The kidney histopathological spectrum of patients with kidney injury following snakebite envenomation in India: scoping review of five decades.

INTRODUCTION: Snakebite is a public health problem leading to about 58,000 deaths every year in India. Kidney injury subsequent to snakebite envenomation is common with a reported prevalence of up to 32%. The current study aims to elucidate the spectrum of kidney histopathology in acute kidney injury (AKI) cases associated with snake bites. METHODS: We searched seven electronic database studies to identify studies describing the histopathological findings in the kidney with snakebite envenomation. Two reviewers independently conducted titles and abstract screening as well as full-text evaluation for the final inclusion decision. Data were extracted as per the standardized form. We conducted narrative synthesis. Studies done exclusively on autopsy findings, in vitro studies, and case reports were excluded. RESULTS: We retrieved 1464 studies and finally included 28 studies which met the eligibility criteria in the analysis. Most studies were single-centre and the majority were cross-sectional. Overall we included a total of 534 renal biopsies. Russell's viper bite was the most common cause related to AKI. Acute tubular necrosis was the most common finding followed by acute interstitial nephritis, acute cortical necrosis (ACN), and thrombotic microangiopathy (TMA). Vasculitis changes in vessels were rarely reported. Lesions such as ACN and TMA were associated with poor outcomes. CONCLUSION: This analysis supports the notion that renal biopsies are important to guide prognosis and increase our knowledge about post-snake bite AKI pathophysiology.

Venom-induced consumptive coagulopathy leading to thrombotic microangiopathy following Echis carinatus sochureki bite: is snake antivenom effective?

The incidence of thrombotic microangiopathy (TMA) following snake bite is reported to be ranging from 3.6 to 15%. We report a 10-year-old boy who developed TMA and due to venom-induced consumptive coagulopathy (VICC) despite receiving adequate and timely doses of snake antivenom following a bite of saw-scaled viper (Echis carinatus sochureki). VICC was managed by plasmapheresis. Though snake bite envenomation-associated renal complications are not uncommon, possibility of TMA should be considered early during management. Our patient developed TMA with subsequent acute cortical necrosis after saw-scaled viper bite despite an adequate and timely dose of snake antivenom which emphasizes the ineffectiveness of antivenom against the venom of given snake species leading to long-term complications.

Renal ischemic adverse drug events related to tranexamic acid in women of child-bearing age: an analysis of pharmacovigilance data.

PURPOSE: In response to a large trial, the World Health Organization broadened their recommendation on tranexamic acid to be used for post-partum hemorrhage. A 2013 French periodic safety update report warned of an abnormally high rate of renal cortical necrosis associated with tranexamic acid and other drugs for severe post-partum hemorrhage. We aimed to identify the reporting incidence of adverse thrombo-embolic events among women in child-bearing age who received tranexamic acid, with a focus on renal vascular and ischemic conditions. METHODS: We analyzed individual case safety reports (ICSRs) on renal vascular and ischemic conditions, pulmonary thrombotic and embolic conditions, and peripheral embolism and thrombosis from the database of the World Health Organization - Uppsala Monitoring Centre (WHO-UMC). ICSRs were restricted to reports including tranexamic acid as a suspected drug, sex reported as female, and reported age between 18 and 44 years. Reporting odds ratios (RORs) and 95% confidence intervals (95% CIs) were calculated by comparing ICSRs on tranexamic acid to all other drugs in VigiBase. RESULTS: Within 2245 included ICSRs on tranexamic acid, we identified 29 reports of adverse renal vascular and ischemic conditions, 42 reports of pulmonary thrombotic and embolic conditions, and 41 reports of peripheral embolism and thrombosis. RORs were statistically significant by 32.6-fold (32.62, 95% CI: 22.50-47.29), 2.5-fold (2.52, 95% CI: 1.85-3.42), and 2.7-fold (2.67, 95% CI: 1.96-3.64), respectively, when compared to any other drug within VigiBase. CONCLUSION: Tranexamic acid might bear an increased risk for renal ischemic adverse drug events in women of child-bearing age.

