Early critical cortical infarction by anti-angiotensin II type 1 receptor antibody: A case report and literature review.

RATIONALE: Anti-angiotensin II type 1 receptor antibodies (AT1R-Abs) have been demonstrated to increase the risk of antibody-mediated rejection. We report a case of AT1R-Ab mediated rejection which caused early critical cortical infarction. PATIENT CONCERNS: A 52-year-old man with end-stage kidney disease underwent preemptive kidney transplantation (KT) from his wife. He had no immunologic risk except ABO incompatibility. Proper desensitization treatment were applied prior to KT. On postoperative day 1, he showed stable clinical course with adequate urine output, but there was no decrease in serum creatinine level and imaging studies showed hypoperfusion in the transplanted kidney. DIAGNOSES: Allograft biopsy revealed total cortical infarction with severe necrotizing vasculitis, but the medullary area was preserved. Serum AT1R-Ab concentration was elevated from 10.9 U/mL before KT to 19.1 U/mL on 7 days after KT. INTERVENTIONS: He was treated with plasmapheresis, intravenous immunoglobulin, rituximab, high-dose methylprednisolone, and bortezomib. OUTCOMES: The treatment showed a partial response, and he was discharged with 7.3 mg/dL creatinine level. At 4 months, his creatinine plateaued at 5.5 mg/dL and AT1R-Ab decreased to 3.6 U/mL. LESSONS: This case highlights the risk of early active antibody-mediated rejection by preformed AT1R-Ab, suggesting its ability to exhibit atypical histopathologic findings, such as total cortical infarction.

Bilateral acute renal cortical necrosis after a dog bite: case report.

BACKGROUND: Capnocytophaga canimorsus is a Gram-negative capnophilic rod and part of dogs/cats' normal oral flora. It can be transmitted by bites, scratches, or even by contact of saliva with injured skin. Asplenic patients and patients with alcohol abuse are at particular risk for fulminant C. canimorsus sepsis. However, also immunocompetent patients can have a severe or even fatal infection. This is the first case of a severe C. canimorsus infection in an immunocompromised host complicated by acute renal cortical necrosis with a "reverse rim sign" in contrast-enhanced computed tomography on hospital admission. CASE PRESENTATION: We report the case of a 44-year functionally asplenic patient after an allogeneic stem cell transplantation, who presented with septic shock after a minor dog bite injury 4 days prior. Because of abdominal complaints, epigastric pain with local peritonism, and radiological gallbladder wall thickening, an abdominal focus was suspected after the initial work-up. The patient underwent emergent open cholecystectomy, but the clinical suspicion of abdominal infection was not confirmed. Septic shock was further complicated by cardiomyopathy and disseminated intravascular coagulation. As a causative pathogen, C. canimorsus could be isolated. The clinical course was complicated by permanent hemodialysis and extensive acral necrosis requiring amputation of several fingers and both thighs. CONCLUSION: We present a severe case of a C. canimorsus infection in a functionally asplenic patient after a minor dog bite. The clinical course was complicated by septic shock, disseminated intravascular coagulation, and the need for multiple amputations. In addition, the rare form of acute renal failure - bilateral acute renal cortical necrosis - was visible as "reverse rim sign" on computed tomography scan. This case is an example of the potential disastrous consequences when omitting pre-emptive antibiotic therapy in wounds inflicted by cats and dogs, particularly in asplenic patients.

Acute kidney injury due to acute cortical necrosis following vivax malaria.

Malaria is a parasitic infection of global importance but has a high prevalence in the developing countries. Renal failure is a common complication of severe Plasmodium falciparum malaria and has been reported in up to 40% of all cases. Acute kidney injury (AKI), however, is not commonly associated with Plasmodium vivax infection. In those patients who develop AKI following P. vivax infection, the cause is commonly attributed to mixed undiagnosed falciparum infection or coexistent sepsis, dehydration, or hypotension. Infrequently, an association of P. vivax infection with thrombotic microangiopathy (TMA) has been reported. The purpose of this report is to describe renal failure due to TMA following malaria caused by P. vivax. A 24-year-old female presented with a history of fever and jaundice of two weeks duration followed by progressive oliguria and swelling of the face and feet five days after the onset of fever. The evaluation revealed normal blood pressure, anemia, thrombocytopenia, azotemia, unconjugated hyperbilirubinemia with mildly elevated transaminases, and elevated lactate dehydrogenase. Peripheral smear was positive for P. vivax, and schistocytes were seen. She was given intravenous artesunate followed by oral primaquine for 14 days. Urine examination showed proteinuria and microscopic hematuria. She remained oliguric and dialysis dependent, and her kidney biopsy revealed patchy cortical necrosis involving 40% of sampled cortex with widespread fibrinoid necrosis of the vessel wall, red blood cell fragmentation, and luminal thrombotic occlusion. Hemodialysis was discontinued after three weeks when there was the improvement of renal function over time, and her serum creatinine decreased to 2.2 mg/dL by six weeks. Patients with P. vivax malaria developing renal failure may have TMA. Renal biopsy, if performed early in the course of the disease, may identify TMA and institution of plasma exchange in such patients could help in early recovery.

