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.

Concomitant Acute Tubular Necrosis and Acute Interstitial Nephritis Induced by Tipifarnib in a Patient with Squamous Cell Carcinoma of the Lung.

Tipifarnib is a novel targeted treatment for hematologic malignancies that is being recently studied for the treatment of advanced solid organ tumors with HRAS mutations. There have been scarce reports on kidney adverse events in initial phase I and II trials. We present a case of acute kidney injury in a patient that had started treatment with tipifarnib for advanced squamous cell carcinoma of the lung. Kidney biopsy revealed acute tubular necrosis together with acute interstitial nephritis. Tipifarnib was discontinued and the patient was started with high-dose corticosteroids with an early taper completing a five-week steroid course, with full recovery of kidney function.

Multiparametric ultrasound findings in acute kidney failure due to rare renal cortical necrosis.

Renal cortical necrosis (RCN) is a rare cause of acute kidney failure and is usually diagnosed on the basis of characteristic enhancement patterns on cross-sectional imaging. Contrast-enhanced ultrasound (CEUS) offers benefits in patients with kidney failure in the clinical setting including the use of a nonnephrotoxic intravascular contrast agent and the fact that it can be performed at the bedside in critical cases. Therefore, the aim of this study is to investigate whether CEUS can reliably identify typical imaging features of RCN. We retrospectively analyzed 12 patients with RCN examined in our department and confirmation of the diagnosis by either histopathology, other contrast-enhanced cross-sectional imaging tests, and/or CEUS follow-up. Assessed parameters in conventional US were reduced echogenicity, loss of corticomedullary differentiation, length and width of kidney, hypoechoic rim, resistance index and in CEUS delayed wash-in of contrast agent (> 20 s), reverse rim sign, maximum nonenhancing rim and additional renal infarction. Furthermore, imaging features in RCN were compared with the findings in renal vein thrombosis (RVT), among them echogenicity, corticomedullar differentiation, hypoechoic rim, RI value, delayed cortical enhancement, total loss of cortical perfusion and enhancement of renal medulla. All 12 patients showed the reverse rim sign, while a hypoechogenic subcapsular rim was only visible in four patients on B-mode ultrasound. A resistance index (RI) was available in 10 cases and was always less than 1. RI was a strong differentiator in separating RVT from RCN (RI > 1 or not measurable due to hypoperfusion as differentiator, p = 0.001). CEUS showed total loss of medullary enhancement in all cases of RVT. With its higher temporal resolution, CEUS allows dynamic assessment of renal macro- and microcirculation and identification of the typical imaging findings of RCN with use of a nonnephrotoxic contrast agent.

COVID-19 Pandemic and Pregnancy in Kidney Disease.

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is a rapidly spreading pandemic. Owing to changes in the immune system and respiratory physiology, pregnant women are vulnerable to severe viral pneumonia. We review the clinical course, pregnancy outcomes, and management of women with COVID-19 in pregnancy with a focus on those with kidney involvement. Current evidence does not show an increased risk of acquiring SARS-CoV-2 during pregnancy and the maternal course appears to be similar to nonpregnant patients. However, severe maternal disease can lead to complex management challenges and has shown to be associated with higher incidence of preterm and caesarean births. The risk of congenital infection with SARS-CoV-2 is not known. All neonates must be considered as high-risk contacts and should be screened at birth and isolated. Pregnant women should follow all measures to prevent SARS-CoV-2 exposure and this fear should not compromise antenatal care. Use of telemedicine, videoconferencing, and noninvasive fetal and maternal home monitoring devices should be encouraged. High-risk pregnant patients with comorbidities and COVID-19 require hospitalization and close monitoring. Pregnant women with COVID-19 and kidney disease are a high-risk group and should be managed by a multidisciplinary team approach including a nephrologist and neonatologist.

COVID-19-associated collapsing glomerulopathy: a report of two cases and literature review.

Nephrotic range proteinuria has been reported during the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and coronavirus disease (COVID-19). However, the pathological mechanisms underlying this manifestation are unknown. In this article, we present two cases of collapsing glomerulopathy (CG) associated with acute tubular necrosis during the course of COVID-19, and review the literature for similar reports. In our two cases, as in the 14 cases reported so far, the patients were of African ancestry. The 14 patients assessed had an APOL1 high-risk genotype. At the end of the reported period, two patients had died and five patients were still requiring dialysis. The 16 cases detailed in the present report strongly argue in favour of a causal link between SARS-CoV-2 infection and the occurrence of CG in patients homozygous for APOL1 high-risk genotype for which the term COVID-associated nephropathy (COVIDAN) can be put forward.

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.

Acute Thrombotic Microangiopathy and Cortical Necrosis Following Administration of Alemtuzumab: A Case Report.

Alemtuzumab, a humanized monoclonal antibody that targets CD52 antigens on lymphocytes and monocytes, has shown efficacy in preventing relapse in relapsing-remitting multiple sclerosis. Despite known severe (yet rare) renal side effects such as anti-glomerular basement membrane disease and membranous glomerulopathy, to our knowledge, alemtuzumab has never been documented to cause drug-induced thrombotic microangiopathy. We describe a 39-year-old woman with relapsing-remitting multiple sclerosis who developed acute kidney injury requiring renal replacement therapy after 1 dose of alemtuzumab, as well as microangiopathic hemolytic anemia and thrombocytopenia. Pathologic examination of a kidney biopsy specimen demonstrated extensive cortical necrosis and arteriolar fibrin thrombi with nonspecific immunofluorescence staining of immunoglobulin M and C3 and absence of immune deposits on electron microscopy. These findings were consistent with the diagnosis of acute thrombotic microangiopathy. She received dexamethasone and underwent plasmapheresis, which was unsuccessful at removing alemtuzumab. The patient received renal replacement therapy for approximately 7 weeks, followed by slow recovery of kidney function that returned close to her baseline.