Renal Biopsy Prognostic Findings in Children With Atypical Hemolytic Uremic Syndrome.

BACKGROUND: The aim of this study was to investigate the histopathological findings in kidney biopsies in children with atypical hemolytic uremic syndrome (aHUS) and to determine whether specific pathological findings in aHUS have a prognostic value. METHODS: Renal biopsy specimens of 29 patients who were recorded in the national Turkish aHUS registry database were available for review. Histopathological findings were compared with the clinical and laboratory features at the presentation and the final outcome. RESULTS: The mean age at presentation and follow-up period was 4.9 ± 3.9 and 3.9 ± 3.0 years, respectively. The median time interval from the first symptom to biopsy was 10 days. Vascular thrombosis and interstitial fibrosis were significantly related to chronic kidney disease (CKD) requiring dialysis or kidney transplantation during follow-up (5.6-fold, for both). Glomerular necrosis, cortical necrosis, and glomerular sclerosis were markedly associated with CKD without dialysis (6.2-fold, 13.3-fold, and 8.8-fold, respectively). However, presence of endothelial swelling, subendothelial widening, and fragmented erythrocytes was found to be correlated with a favorable final outcome. CONCLUSIONS: Presence of vascular thrombosis, cortical necrosis, and glomerular sclerosis in histopathological evaluation correlated with developing CKD. Chronic changes in the interstitial compartment were also related to poor prognosis, a finding that has been shown for the first time in pediatric aHUS cases.

Radiation-induced focal cortical necrosis of the femur presenting as a lytic lesion.

Management of soft tissue sarcomas is often complicated, requiring radiation before and in some cases after limb-sparing surgery. Radiation necrosis is a severe complication after radiation treatment and is typically dose related and involves medullary bone. We report on two cases of hitherto unreported focal circumscribed intra-cortical lytic lesions within the radiation portal, which appeared 19 months and 31 months, respectively, after the conclusion of radiation treatment. Both patients had a history of soft tissue sarcoma treated with radiation (66 Gy) and surgical resection. Biopsy of these lesions showed necrotic bone attributed to radiation.

Fatal Cryocrystalglobulinemia With Intravascular and Renal Tubular Crystalline Deposits.

Cryocrystalglobulinemia is a rare variant of cryoglobulinemia in which monoclonal immunoglobulins self-assemble into crystalline arrays. We report a case of a 53-year-old man who presented with systemic thrombotic microangiopathy causing multiorgan failure, including decreased kidney, lung, and gastrointestinal function; skin necrosis; and mental status changes. Skin and kidney biopsy specimens showed intravascular thrombi, along with intravascular, intratubular, and periglomerular crystalline deposits. Typical morphologic features of cryoglobulinemia, such as a leukocytoclastic vasculitis and pseudothrombi, were absent. Spindled crystals precipitated in the cryoglobulin assay, and immunofixation showed them to be composed of monoclonal immunoglobulin G κ light chains. Ultrastructural analysis demonstrated deposits to have an array-like substructure. The patient was successfully treated with a combination of plasmapheresis, steroids, and bortezomib, but experienced a relapse and died 12 months after his initial diagnosis. Cryocrystalglobulinemia causes significant morbidity and mortality and should be classified as a monoclonal gammopathy of renal significance when it occurs in patients not meeting diagnostic criteria for multiple myeloma.

Renal Cortical Necrosis in Postpartum Hemorrhage: A Case Series.