[Renal cortical necrosis after application of tranexamic acid in peripartal hemorrhage]. / Renale Rindennekrose nach Gabe von Tranexamsäure bei geburtsassoziierter Blutung.

HISTORY: A 28-years old patient delivers a daughter by primary caesarian section (41. WOP) in breech presentation after a complication-free pregnancy except increased blood pressure readings at the morning of caesarian section. During the caesarian section a major bleeding of the atonic uterus with hemorrhagic shock appears. Haemostasis is achieved by mechanical tamponade, the application of red blood cell concentrates and the substitution of clotting factors, also tranexamic acid. Because of an anuric renal failure due to the shock hemodialysis is initiated. EXAMINATIONS/FINDINGS: Clinical examination and blood tests show the constellation of a thrombotic microangiopathy. There are no hints for a thrombotic thrombocytopenic purpura (TTP) or a hemolytic-uremic syndrome (HUS). In addition, a genetic testing gives no hints for an atypical HUS. After 4 weeks of dialysis duty a renal biopsy is performed. The renal biopsy shows a partly reversible tubular damage with an older ischemic cortical necrosis. DIAGNOSIS/THERAPY: In the further course the resumption of the diuresis can be observed. The dialysis treatment has to be continued because of an insufficient excretory renal function. Fortunately a living-donor kidney transplantation (mother) can be carry out successfully already one year after the hemorrhagic shock. CONCLUSION: The combination of peripartal bleeding with hemorrhagic shock, possibly aggravated by (pre-)eclampsia or HELLP-syndrome, and the application of tranexamic acid with its prothrombotic effect seems to be responsible for the major renal cortical necrosis.

Bilateral renal cortical necrosis following acute pancreatitis - A rare complication of a common disease.

Acute renal cortical necrosis is a rare cause of intrinsic acute kidney injury (AKI) which is commonly associated with obstetric complications such as placental abruption and some serious systemic disorders such as hemolytic-uremic syndrome, sepsis, severe burns, and snake bite. Acute pancreatitis is an extremely rare cause of renal cortical necrosis, and only less than 10 cases are reported in the literature. Here, we present a 24-year-old male presented with features of acute pancreatitis and oliguric AKI. His pancreatic enzymes were above 1000 IU/mL at admission. He was initiated on hemodialysis. Percutaneous renal biopsy done at 4th week of illness showed features of diffuse renal cortical necrosis. Contrast-enhanced computed tomography demonstrated hypoattenuation of cortex compared to medulla consistent with renal cortical necrosis. He developed complications such as acute necrotic collection, pleural effusion and retinal detachment in addition to renal cortical necrosis which was managed conservatively. Since there was no improvement in the renal function now, he is being evaluated for renal transplantation.

[CME: Ethylene Glycol Intoxication]. / CME: Ethylenglykol-Intoxikation.

CME: Ethylene Glycol Intoxication Abstract. Ethylene glycol is a sweet-tasting alcohol used in common antifreeze and other industrial solutions. Without appropriate therapy, intoxication with ethylene glycol can result in severe metabolic acidosis, acute renal failure, and in death. After gastrointestinal resorption, hepatic metabolism starts with oxidation by alcohol dehydrogenase and results in severe anion gap metabolic acidosis. Other metabolic products are calcium oxalate crystals, which can deposit in several tissues like the kidneys and lead to acute tubular necrosis with reversible renal failure. The crucial therapeutic step is rapid inhibition of alcohol dehydrogenase with fomepizole or ethanol to avoid the formation of toxic metabolites. Additionally, haemodialysis is the most effective way to eliminate ethylene glycol as well as its toxic metabolites. If therapy is initiated rapidly, prognosis is favorable.

