scholarly journals P0494UNUSUAL CASE OF ACUTE KIDNEY INJURY (HISTOLOGICAL EVALUATION: COLLAPSING GLOMERULOPATHY) IN HEMOPHAGOCYTIC SYNDROME ASSOCIATED WITH NK/T LYMPHOMA

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Elisabetta Ascione ◽  
Riccardo Magistroni ◽  
Marco Leonelli ◽  
Gianni Cappelli
Keyword(s):  
Bone Marrow ◽  
Acute Kidney Injury ◽  
Clinical Judgment ◽  
Antimicrobial Agents ◽  
Early Recognition ◽  
Cytotoxic T Cells ◽  
Renal Involvement ◽  
Kidney Injury ◽  
Histological Evaluation ◽  
Collapsing Glomerulopathy

Abstract Background and Aims Hemophagocytic lymphohistiocytosis (HLH) is a severe hyperinflammatory syndrome induced by aberrantly activated macrophages and cytotoxic T cells. The primary (genetic) form, caused by mutations affecting lymphocyte cytotoxicity and immune regulation, is most common in children, whereas the secondary (acquired) form is most frequent in adults. Secondary HLH is commonly triggered by infections or malignancies but may also be induced by autoinflammatory/autoimmune disorders, in which case it is called macrophage activation syndrome. The diagnosis of HLH in adults should be based on the HLH-2004 diagnostic criteria in conjunction with clinical judgment and the patient’s history. Renal involvement has previously been reported in 24 adult cases, mostly as acute renal failure. Collapsing glomerulopathy is extremely rare with only six previous cases reported in the literature. Case presentation We report the case of an African man, 31 years old, presented with fever, acute kidney injury: serum creatinine 10.3 mg/dl; urine protein 600 mg/dl, macrohematuria, ANA/ANCA were negative, low serum C3, organomegaly, anemia, thrombocytopenia, hypertriglyceridemia, hypofibrinogenemia, hyperferritinemia, direct and indirect antiglobulin (Coombs) tests were negative, low haptoglobin; elevated LDH; normal partial thromboplatin time. Peripheral blood smear examination reveal few schistocytes. ADAMTS13 activity was found to be 25%. HBV-DNA and HIV were negative. Anticardiolipin antibodies were negative. Lab exam suggested the relapse of an EBV infection and primary mycoplasma infection. Because of uremic symptoms and persisting oliguria we started replacement therapy by hemodialysis. Plasmapheresis was started because of suspected thrombotic microangiopathy. Suprisingly the kidney biopsy was consistent with collapsing glomerulopathy with evidence of tubular injury while the bone marrow biopsy diagnosed an EBV NK/T-Cell lymphoma. During the course of his hospitalization, the patient suffered high fever. C-reactive protein, WBC and procalcitonin levels were elevated. Antimicrobial agents were initiated, starting with ceftriaxone then upgraded to piperacillin/tazobactam and then the shifted to teicoplanin and meropenem. Blood, urine and stool cultures were negative.VRE positive, IgM Mycoplasma pneumoniae were positive; EBV PCR on bone marrow blood was positive. Malaria screening was negative. The antibiotic therapy was finally switched to doxycycline as unique agent. Steroid therapy (dexamethasone daily 40 mg) and IVIG (daily 35g) were initiated then these drug were stopped. CHOP-like regimen ( Etoposide 75 mg/m2, twice a week for two weeks then once a week until the seventh week) and Rituximab (375 mg/m2, once a week for 4 weeks) were initiated and continued for two weeks. Later on the patient died because of sepsis and multi-organ failure. Conclusions The multidisciplinary approach is very important. Physicians should be aware of HLH, because early recognition may prevent irreversible organ damage and subsequent death.4,5 In adults, HLH-associated mortality remains high, especially in patients with underlying malignancies. Collapsing glomerulopathy is the most commonly reported finding on renal biopsy. Renal prognosis appears to be poor with most patients remaining dialysis-dependent. The increased awareness of HLH, together with a more rapid diagnostic workup and new therapeutic approaches, will improve the prognosis of HLH in adults.

scholarly journals It’s complicated: A case report on a COVID-19-positive HIV patient presenting with rhabdomyolysis and acute kidney injury

