Vocal Fold Paralysis Following COVID-19 Vaccination in a Patient on Hemodialysis

Introduction: With the increase in number of the people receiving COVID-19 vaccination, different adverse effects associated with vaccine are being described. While vocal fold paresis (VFP) after both COVID-19 disease and COVID-19 vaccination has been rarely reported, data on this entity in dialysis population is still lacking. We present a case of VFP in a hemodialysis patient following the administration of Pfizer-BioNTech COVID-19 vaccine. Case Description: 45-year-old West Indian female with DM, HTN and End Stage Kidney Disease 2/2 Focal Segmental Glomerulosclerosis s/p kidney transplant that failed after 16 years (on low dose tacrolimus) requiring to start hemodialysis presented to the ED with complaints of voice hoarseness with dysarthria and throat itching that started ~30- 45 minutes after having received the first dose of Pfizer-BioNTech COVID-19 vaccine. She underwent Fiberoptic Indirect Laryngoscopy that showed widely patent airway with mobile vocal cords bilaterally. Symptoms were thought to be secondary to a reaction to the vaccine vs mild GERD. She received steroids and was discharged home within 24 hours after symptomatic improvement on steroid therapy. Her voice normalized within a week. Six months later, she received the second dose of Pfizer-BioNTech vaccine, ~30 minutes after which again developed dysphonia and dysarthria. This time, she was found to have bilateral VFP with incomplete closure. Steroid therapy was reinitiated and is slowly being tapered. Her dysarthria has improved;however, she continues to have hoarseness of voice even after 9 months of having received 2nd dose of vaccine. She has not received the booster dose of vaccine. Discussion(s): Current guidelines recommend booster doses of COVID-19 vaccine for immunocompromised individuals including those on dialysis. The benefits of vaccination markedly outweigh the risk of very rarely reported development of VFP after vaccination. Further research is needed to determine the prevalence of this complication in dialysis patients and to elucidate the underlying mechanisms leading to it.

Kidney Biopsy Proven Thrombotic Microangiopathy in a Heart Transplant Recipient

Introduction: Thrombotic Microangiopathy (TMA) after non renal solid organ transplantation is very rare. While few cases of TMA following liver and lung transplants have been published, it has been very rarely reported following orthotopic heart transplant (OHT). We report the first case of kidney biopsy proven De Novo TMA after OHT. Case Description: 58-year-old male with non ischemic cardiomyopathy undergoes OHT in Jan 2021. He had normal renal function pre transplantation. Post-operatively he had pericardial effusion and in that setting developed oliguric AKI from ATN requiring dialysis. His renal function recovered and was discharged without dialysis. He was on tacrolimus, MMF and steroid regimen. Frequent heart biopsies were negative for rejection. In March 2021 the patient was admitted for GI bleed and again noted to have AKI. However, during this episode he developed proteinuria of over 2gm, new compared to previous urine studies. He was discharged with a serum creatinine of 2.6mg/dL. By July 2021 renal function worsened and he underwent a renal biopsy on 7/30/21 which showed acute and chronic TMA, related to calcineurin inhibitor use. Viral causes and other medications were ruled out (CMV, BK, adenovirus, SARs-COV2). Tacrolimus was held and he was initiated on Everolimus. Genetic and complement testing revealed normal complement levels, an elevated SC5b-9 complex, heterozygous for the APOL1 gene mutation (c.[1024A>G;1152T>G] p.[Ser342Gly;Ile384Met] (G1 allele)), and heterozygous for the CFHR5 gene mutation, suggestive for complement mediated TMA. He was initiated on Eculizumab. After two doses of Eculizumab he was again admitted with acute respiratory failure requiring intubation secondary to mTOR induced pneumonitis. His renal function worsened and he was reinitiated on dialysis. After a multidisciplinary discussion, he was transitioned to cyclosporine for immunosuppression. He continues to be on dialysis and cyclosporine with eculizumab without other non-renal findings of TMA. He is currently being evaluated for kidney transplantation. He has no signs of OHT rejection on heart biopsies. Discussion(s): The early identification and treatment of TMA in OHT is important in preventing further complications associated with it. Although rare as compared to other solid organ transplants, it is essential to maintain TMA as a differential diagnosis for AKI following OHT.