BACKGROUND: Pregnancy-related renal cortical necrosis may lead to end-stage renal disease. Although this obstetric complication had virtually disappeared in high-income countries, we have noted new cases in France over the past few years, all following postpartum hemorrhage. STUDY DESIGN: Case series. SETTING & PARTICIPANTS: We retrospectively identified 18 patients from 5 French nephrology departments who developed renal cortical necrosis following postpartum hemorrhage in 2009 to 2013. OUTCOMES: Obstetric and renal features, therapeutic measures, and kidney disease outcome were studied. RESULTS: All patients had a severe postpartum hemorrhage (mean blood loss, 2.6±1.1 [SD] L). Hemodynamic instability and disseminated intravascular coagulation were reported in 5 and 11 patients, respectively. All developed rapid onset of acute kidney injury and required hemodialysis. Diagnosis of renal cortical necrosis was performed 4 to 33 days following delivery. At 6 months postpartum, 8 patients remained dialysis dependent and none recovered normal kidney function. The length of exposure to tranexamic acid treatment was significantly more prolonged in women whose estimated glomerular filtration rate remained <15mL/min/1.73m(2) (7.1±4.8 vs 2.9±2.4 hours; P=0.03). LIMITATIONS: Retrospective study; small sample size. CONCLUSIONS: In the setting of gravid endothelium, the conjunction of disseminated intravascular coagulation with the life-saving use of procoagulant and antifibrinolytic agents (recently implemented in France in a postpartum hemorrhage treatment algorithm) may give rise to a risk for uncontrolled clotting in the renal cortex and hence irreversible partial or diffuse cortical necrosis.

Acute kidney injury in pregnancy--a single center experience.

BACKGROUND: Acute kidney injury (AKI) is a serious complication in pregnancy, resulting in significant maternal morbidity/mortality and fetal loss. Although the incidence of pregnancy-related acute kidney injury (PRAKI) has decreased in developed countries, it is still common in developing nations. METHODS: A prospective observational study was done between January 2010 and December 2014 to report the incidence, clinical spectrum, maternal and fetal outcome of AKI in pregnancy. RESULTS: Total number of patients: 130; mean age: 25.4 ± 4.73 years. The incidence of AKI in pregnancy was 7.8%. Most of the AKI was noted in postpartum period (68%). Etiology of AKI was sepsis (39%), pre-eclampsia (21%), placental abruption (10%), acute diarrheal disease complicating pregnancy (10%), thrombotic microangiopathy (TMA) (9%), postpartum hemorrhage (2%) and glomerular diseases (9%). Renal biopsy (n = 46) done in these patients showed renal cortical necrosis (16), TMA (11), acute tubular injury (9), acute tubulointerstitial disease (1) and glomerular disease (9). Live births occurred in 42% of patients with vaginal delivery in 34% cases. Thirty-four patients were managed conservatively, while 96 required dialysis. Complete recovery occurred in 56% and about 36% had persistent renal failure at 3 months. Mortality rate observed was 8%. In univariate analysis, low mean platelet count, higher peak serum creatinine, dialysis dependency at presentation and histopathologically presence of cortical necrosis and TMA predicted the progression to chronic kidney disease. CONCLUSION: AKI in pregnancy was common in postpartum period and sepsis being the commonest cause.

Renal cortical necrosis is a disappearing entity in obstetric acute kidney injury in developing countries: our three decade of experience from India.

RATIONAL: Obstetrical complications are the commonest causes of Renal Cortical Necrosis (RCN). However, the overall incidence of RCN in obstetric acute kidney injury in developing countries has been decreasing in recent years. OBJECTIVE: The aim of this study was to evaluate the changing profile of RCN in obstetric AKI over the last three decades. METHODS: This single center study included patients with biopsy proven renal cortical necrosis over a period of 32 years from 1982 to 2014. The diagnosis of RCN was suspected in patients with prolonged AKI (>4 weeks) with absolute anuria in the setting of hemorrhage, hypotension and sepsis; and was confirmed by renal biopsy. The changing pattern in the incidence, etiology and outcome of RCN in patients with obstetric AKI was compared in the three study periods, namely 1982-1991, 1992-2002 and 2003-2014. RESULTS: Over a period of 32 years, RCN was diagnosed in 15/259(5.8%) cases of obstetric AKI. Diffuse and patchy cortical necrosis were noted in 8(53.3%) and 7(46.7%) patients, respectively. RCN occurred in 17%(11/65), 2.4%(3/125) and 1.44%(1/69) patients in 1982-1991, 1992-2002 and 2003-2014, respectively. Septic abortion was commonest cause of RCN in the first two study periods but no case was observed in last decade. The decrease in incidence of RCN over the three decades was statistically significant (p-value < 0.001). Maternal mortality decreased to zero in 2003-2014 from 72.7% in 1982-1991. CONCLUSIONS: The incidence of RCN in obstetric AKI in developing countries has declined low enough to label it as a disappearing entity.