[Acute kidney injury in children].

Acute kidney injury (AKI) is a clinical condition considered to be the consequence of a sudden decrease (> 25%) or discontinuation of renal function. The term AKI is used instead of the previous term acute renal failure, because it has been demonstrated that even minor renal lesions may cause far-reaching consequences on human health. Contemporary classifications of AKI (RIFLE and AKIN) are based on the change of serum creatinine and urinary output. In the developed countries, AKI is most often caused by renal ischemia, nephrotoxins and sepsis, rather than a (primary) diffuse renal disease, such as glomerulonephritis, interstitial nephritis, renovascular disorder and thrombotic microangiopathy. The main risk factors for hospital AKI are mechanical ventilation, use of vasoactive drugs, stem cell transplantation and diuretic-resistant hypervolemia. Prerenal and parenchymal AKI (previously known as acute tubular necrosis) jointly account for 2/3 of all AKI causes. Diuresis and serum creatinine concentration are not early diagnostic markers of AKI. Potential early biomarkers of AKI are neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule-1 (KIM-1), interleukins 6, 8 and 18, and liver-type fatty acid-binding protein (L-FABP). Early detection of kidney impairment, before the increase of serum creatinine, is important for timely initiated therapy and recovery. The goal of AKI treatment is to normalize the fluid and electrolyte status, as well as the correction of acidosis and blood pressure. Since a severe fluid overload resistant to diuretics and inotropic agents is associated with a poor outcome, the initiation of dialysis should not be delayed. The mortality rate of AKI is highest in critically ill children with multiple organ failure and hemodynamically unstable patients.

Renal cortical necrosis secondary to thrombotic microangiopathy in the context of acute promyelocytic leukaemia blast crisis.

A 37-year-old patient was transferred to Haematology from the ENT Emergency Department where he had been admitted due to tonsillitis. He displayed anaemia and leukopenia and had agranulocytosis in the study. A day later the patient had blast crisis, and was diagnosed with myeloid acute leukaemia. Due to blast crisis the patient experienced sudden back pain, with oliguria and renal function deterioration followed by anaemia, in the context of haemolysis consistent with thrombotic microangiopathy, and as such, we were consulted. We began treatment with plasmapheresis and on the following day we performed haemodialysis (we carried out a total of 12 sessions of plasmapheresis until haemolysis disappeared). Five days later there was respiratory failure, and the patient was consequently transferred to the Intensive Care Unit, where he continued treatment with plasmapheresis and haemodialysis. The patient remained anuric thereafter, requiring haemodialysis, with no sign of renal recovery. Once platelet levels normalised with haematology chemotherapy, a percutaneous renal biopsy was performed, which confirmed the diagnosis of cortical necrosis. Finally, the patient underwent renal replacement therapy by regular haemodialysis.

Transient IgA nephropathy with acute kidney injury in a patient with dengue fever.

Dengue virus infection can clinically manifest as dengue fever, dengue shock syndrome and dengue hemorrhagic fever. Acute kidney injury as a result of dengue virus infection can occur due to various reasons including hypotension, rhabdomyolysis, sepsis and rarely immune complex mediated glomerular injury. However, glomerulonephritis associated with IgA Nephropathy in dengue virus infection has not been reported previously. We report a case of 15-year-old boy who was admitted with dengue fever and dialysis dependant acute kidney injury. Urine examination showed microscopic glomerular hematuria and proteinuria. Kidney biopsy showed mesangial proliferation with mesangial IgA dominant immune complex deposits and acute tubular necrosis. A repeated kidney biopsy 6 weeks after clinical recovery showed reversal of glomerular changes as well as resolution of mesangial IgA deposits.

Obstetrical associated renal, cortical necrosis: uncommon but not rare!