Minimal Change Disease Relapse After SARS-CoV-2 Booster Vaccine

Immune dysregulation has been postulated as a pathogenetic mechanism for minimal change disease (MCD) and several vaccines have been reported to act as a trigger for relapse. While cases of both de-novo MCD and MCD relapse have been reported following severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) mRNA vaccinations, we report, to the best of our knowledge, the first case of MCD relapse following booster dose of Pfizer-BioNTech SARS-CoV-2 vaccine. 63-year-old Italian male, with history of nephrotic syndrome secondary to kidney biopsy proven MCD, who had achieved complete remission with steroid therapy, had follow up labs done that showed spot urine protein: creatinine of 10.1 and albumin of 3.0g/dL. He had received the booster dose of Pfizer-BioNTech SARS-CoV-2 vaccine 2 weeks ago, and endorsed generalized weakness, puffiness over face, edema over upper extremities that appeared within a week after administration of the vaccine, and weight gain of 10 lbs over past week. Blood pressure was elevated (152/78 mmHg). He denied any recent infections, use of Nonsteroidal Anti-Inflammatory Drugs, or antibiotics. Other diagnostic work up revealed hypertriglyceridemia, normal serum creatinine. Serological work up for secondary causes of glomerular diseases was negative. He was initiated on oral prednisone therapy. Spot urine protein:creatinine decreased to 1.1, 2 weeks after initiation of steroids. Vaccination is a recognized trigger for relapse of nephrotic syndrome. mRNA vaccines are expected to produce a higher antibody response as well as increased production of cytokines and chemokines. This can lead to dysregulation in permeability factors that can result in relapsing glomerulonephritis. As data on adverse effects of SARS-CoV-2 vaccines continue to evolve, we suggest to closely monitor patients with history of nephrotic syndrome for relapse after receipt of the SARS-CoV-2 vaccine, including the booster dose. Further studies are needed to determine whether relapse of MCD is specific for SARS-CoV-2 mRNA vaccination and to decipher mechanisms for possible immune dysregulation in those patients. This may help in formulation of protocol for vaccination in patients with nephrotic syndrome and contribute to informed decision making.

A case of severe hyponatremia in a patient with COVID-19

Introduction: Hyponatremia is a common electrolyte disturbance seen in association with conditions such as malignancy and infections. In the recent literature, hyponatremia has been linked to SARS-CoV2 infection. To date, the most likely reported etiology of hyponatremia in setting of COVID-19 has been SIADH. We describe a severe case of hyponatremia, not due to SIADH, seen in a patient with COVID-19 Case Description: 49-year-old male with history of hypertension, hyperlipidemia, positive novel coronavirus nasopharyngeal swab done as outpatient, presented to the emergency department with fever, cough and dyspnea for a week. On admission, he was afebrile with respiratory rate of 18 and oxygen saturation of 84% on ambient air. His BP was not low, and heart rate ranged from 95-105 beats per minute. Pulmonary examination revealed rales bilaterally. Initial laboratory test showed serum sodium of 104 mEq/L and serum creatinine 0.58 mg/dL. Additionally, C-reactive protein was elevated to 7.19, serum ferritin elevated at 1798 and D-dimer was 158. CXR showed bilateral infiltrates. Serum osmolality was low at 217, and urine studies showed elevated urine osmolality (328) and low urine sodium (< 35), suggestive for diagnosis of hypotonic hyponatremia from volume depletion. He received treatment with 3% hypertonic saline with a subsequentdecrease in urine osmolality to 83. Serum sodium rapidly corrected to 118 requiring hypotonic fluids to manage overcorrection. Subsequently, serum sodium improved to a level of 133 mEq/L in the next 5 days after admission Discussion: As the COVID-19 pandemic continues to evolve, cases of related hyponatremia in this setting are being reported, mostly SIADH being the underlying etiology. Various mechanisms for SIADH development, including cytokine storm, and hypoxic pulmonary vasoconstriction have been postulated, however, the common aspect of volume depleted state in setting of viral infection, leading to appropriate ADH release should not be forgotten.

