Multiple Myeloma as the Underlying Cause of Thrombotic Microangiopathy Leading to Acute Kidney Injury: Revisiting a Very Rare Entity

Thrombotic microangiopathy (TMA) describes a pathological process of microvascular thrombosis, consumptive thrombocytopenia, and microangiopathic hemolytic anemia, leading to end-organ ischemia and infarction, affecting particularly the kidney and brain. TMA is a pathological feature of a number of clinical disorders including thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, and atypical hemolytic uremic syndrome. Rare but important, TMA may also occur in malignancy, connective tissue disease, malignant hypertension, and renal transplantation (rejection or drug toxicity). We present a very rare case where the patient developed acute kidney injury from TMA but found to have multiple myeloma as the possible underlying etiology

Thrombotic Microangiopathy Associated With Synthetic Cannabinoid Receptor agonists

Marijuana is one of the most commonly used recreational drugs in the United States. As marijuana is illegal in the majority of countries, the use of readily available and unregulated synthetic cannabinoids (SCBs) has increased. Little is known about the potential adverse effects of SCBs especially in regards to their nephrotoxicity. Case reports of acute kidney injury (AKI) from acute tubular injury secondary to their use have been reported. However, the exact pathology, mechanism, and extent of renal injury remain unknown. We report the first case of biopsy proven thrombotic microangiopathy (TMA) associated with SCBs resulting in AKI. The patient suffered significant morbidity with loss of renal function eventually requiring renal replacement therapy

Managing Acute Kidney Injury (AKI) in the Setting of the COVID-19 Patient Surge

Presented by the Greater New York Hospital Association This panel of nephrologists cared for patients at the height of the spring surge in the Northeast. The aim of the webinar is to share highly technical clinical knowledge and experiences with clinicians across the country who are or will be encountering critically ill patients with Acute Kidney Injury due to COVID-19. Examples of topics include discussion of therapeutic options, use of treatment modalities, and strategies for managing scarce resources. Featured Speakers: Dr. Alan Kliger, Yale School of Medicine Dr. Renee Garrick, New York Medical College-Westchester Medical Center Dr. Leslie Wong, The Cleveland Clinic Dr. David Chartyan, NYU Langone Health Dr. George Coritsidis, NYC Health+Hospitals/Elmhurst Dr. Jeffrey Silberzweig, NewYork-Presbyterian Hospital Dr. Savneek Chugh, New York Medical-Westchester Medical Cente

Dosing of Radioactive Iodine in End-stage Renal Disease Patient with Thyroid Cancer

We describe detailed administration of thyroidal and extrathyroidal doses of radioiodine to a patient with end-stage renal disease on hemodialysis. A thorough description of area under curve measurements in a patient with compromised renal function has rarely been described in the literature. Few publications have described thyroid cancer management of patients on hemodialysis, and we believe our management will aid in patient treatment in the future. Learning points: Scheduling of hemodialysis is important when administering radioactive iodine.Treatment of thyroid cancer with radioiodine in patients with end-stage renal disease requires multidisciplinary approach coordinating dialysis, nuclear medicine and endocrinologists care.Balancing ideal dosage of I(131) and the timing of dialysis to insure maximal thyroidal uptake and minimal extra thyroidal I(131) concentration is necessary

Uremic- and Dialysis-Associated Pericarditis

Uremic pericarditis occurs as a result of inflammation of the pericardium due to toxins and immune complexes in patients with renal disease. The initial clinical manifestations of pericarditis and acute coronary syndrome may be similar, and initial EKG findings may overlap. The management of this disease needs the combined efforts of internists, cardiologists, and nephrologists. Its incidence has been reduced since the introduction of renal replacement therapy. Dialysis continues to be the mainstay of treatment

Multiple Myeloma as the Underlying Cause of Thrombotic Microangiopathy Leading to Acute Kidney Injury: Revisiting a Very Rare Entity

Thrombotic microangiopathy (TMA) describes a pathological process of microvascular thrombosis, consumptive thrombocytopenia, and microangiopathic hemolytic anemia, leading to end-organ ischemia and infarction, affecting particularly the kidney and brain. TMA is a pathological feature of a number of clinical disorders including thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, and atypical hemolytic uremic syndrome. Rare but important, TMA may also occur in malignancy, connective tissue disease, malignant hypertension, and renal transplantation (rejection or drug toxicity). We present a very rare case where the patient developed acute kidney injury from TMA but found to have multiple myeloma as the possible underlying etiology

Atypical Hemolytic Uremic Syndrome Presenting as Acute Heart Failure—A Rare Presentation: Diagnosis Supported by Skin Biopsy

Atypical hemolytic uremic syndrome (aHUS) is a rare disorder of uncontrolled complement activation that manifests classically as anemia, thrombocytopenia, and renal failure, although extrarenal manifestations are observed in 20% of the patient most of which involving central nervous system, with relatively rare involvement of the heart. In this article, we report the case of a 24-year-old male with no history of heart disease presenting with acute systolic heart failure along with microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury. Given his presentation of thrombotic microangiopathy (TMA), along with laboratory results significant for low haptoglobin, platelets, hemoglobin, C3, C4, CH50, and normal ADAMTS13 levels, with no diarrhea and negative STEC polymerase chain reaction in stool, aHUS diagnosis was established with strong clinical suspicion, and immediate initiation of treatment was advised. Kidney biopsy to confirm diagnosis of aHUS was inadvisable because of thrombocytopenia, so the skin biopsy of a rash on his arm was done, which came to be consistent with thrombotic microangiopathy. Our case highlights a relatively rare association between aHUS and cardiac involvement, and the use of skin biopsy to support diagnosis of aHUS in patients who cannot undergo renal biopsy because of thrombocytopenia

Tenofovir and Severe Symptomatic Hypophosphatemia

Tenofovir is a broadly used drug used for the treatment of human immunodeficiency virus (HIV). Although the initial results of the clinical trials supported the renal safety of Tenofovir, clinical use of it has caused a low, albeit a significant, risk of renal damage either in the form of AKI or CKD. The pathophysiology has been linked to the effect of this medication on the proximal tubular cell. Although the exact mechanism is unknown, studies have suggested that Tenofovir accumulates in proximal tubular cells which are rich in mitochondria. It is both filtered in the glomerulus and actively secreted in the tubules for elimination and is excreted unchanged in the urine. Studies have shown an active transportation of 20-30% of this drug into the renal proximal tubule (PCT) cells via the organic anion transporters in the baso-lateral membrane (primarily hOAT1, and OAT3 to a lesser extent) and ultimate excretion of the drug into the tubular lumen via the transporters in the proximal tubular apical membrane MRP4 and MRP2 (multidrug resistance-associated proteins 2 & 4). Subsequently, the mitochondrial injury caused by Tenofovir can lead to the development of Fanconi’s syndrome which causes renal tubular acidosis, phosphaturia, aminoaciduria, glucosuria with normoglycemia, and tubular proteinuria. Here we present a case where Tenofovir treatment resulted in severe hypophosphatemia requiring hospitalization for parentral phosphate repletion