daily, with creatinine stabilizing at 0.4 mg/dL by one month. Serial ultrasounds showed persistent patency of the IVC and bilateral renal veins. The patient was heterozygous for the Factor V Leiden mutation and pathology demonstrated evidence of placental thrombosis. We have shown that neonatal anuric renal failure secondary to bilateral renal vein thrombosis can be successfully managed with early surgical thrombectomy without the need for nephrectomy. Restoration of renal function after surgical thrombectomy in this patient illustrates the potential reversibility of acute renal failure even in severe cases.

Acute Peritoneal Dialysis in the Newborn Period: A 7-Year Single-Center Experience at Tertiary Neonatal Intensive Care Unit in Turkey

To evaluate the underlying causes and outcomes of neonates who underwent acute peritoneal dialysis (APD). This report describes a 7-year experience with APD in 77 neonates. Underlying causes requiring APD were acute tubular necrosis (ATN; n = 53), inborn error of metabolism (n = 18), bilateral renal vein thrombosis (n = 3), obstructive uropathy (n = 2; posterior urethral valve and neurogenic bladder), and bilateral renal artery thrombosis (n = 1). Fifteen of the 53 patients developed post-cardiac surgery ATN. The mean dialysis duration was 6.2 ± 10.7 days (range 1 to 90 days). Complications of procedure were hyperglycemia (n = 35), leaking of dialysate (n = 13), peritonitis (n = 10), catheter obstruction (n = 3), bleeding when inserting the catheter (n = 3), exit site infection (n = 2), and bowel perforation (n = 1). There were 57 deaths (74%) in this high-risk group due to underling causes. Of the 20 survivors, 16 patients showed a full renal recovery, but mild chronic renal failure developed in 1 patient and proteinuria with/without hypertension in 3 patients. Peritoneal dialysis is an effective means of renal replacement therapy in the neonatal period in the management of metabolic disturbances as well as renal failure. Although major complications of procedure are not so common, these patients have high mortality rates due to the serious nature of the primary causes.

Complete renal recovery from severe acute renal failure after thrombolysis of bilateral renal vein thrombosis

A previously healthy young man presented with acute renal failure due to extensive spontaneous deep vein thrombosis, including the inferior vena cava (IVC) and both renal veins. The patient was treated with selectively delivered thrombolytic therapy over a 7-day-period, which resulted in renal vein patency and complete recovery of renal function. A stent was placed over a segment stenosis of the IVC. No thrombophilic factors were identified. Bilateral renal vein thrombosis in young fit individuals is an unusual cause of acute renal failure. Thrombolytic therapy, even with delay, can completely restore renal function.

Anti-neutrophil cytoplasmic antibody vasculitis presenting with bilateral renal vein thrombosis.

We report a case of anti-neutrophil cytoplasmic antibody (ANCA)-associated necrotizing crescentic glomerulonephritis presenting with bilateral renal vein thrombosis and pulmonary emboli in a patient who also had a lupus anticoagulant and anti-cardiolipin antibodies. Although the link between venous thrombosis and ANCA vasculitis is well established, the coexistence of renal vein thrombosis is unusual. Furthermore, despite the positive ANCA, he was initially negative for antibodies to myeloperoxidase (MPO) and proteinase-3 (PR3), illustrating that a positive ANCA may be significant despite a negative test for antibodies to MPO and PR3.