Antineutrophil cytoplasmic antibody (ANCA) vasculitis with glomerulonephritis in COVID-19

Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the disease it inflicts, coronavirus disease 2019 (COVID-19), has become a global pandemic in 2020. To date, only one case of ANCA associated vasculitis (AAV) with COVID-19 has been reported from Iran. We describe the first two cases of AAV and glomerulonephritis in the United States. Case Description: Case one: 64 year old African American male with a distant (> 10years) history of cryptogenic organizing pneumonia presented to the hospital with hypoxic respiratory failure secondary to COVID19. He had an acute kidney injury(AKI) with elevated creatinine(Cr) of 7.87mg/dL. Urinalysis revealed active sediment with 55 RBC/ hpf, 65 WBC/hpf, and nephrotic range proteinuria: 5 gm/gm of creatinine. He was initiated on renal replacement therapy and received convalescent plasma along with Tocilizumab for the treatment of COVID-19. Serologic testing revealed a positive perinuclear (p)-ANCA (1:320), myeloperoxidase (32.5). Kidney biopsy was consistent with a pauci immune glomerulonephritis;cellular crescent present in 40% of glomeruli. He received pulse dose steroids and Rituximab. The patient had a good clinical response and was able to discontinue hemodialysis and serum Cr decreased to 3.5mg/dL. Case Two: 46 year old South Asian male presented with rash from leukocytoclastic vasculitis and was diagnosed with COVID-19. He had an AKI, serum Cr peaked at 4.0mg/dL with proteinuria, leukocyturia, and microhematuria on urinalysis. Cytoplasmic(c)-ANCA and proteinase-3(PR-3) were positive. A kidney biopsy was performed which revealed a necrotizing glomerulonephritis. He was treated with steroids and Rituximab with a positive response, Cr decreased to 2.0mg/dL. Discussion: It is now well known that SARS-CoV-2 affects organs outside of the respiratory system, with the kidneys being a usual target. The most commonly reported presentation of COVID-19 and the kidneys is AKI, the etiology of which is predominantly acute tubular necrosis (ATN). Collapsing GN is by far the most described glomerular lesion. Clinicians should be aware of AAV with GN as another potential pathology, and concurrent use of immunosuppression with treatment of infection, can lead to favorable clinical outcomes.

Rhabdomyolysis as initial presentation of COVID-19

Introduction: Rhabdomyolysis has infectious etiology including Mycoplasma pneumoniae infection, Legionella, and Influenza. To date, there has been one case report from Wuhan China of a patient who developed rhabdomyolysis from COVID-19 during their hospitalization. We report a case where acute kidney injury and rhabdomyolysis was the initial presentation. Case Description: A 57 year old African American male with history of HTN for more than 10 years, presented with complaints of decreased urine output for 3 days associated with dark urine that progressed to anuria, fever for 11 days, decreased appetite and oral intake and generalized muscle weakness. Labs on admission were notable for acute kidney injury (creatinine 1.77mg/dL) which progressed rapidly to a peak creatinine of 11.10mg/dL within 72 hours, and other electrolyte abnormalities including mild hyperkalemia and acidosis. His CPK was >92,000U/L on admission and COVID-19 PCR was positive. Other labs included: peak AST 1692 U/L and ALT 291U/L, ferritin 1436 ng/mL, 4.86mg/dL, DDimer 2330 DDU, urinalysis specific gravity 1.030 with large blood, 10RBCs, 20WBCs, urine spot protein/creatinine 2.1 and random urine sodium 65. Serologic workup was negative for glomerular etiology. He was presumed to have acute tubular necrosis from rhabdomyolysis. He was started on hemodialysis on day 3 of admission for anuria and worsening of renal function. He was maintained on hemodialysis with minimal ultrafiltration three times a week, intravenous fluid resuscitation along with intermittent doses of bumex. He received total of five hemodialysis treatments until he became non-oliguric and started showing signs of recovery. He was taken off dialysis approximately three weeks after his initial presentation. His creatinine decreased and is 1.4 mg/dL one month after being taken off of hemodialysis. Discussion: COVID-19 has its usual presentation of fevers, shortness of breath, dry cough and myalgias. This case highlights the importance that rhabdomyolysis can be one of the only presenting features of COVID-19. Checking CPK levels should be an integral part of not only an acute kidney injury workup in the COVID-19 patient but also for any COVID-19 newly diagnosed case as this diagnosis requires prompt and specific treatment.