Unilateral renal cortical necrosis.

A 51-year-old woman presented to her local emergency department with acute onset right-sided flank pain and nausea. Her blood results on admission were largely unremarkable aside from leucocytosis and neutrophilia. Two days after admission, she developed the following: stage 3 AKI with oliguria, anaemia, thrombocytopenia, and acute derangement of liver function tests. A computed tomography of the kidney ureter bladder demonstrated a right-sided 4 mm obstructing vesicoureteric junction stone with associated hydronephrosis and hydroureter. She was transferred to a tertiary care centre; gram negative sepsis was confirmed with a Proteus on blood culture and laboratory findings were in keeping with DIC. She was treated with Tazobactam/Piperacillin and intravenous fluids. In addition, further imaging showed improving right-sided hydronephrosis and left renal cortical necrosis. The aetiology of this presentation was sepsis complicated by disseminated intravascular coagulation. The coagulopathy likely contributed to the unilateral renal cortical necrosis. Cortical necrosis usually affects both kidneys, and is typically a complication of sepsis, shock, or obstetrical trauma. To our knowledge, there are only 2 reported cases of unilateral renal cortical necrosis and contralateral hydronephrosis with renal colic and septic shock. Potential pathogenetic mechanisms are discussed.

Urinary GM2AP coincides with renal cortical damage and grades cisplatin nephrotoxicity severity in rats.

Nephrotoxicity, including electrolytic disorders and acute kidney injury (AKI), limits the clinical dosage and utility of platinated antineoplastics such as cisplatin. Cisplatin nephrotoxicity embodies a tubulopathy involving the medullary S2 and S3 segments of the proximal and the distal tubules. Higher dosage extends damage over the cortical S1 segment and intensifies overall injury. However, the standard diagnosis based on plasma creatinine as well as novel injury biomarkers lacks enough pathophysiological specificity. Further granularity in the detection of renal injury would help understand the implications of individual damage patterns needed for personalized patient handling. In this article, we studied the association of urinary ganglioside GM2 activator protein (GM2AP) with the patterns of tubular damage produced by 5 and 10 mg/kg cisplatin in rats. Our results show that GM2AP appears in the urine only following damage to the cortical segment of the proximal tubule. The information provided by GM2AP is not redundant with but distinct and complementary to that provided by urinary neutrophil gelatinase-associated lipocalin (NGAL). Similarly, treatment with 150 mg/kg/day gentamicin damages the renal cortex and increases GM2AP urinary excretion; whereas renal ischemia, which does not affect the cortex, has no effect on GM2AP. Because of the key role of the cortical proximal tubule in renal function, we contend GM2AP as a potential diagnostic biomarker to stratify AKI patients according to the underlying damage and follow their evolution and prognosis. Prospectively, urinary GM2AP may help grade the severity of platinated antineoplastic nephrotoxicity by forming part of a non-invasive liquid biopsy.

Features of Postpartum Hemorrhage-Associated Thrombotic Microangiopathy and Role of Short-Term Complement Inhibition.