BACKGROUND: Renal cortical necrosis (RCN) carries high morbidity and mortality in South East Asia. The purpose of this study was to look specifically at the incidence of obstetrical related RCN in renal biopsies and to evaluate its precipitating factors. In addition, prognosis, impact of aetiology and outcomes on discharge were also considered. METHODS: The study was conducted in the Department of Nephrology, Lady Reading Hospital Peshawar, Pakistan. Renal biopsies of 1,670 patients were analysed during the study period of 1998 to 2008. All the patients with obstetrical related RCN were included. Patient records, demographic data, urine output on admission and preceding history of ante-partum haemorrhage (APH), post-partum haemorrhage (PPH), septicaemia, operative interventions and retained product of conception (ROPC) was noted and need for dialysis was considered. RESULTS: Out of 1670 kidney biopsies analysed, 48 turned out to be RCN. Among them 39 patients (81.3%) had diffuse cortical necrosis, 6 patients (12.5%) had patchy cortical necrosis with ATN while 3 patients (6.3%) had predominant ATN with partial patchy cortical necrosis. Out of 48 patients, 25 (52.1%) were oliguric, 18 (37.5%) were anuric while 5 (10.4%) had urine output > 800 ml 24 hr. Operative interventions were found in 29 patients while 19 patients had normal vaginal delivery (NVD). 16 (55.2%) patients with operative intervention had PPH. Thus the association proved to be significant (p = 0.037). CONCLUSION: Overall incidence of RCN was 2.9%. Oliguria/anuria on admission and dialysis dependency are associated with RCN. PPH and history of operative intervention have significant association and are contributing factors to development of RCN.

Waterhouse-Friderichsen syndrome and bilateral renal cortical necrosis in meningococcal sepsis.

Waterhouse-Friderichsen syndrome and bilateral renal cortical necrosis (BRCN) are rare complications of meningococcal sepsis associated with high mortality rates. We describe a 20-year-old man who presented with a 1-day history of fever, chills, malaise, and vomiting. He collapsed in the emergency room, requiring mechanical ventilation and intravenous vasopressors for resuscitation. He was noted to be anuric, and computed tomography showed adrenal hemorrhage and BRCN. Blood cultures later confirmed Neisseria meningitidis sepsis, and a biopsy confirmed renal cortical infarction. The patient was treated aggressively with intravenous antibiotics, corticosteroids, and immunoglobulins, in addition to plasmapheresis, dialysis, and supportive measures. He recovered his adrenal function and was discharged from the hospital, but he remains dialysis dependent. To our knowledge, this is the first reported case of concomitant Waterhouse-Friderichsen syndrome and BRCN in a patient with meningococcal sepsis.

Bilateral renal cortical necrosis associated with cefuroxime axetil.

Cefuroxime axetil has been associated with few reported adverse effects. We report a case of bilateral renal cortical necrosis in a female after receiving 7 doses over 4 treatment days. The patient presented with worsening symptoms consisting of arthralgias, pruritus, and abdominal pain. Laboratory data obtained was indicative of worsening renal failure and thrombocytopenia. The patient required hemodialysis by the third day. Kidney biopsy revealed cortical necrosis. The possible pathogenesis of cefuroxime axetil causing cortical necrosis in this case and a review of other reported cases of chemical induced renal cortical necrosis is discussed.

Necrosis renal cortical aguda / Acute renal cortical necrosis

La necrosis renal cortical aguda (NRCA) es la destrucción parcial o total de todos los elementos de la corteza renal. Se caracteriza por oliguria prolongada y recuperación incompleta de la función renal. Se ha implicado al vasoespasmo y a la liberación de toxinas en los eventos fisiopatológicos que producen esta enfermedad. Las causas más comunes de ARCN son complicaciones del enbarazo, síndrome urémico hemolítico, pancreatitis, sepsis, quemaduras, trauma, mordeduras de serpientes, shock y rechazo de injertos. La mortalidad es muy alta y muchos de los sobrevivientes requieren substitución permanente de la función renal

[Postpartum renal cortical necrosis]. / La nécrose corticale rénale du post-partum.

The authors report two cases of post-partum cortical renal necrosis. The diagnosis was made on clinical and biological criteria (severe, prolonged oliguria, the signs of intra-vascular coagulation defects, a rise in L.D.H. and anaemia with micro-angiopathy. It is confirmed by selective renal arteriography and renal punch-biopsy. There is a threefold method of treatment: --of the kidney condition by repeated haemodialysis and diuretics; --antihypertensive treatment; --treatment aimed at the aetiological pathology (heparin, anti-platelet aggregation and fresh plasma). Functional recovery of the kidney was obtained in both cases (after an interval of 1 year and an interval of 1 1/2 year). The authors review the diagnostic, physiopathological, morphological and therapeutic elements in the condition of cortical renal necrosis.