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.

Assessment of Kidney Function in Mouse Models of Glomerular Disease.

The use of murine models to mimic human kidney disease is becoming increasingly common. Our research is focused on the assessment of glomerular function in diabetic nephropathy and podocyte-specific VEGF-A knock-out mice; therefore, this protocol describes the full kidney work-up used in our lab to assess these mouse models of glomerular disease, enabling a vast amount of information regarding kidney and glomerular function to be obtained from a single mouse. In comparison to alternative methods presented in the literature to assess glomerular function, the use of the method outlined in this paper enables the glomerular phenotype to be fully evaluated from multiple aspects. By using this method, the researcher can determine the kidney phenotype of the model and assess the mechanism as to why the phenotype develops. This vital information on the mechanism of disease is required when examining potential therapeutic avenues in these models. The methods allow for detailed functional assessment of the glomerular filtration barrier through measurement of the urinary albumin creatinine ratio and individual glomerular water permeability, as well as both structural and ultra-structural examination using the Periodic Acid Schiff stain and electron microscopy. Furthermore, analysis of the genes dysregulated at the mRNA and protein level enables mechanistic analysis of glomerular function. This protocol outlines the generic but adaptable methods that can be applied to all mouse models of glomerular disease.

Acute renal cortical necrosis in pregnancy: Clinical course and changing prognosis.

Obstetric cortical renal necrosis is a serious complication that can lead to chronic renal failure and the need for chronic dialysis. The aim of renal cortical necrosis therapy is to restore hemodynamic stability, institute early dialytic therapy, and treat the underlying cause of the disease. Most cases of renal cortical necrosis do not recover a normal renal function despite intensive care. We describe the course of a patient who was diagnosed with acute renal cortical necrosis in pregnancy treated with hemodialysis for three years but then she recovered her renal function.

The Impact of Kidney Disease on Acute Tubular Necrosis and Surgical Site Infection After Lumbar Fusion.

BACKGROUND: Kidney disease in spine surgery can be associated with serious complications. OBJECTIVE: To investigate the rate of acute tubular necrosis (ATN) and surgical site infection (SSI) after lumbar fusion in patients with kidney disease. METHODS: A review of the U.S. Nationwide Inpatient Sample from 2002 to 2011 was performed to identify patients who underwent lumbar fusion for degenerative spine disease or disk herniation. Four groups were established: no kidney disease, chronic kidney disease (CKD), end-stage renal disease (ESRD), and posttransplant. A multivariate analysis was performed to control for age, sex, and comorbidities. RESULTS: A total of 268,158 patients met the criteria; 263,757 with no kidney disease (98.4%), 3576 with CKD (1.3%), 586 with ESRD (0.2%), and 239 posttransplant (0.1%). Rates of ATN were 0.1%, 2.9%, 3.6%, and 0.0% for the 4 groups, respectively (P < 0.001). Rates of SSI were 0.3%, 0.4%, 1.0%, and 0.0%, respectively (P = 0.002). After controlling for patient age, sex, and medical comorbidities, patients with CKD (odds ratio [OR], 5.42; 95% confidence interval [CI], 4.14-7.09; P < 0.001) and ESRD (OR, 6.32; 95% CI, 3.89-10.33; P < 0.001) were significantly more likely to develop ATN compared with patients without kidney disease. However, CKD (OR, 0.80; 95% CI, 0.20-3.12; P = 0.754) or ESRD (OR, 1.96; 95% CI, 0.38-10.00; P = 0.415) did not increase the risk for SSI on multivariate analysis. DISCUSSION: The rate of ATN significantly increases based on severity of kidney disease. However, patients with transplants have ATN and SSI rates comparable with patients without kidney disease.

The urine sediment as a biomarker of kidney disease.

The modern era of medicine has ushered in new diagnostic technologies to assist the clinician in evaluating patients with kidney disease. The birth of automated urine analysis technology and centralized laboratory testing has unfortunately made examination of urine sediment by physicians a rare event. At the same time, identifying novel urine biomarkers for kidney disease has become a research priority in nephrology, and the search for the "renal troponin" has progressed at a fast pace. Despite this, urine sediment examination remains a time-honored test that provides a wealth of information about the patient's kidney condition and performs favorably as a urinary biomarker. It alerts the clinician to the presence of kidney disease and provides diagnostic information that often identifies the compartment of kidney injury. In addition, sediment findings may guide therapy and assist in prognostication. As such, it is premature to abandon urine sediment examination. It may be more appropriate to combine urine sediment examination with new candidate biomarkers that enter clinical practice to create a "diagnostic panel" that provides clinicians with a useful battery of diagnostic tests. To accomplish this, we as nephrologists must encourage continued training and maintenance of competency in urine sediment examination.

[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.

Post-partum bilateral renal cortical necrosis in antiphospholipid syndrome and systemic lupus erythematosus.

In the presence of systemic lupus erythematosus or related autoimmune disorders, antiphospholipid syndrome (APS) is termed secondary APS. Pregnancy-related renal failure due to SAPS is rarely reported in the literature. We present the case of a young primgravida woman with bilateral renal cortical necrosis due to secondary APS in late pregnancy.