Introduction: In pregnancy-related atypical hemolytic uremic syndrome (p-aHUS), transferring recommendations for treatment decisions from nonpregnant cohorts with thrombotic microangiopathy (TMA) is difficult. Although potential causes of p-aHUS may be unrelated to inherent complement defects, peripartal complications such as postpartum hemorrhage (PPH) or (pre)eclampsia or Hemolysis, Elevated Liver enzymes and Low Platelets (HELLP) syndrome may be unrecognized drivers of complement activation. Methods: To evaluate diagnostic and therapeutic decisions in the practical real-life setting, we conducted an analysis of a cohort of 40 patients from 3 German academic hospitals with a diagnosis of p-aHUS, stratified by the presence (n = 25) or absence (n = 15) of PPH. Results: Histological signs of TMA were observed in 84.2% of all patients (100% vs. 72.7% in patients without or with PPH, respectively). Patients without PPH had a higher likelihood (20% vs. 0%) of pathogenic genetic abnormalities in the complement system although notably less than in other published cohorts. Four of 5 patients with observed renal cortical necrosis (RCN) after PPH received complement inhibition and experienced partially recovered kidney function. Patients on complement inhibition with or without PPH had an increased need for kidney replacement therapy (KRT) and plasma exchange (PEX). Because renal recovery was comparable among all patients treated with complement inhibition, a potential beneficial effect in this group of pregnancy-associated TMAs and p-aHUS is presumed. Conclusion: Based on our findings, we suggest a pragmatic approach toward limited and short-term anticomplement therapy for patients with a clinical diagnosis of p-aHUS, which should be stopped once causes of TMA other than genetic complement abnormalities emerge.

Postpartum Renal Cortical Necrosis: A Case Series.

Rationale & Objective: Postpartum renal cortical necrosis (postpartum RCN) is a severe form of obstetric acute kidney injury. This study aimed to identify clinicopathologic features in Chinese postpartum RCN cases to determine how pathologic findings may contribute to the treatment and prognosis. Study Design: Single-center, case series. Setting & Participants: Twelve patients with postpartum RCN had kidney biopsies at Peking University First Hospital between 2014 and 2021. The diagnosis of postpartum RCN was made according to typical magnetic resonance imaging or pathologic features. Clinical, laboratory, and pathologic data were compared between patients with estimated glomerular filtration rate <30 (poor outcome) and ≥30 mL/min/1.73 m2 after 6 months. Observations: All patients with postpartum RCN presented with stage 3 acute kidney injury attributed to a probable atypical hemolytic uremic syndrome. Pregnancy terminations occurred at a median gestational age of 35.5 weeks. Kidney biopsy was performed from 18 days to 4 months from delivery. On biopsy, hemoglobin, platelet count, and lactate dehydrogenase levels had been restored to 137 g/L, 214 × 109/L, and 231.50 ± 65.01 U/L, respectively. Four patients exhibited poor outcome, demonstrating higher schistocyte count, serum creatinine, and mean arterial pressure at onset. Pathologically, glomerular segmental sclerosis was prevalent. The "not otherwise specified" variant was the most common type, followed by collapsing variant, cellular variant, and tip variant. Patients with poor kidney outcome had more glomerular coagulative necrosis, capillary thrombosis, extensive cortical coagulative necrosis, and pronounced arteriole/artery lesions including increased interlobular arteriole intimal edema and fibrin thrombosis, but a lower occurrence of segmental sclerosis. Limitations: Limited sample size and retrospective design. Conclusions: We identified key pathologic features in patients with postpartum RCN and atypical hemolytic uremic syndrome, highlighting the necessity for more effective therapeutic options. There is a clear demand for noninvasive biomarkers that can accurately track disease progression and inform treatment duration for long-term outcomes improvement.