2020 ◽  
Vol 8 ◽  
pp. 2050313X2096542
Author(s):  
Allison Foster ◽  
Zohaib Khan ◽  
Aisha Siddiqui ◽  
Sukhdev Singh ◽  
Muhammed Atere ◽  
...  
Keyword(s):  
New York ◽  
Acute Kidney Injury ◽  
Highly Active Antiretroviral Therapy ◽  
Early Recognition ◽  
Renal Involvement ◽  
Supportive Therapy ◽  
Kidney Injury ◽  
Hiv Positive ◽  
Highly Active ◽  
The Impact

The SARS-Cov-2/COVID-19 pandemic in early 2020 has had a devastating impact on health systems around the world. While viral pneumonia remains the most common complication, reports are surfacing of cases with neurological, cardiac, and renal involvement. Even less is known about the implications in special high-risk populations. In this report, we discuss a unique case of an HIV-positive patient in New York City who presented with a 2-week history of worsening fatigue, cough, dyspnea, and myalgias and was found to have COVID-19 pneumonia and acute kidney injury. He was managed for severe uremic metabolic acidosis and electrolyte abnormalities with emergent hemodialysis and supportive therapy with subsequent improvement. Direct involvement of SARS-CoV-2 and pneumonia-induced rhabdomyolysis were identified as the precipitating factors of his acute kidney injury. The pathophysiologic mechanisms of acute kidney injury, SARS-CoV-2 renal tropism, and the impact of highly active antiretroviral therapy on COVID-19 pneumonia are discussed. We highlight the importance of clinician awareness of this potentially fatal complication of COVID-19 pneumonia, particularly in the HIV-positive population as early recognition and management can have favorable outcomes.

scholarly journals Severe bone marrow suppression due to methotrexate toxicity following aceclofenac-induced acute kidney injury

2018 ◽  
pp. bcr-2018-224722 ◽  
Author(s):  
Robin George Manappallil ◽  
Durga Prasan ◽  
Jayameena Peringat ◽  
Illolil Kuniyil Biju
Keyword(s):  
Bone Marrow ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Bone Marrow Suppression ◽  
Methotrexate Toxicity

scholarly journals The Phenotypic Fate of Bone Marrow-Derived Stem Cells in Acute Kidney Injury

2013 ◽  
Vol 32 (5) ◽  
pp. 1517-1527 ◽  
Author(s):  
Guowei Feng ◽  
Duo Mao ◽  
Yongzhe Che ◽  
Weijun Su ◽  
Yuebing Wang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Acute Kidney Injury ◽  
Kidney Injury

scholarly journals Acute kidney injury as initial presentation of renal lymphoma: Diagnostic and therapeutic challenges in a resource-limited setting

2019 ◽  
Vol 7 ◽  
pp. 2050313X1984525 ◽  
Author(s):  
Jeannine Anyingu Aminde ◽  
Nkweta Eugene Adze ◽  
Guisilla Ankwatia Dedino ◽  
Leopold Ndemnge Aminde
Keyword(s):  
Acute Kidney Injury ◽  
State Of The Art ◽  
Renal Involvement ◽  
Kidney Injury ◽  
Abdominal Distension ◽  
Lymphoma Patient ◽  
Limited Data ◽  
Resource Limited ◽  
History Of ◽  
Limited Setting

Non-Hodgkin’s lymphoma is reportedly common in Africa; however, there is limited data on renal involvement. Acute kidney injury only at presentation is rare for lymphoproliferative malignancies. A 7-year old presented to our facility with a 2-week history of progressive abdominal distension and pain, examination revealed anasarca and hypertension. On further evaluation, there were bilateral nephromegaly, acute kidney injury (AKI) and cytomorphological findings suggestive of lymphoma. Patient management was mostly supportive, and evolution was unfavourable leading to his demise. We discuss diagnostic and therapeutic challenges due to unavailability of state-of-the-art facilities in resource-constrained settings.

The patient with sarcoidosis

2015 ◽  
Author(s):  
Ravindra Rajakariar ◽  
Muhammad M. Yaqoob
Keyword(s):  
Acute Kidney Injury ◽  
Renal Impairment ◽  
Renal Disease ◽  
Low Dose ◽  
Clinical Presentation ◽  
Tubulointerstitial Nephritis ◽  
Renal Involvement ◽  
Kidney Injury ◽  
Chronic Renal Impairment

Renal involvement in sarcoidosis is common and often under-recognized. The most frequent manifestation is acute kidney injury secondary to hypercalcaemia and granulomatous tubulointerstitial nephritis. The latter can lead to both acute kidney injury and to slowly progressive chronic renal impairment with concomitant chronic damage seen on histology. This chapter describes the types of renal disease that may occur in sarcoidosis and the pathogenesis, clinical presentation, diagnosis, and treatment of the patient with sarcoidosis. Corticosteroid therapy is the cornerstone of therapy. In patients with granulomatous tubulointerstitial nephritis, the authors recommend long-term, low-dose maintenance steroids.

Acute kidney injury

2017 ◽  
Author(s):  
Edward Sharples
Keyword(s):  
Acute Kidney Injury ◽  
Early Recognition ◽  
Kidney Injury ◽  
Epidemiological Studies ◽  
Hospitalized Patients ◽  
Early Management ◽  
Common Causes ◽  
Definition Of ◽  
End Stage

Acute kidney injury (AKI) is a common, major cause of morbidity and mortality in hospitalized patients, and contributes significantly to length of stay and hence costs. Large epidemiological studies consistently demonstrate an incidence of AKI of 5–18% depending on the definition of AKI utilized. Even relatively small changes in renal function are associated with increased mortality, and this has led to strict definition and staging of AKI. Early recognition with good clinical assessment, diagnosis, and management are critical to prevent progression of AKI and reduce the potential complications, including long-term risk of end-stage renal failure. In this chapter, the pathophysiology, causes, and early management of AKI are discussed. Hypovolaemia and sepsis are the most common causes in hospitalized patients, across medical and surgical specialities. Other common causes are discussed, as well as diagnostic criteria.

scholarly journals 1481. A Study for Risk Factors of Acute Kidney Injury in Leptospirosis in a Tertiary Health Center in South India

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S540-S540
Author(s):  
Bhavana Surapareddy ◽  
Muralidhar Varma ◽  
Shashidhar V
Keyword(s):  
Risk Factors ◽  
Acute Kidney Injury ◽  
Early Recognition ◽  
Care Center ◽  
Tertiary Care ◽  
Laboratory Data ◽  
Kidney Injury ◽  
Serum Lactate ◽  
Significant Difference ◽  
Serum Bicarbonate Level

Abstract Background Leptospirosis is the most widespread zoonotic disease in the world. In India, it is endemic in coast lined states. Renal failure is a severe complication with mortality approaching 22%, early recognition of which helps clinicians in acting fast. This study aimed to investigate the predictors of Acute Kidney Injury (AKI) in Leptospirosis Methods This is a prospective, case–control study done in a tertiary care center in Southern India carried out between October 2017 and December 2018. Patients with confirmed Leptospirosis as per CDC 2013 and Faine’s criteria (2012) having AKI as per KDIGO criteria were defined as cases. Subjects without AKI were controls. Demographic, clinical and laboratory data were compared between the groups and analyzed. Logistic regression was performed to analyze the possible risk factors associated with AKI in Leptospirosis. Results A total of 329 subjects met the inclusion criteria of the study. 187 patients with AKI (CASES) and 142 patients without AKI (CONTROLS) were studied. Patients with AKI were older, (mean age- 46.99 ± 13.21 vs. 42.99 ± 15.15 years) had longer hospital stay (9.04 ± 5.62 vs. 6.27 ± 3.27 days) had higher SOFA (7.97 ±2.9 vs. 3.37 ± 2.6) and APACHE 2 scores (14.37±5.93 vs. 4.66 ± 4.4), lower mean arterial pressure (84.01 ± 14.45 vs. 89.01 ± 10.63 mmHg; P = 0.001) lower serum bicarbonate level (21.70 ± 2.35 vs. 18.73 ± 3.78 mEq/dL; P < 0.001). Factors like serum lactate, AST, ALT had no significant difference between the groups. Serovar identification was done in 88 patients, of which 57 had AKI. Australis (16.7%), Pyrogenes (16.7%) and Grippotyphosa (11.1%) were the commonest serovars isolated. Serovar most commonly associated with AKI was Pyrogenes (17.5%) Predictors for AKI were jaundice (P = 0.01, OR 2.25; CI 1.21 –3.26), vomiting (P = 0.017, OR 1.9, CI 1.12- 3.26) Hypotension (P = 0.02, OR = 12.3, CI 1.85 – 107.2), tachypnea (P = 0.006, OR = 2.55, CI 1.11- 3.24), leukocytosis (P < 0.001, OR 5.45, CI 1.86- 4.89), thrombocytopenia (P < 0.001, OR 6.49, CI 2.33 – 6.75) Conclusion Identification of features like hypotension, tachypnea, acidosis, leukocytosis, thrombocytopenia, the occurrence of serovar Pyrogenes should alert the clinician on risk of developing AKI Disclosures All authors: No reported disclosures.