Our study investigated postpartum renal cortical necrosis (RCN) in 12 Chinese women, a severe form of kidney injury that occurs after childbirth, often linked to atypical hemolytic uremic syndrome (aHUS). We aimed to identify clinical and pathologic features to improve treatment and predict patient outcomes. The women experienced stage 3 acute kidney injury, with kidney biopsies revealing various degrees of glomerular and vascular damage. Key findings included segmental glomerular sclerosis and arteriole lesions, which were more pronounced in patients with poor outcomes. The study, though limited by its small and retrospective design, underscores the importance of recognizing aHUS in postpartum RCN for better management and highlights the urgent need for noninvasive biomarkers to monitor disease progression and improve long-term prognosis.

Renal Allograft Cortical Necrosis in a COVID-19 Positive Patient.

The incidence of acute kidney injury (AKI) has been reported to be higher in kidney transplant recipients infected with SARS-CoV-2 compared with the general population. Here, we report a case of cortical necrosis in the graft kidney due to COVID infection in a patient with stable graft function over the years. The patient was started on hemodialysis and treated with steroids, and anticoagulants for COVID infection. Later, he had gradual improvement in his graft function and became dialysis independent on follow up.

Rubber Dam Clamp May Cause Cortical Necrosis: A Case Report.

Tooth isolation methods used during endodontic procedures are necessary to create an aseptic field and protect the patient's alimentary tract from irrigation and instrument insult. This case details changes that can occur in mandibular cortical bone architecture after the use of a stainless steel rubber dam clamp during an endodontic procedure. A 22-year-old, otherwise healthy woman underwent nonsurgical root canal therapy on tooth #31 (mandibular right second molar, symptomatic irreversible pulpitis and periapical periodontitis.) Cone-beam computed tomographic imaging obtained between treatments revealed irregular erosive and lytic changes of the crestal-lingual cortical bone, resulting in sequestrum formation with infection and exfoliation. Continued monitoring and 6-month post-treatment CBCT imaging revealed complete resolution without further intervention. When a stainless steel rubber dam clamp is placed onto gingiva overlying mandibular alveolar bone, bony changes can occur presenting with radiographic signs of cortical erosion and may result in necrosis of the cortical bone with sequestrum formation. Knowledge of this potential outcome improves our understanding of the normal course progression after dental procedures using a rubber dam clamp for tooth isolation.

Pregnancy-Associated Renal Cortical Necrosis and Nonenhanced Functional Magnetic Resonance Imaging: A Case Series.

Rationale & Objective: Pregnancy-associated renal cortical necrosis is a critical illness with a poor prognosis. We aimed to describe the clinical and magnetic resonance imaging (MRI) characteristics of a case series of patients with acute kidney injury in the setting of pregnancy-associated renal cortical necrosis. Study Design: Case series. Setting & Participants: Seventeen patients from a single center diagnosed by nonenhanced functional MRI and/or kidney pathology. Results: All patients presented with postpartum acute kidney injury stage 3. Of the 17 patients, 15 (88%) had pregnancy-associated atypical hemolytic uremic syndrome, 11 (65%) had postpartum hemorrhage, 7 (41%) had preeclampsia/hemolysis elevated liver enzymes low platelet count syndrome, and 4 (24%) had disseminated intravascular coagulation. On T2-weighted MRI, the diffuse phenotype showed outer cortex swelling in the early phase, with a dark signal rim involving the inner cortex and Bertin column, which became more apparent over time along with cortical thinning, substantially decreasing T2 signal intensity. The focal phenotype showed focally distributed hypointense signals in the cortex. After 8-101 (median: 60) months of follow-up, 4 individuals had estimated glomerular filtration rates ≥60 mL/min/1.73 m2, 6 had estimated glomerular filtration rates of 15-60 mL/min/1.73 m2, and 7 had kidney failure requiring kidney replacement therapy. The diffuse phenotype was present in all of the individuals who remained kidney replacement therapy dependent. Limitations: Retrospective study; small sample size. Conclusions: Different forms of pregnancy-associated thrombotic microangiopathy were the major causative diseases in our pregnancy-associated renal cortical necrosis case series. Nonenhanced functional MRI may provide valuable data for establishing diagnosis and kidney prognosis.

Evanescing renal allograft cortical necrosis from living donor renal transplantation: A lesson learned over two decades.

BACKGROUND: Renal graft cortical necrosis (GCN) is a catastrophic cause of graft failure. We evaluated the incidence, causes, management, and outcome of GCN across two decades from our center. METHODS: This is a retrospective analysis of transplant patients who had biopsy-proven GCN transplanted between 2000 and 2020. The clinical details, immunological workup, induction, maintenance regimen, causes of cortical necrosis, and the outcomes were compared between the first period 2000-2012, and the second period 2013-2020, when Flow cytometric and Luminex based crossmatch were included in the workup plan. RESULTS: Among 2333 live ABO-compatible renal transplants, 37 (0.015%) patients (36 patients between 2000 and 2012 and 1 between 2013 and 2020) developed GCN (60% had diffuse and 40% patchy GCN) at a median of 8 days after transplantation.Twenty-six (60%) received ATG, 4 received plasmapheresis and ATG (10.8%) as antirejection therapy. The cyclosporine-based regimen was associated with a higher risk of GCN (RR 2.54; 95% CI 1.26 to 5.12, p = 0.009), whereas tacrolimus-based therapy had a lower risk (RR 0.39; 95% CI 0.19 to 0.79, p = 0.009). The introduction of flow cytometry and DSA assay has significantly decreased the incidence of acute rejection and GCN. Only one patient had GCN during the 2013-2020 period because of graft's mucormycosis. Twenty-five (67.56%) patients had no recovery, and 12 (32.43%) had partial recovery of graft function. CONCLUSION: GCN is mainly associated with rejection, and cyclosporin-based maintenance regimen had a higher incidence. The remarkable decrease in GCN after 2012 onwards could be attributed to the use of Flowcytometry, Luminex-based DSA assays, and tacrolimus-based regimens.

Prolonged Hemiplegic Migraine Led to Persistent Hyperperfusion and Cortical Necrosis: Case Report and Literature Review.

Hemiplegic migraine (HM) is a rare subtype of migraine characterized by aura of motor weakness accompanied by visual, sensory, and/or speech symptoms. Aura symptoms usually resolve completely; permanent attack-related deficit and radiographic change were rare. Here, we reported a case presented with progressively aggravated hemiplegic migraine episodes refractory to medication. He experienced two prolonged hemiplegic migraine attacks that led to irreversible visual impairment and cortical necrosis on brain MRI. Multimodal MRI during attack showed persistent vasodilation and hyperperfusion in the affected hemisphere associated with deterioration of clinical symptoms and worsening of brain edema. Patent foramen ovale (PFO) was found on the patient. PFO closure resulted in a significant reduction of HM attacks. This case indicated that prolonged hemiplegic migraine attack could result in irreversible neurological deficit with radiographic changes manifested as cortical necrosis. Persistent hyperperfusion might be an important factor contributing to prolonged attack and persistent attack-related neurological deficit. We recommend screening for PFO in patients with prolonged or intractable hemiplegic migraine, for that closure of PFO might alleviate the attacks thus preventing the patient from disabling sequelae.

A Rare Case of Unilateral Renal Cortical Necrosis.

Unilateral cortical necrosis is a rare condition, and only described in a few case reports. We present a case of a previously healthy 24-year-old male with acute unilateral cortical necrosis, where contrast-enhanced ultrasound (CEUS) became a valuable diagnostic tool. Antiphospholipid syndrome was subsequently diagnosed. Primary antiphospholipid syndrome is a well-known, but rare cause of cortical necrosis. It promotes thrombosis in renal arteries, capillaries and veins, and usually affects both kidneys. Unilateral cortical necrosis due to antiphospholipid syndrome has, to our knowledge, not been previously described.