scholarly journals SAT-107 BONE MARROW STROMAL CELL ANTIGEN-1 MEDIATES ACUTE KIDNEY INJURY AND KIDNEY FIBROSIS

2019 ◽  
Vol 4 (7) ◽  
pp. S50-S51
Author(s):  
T. INOUE ◽  
J. Yao ◽  
L. Huang ◽  
D. Rosin ◽  
K. Ishihara ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Kidney Injury ◽  
Stromal Cell ◽  
Bone Marrow Stromal Cell ◽  
Kidney Injury ◽  
Kidney Fibrosis ◽  
Marrow Stromal Cell ◽  
Cell Antigen

scholarly journals P0544INHIBITION OF 15-HYDROXYPROSTAGLANDIN DEHYDROGENASE (15-PGDH) PROTECTS MICE AGAINST CONTRAST-INDUCED ACUTE KIDNEY INJURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Byeong Woo KIm ◽  
Sun hee Kim ◽  
Ki beom Bae
Keyword(s):  
Acute Kidney Injury ◽  
Blood Flow ◽  
Protective Effect ◽  
Renal Blood Flow ◽  
Smooth Muscle Actin ◽  
Kidney Injury ◽  
Plasma Creatinine ◽  
Histological Evaluation ◽  
Vehicle Group ◽  
Before And After

Abstract Background and Aims Although the mechanism of contrast-induced acute kidney injury (CI-AKI) is not fully known, the imbalance of vasoconstrictive and vasodilative mediators plays a major role. Prostaglandin E2 (PGE2) is one of the vasodilators involved in this process. Inhibition of 15-hydroxyprostaglandin dehydrogenase (15-PGDH) causes elevation of PGE2 level in tissue by delaying the rapid degradation of PGE2 by the enzyme. We tested the hypothesis that the 15-PGE2 inhibitor would protect against CI-AKI in a mouse model and attempted to elucidate the mechanism involved. Method 10-week aged male C57/BL6 Mice were injected with 10gI/kg of iodixanol by tail vein. Renal blood flow measurement, right nephrectomy, and blood sampling were taken at 48 hours after iodixanol injection. The 15-PGDH inhibitor was injected before and after iodixanol administration. Plasma creatinine, NGAL, KIM-1 were measured as biomarkers for renal function. Histological evaluation was analyzed by the necrosis scoring system and TUNEL assay. Arteriolar area of outer medulla was analyzed by α-smooth muscle actin stain. Renal blood flow was measured by the non-invasive laser doppler. Results Plasma creatinine (1.94±0.75 vs 1.11±0.44 mg/dL, p=0.005), NGAL (299.7±115.87 vs 140.4±76.56 ng/mL, p=0.004), and KIM-1 (2.09±2.34 vs 0.43±0.89 ng/mL, p=0.024) levels were significantly lower when the 15-PGDH inhibitor was injected before and after iodixanol administration than the vehicle group. But no significant renal protective effect was shown when the 15-PGDH inhibitor was injected before or after iodixanol administration. The 15-PGDH inhibitor administration before and after iodixanol injection showed a significantly wider renal arteriolar area (683.63±248.46 vs 1132.97±357.46 μm2, p=0.039) and larger renal blood flow (360.0±49.72 vs 635.1±27.20, p=0.011) than vehicle administration. Conclusion The 15-PGDH inhibitor has a renal protective effect against CI-AKI in mice by increasing renal blood flow when injected intravenously before and after iodine contrast media administration.

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