Acute Kidney Injury Due To Myoglobin Cast Nephropathy in The Setting Of Coronavirus Disease 2019-mediated Rhabdomyolysis: A Case Report

Abstract Background: We present this case of coronavirus disease 2019-associated acute kidney injury with rhabdomyolysis—with noteworthy renal biopsy findings demonstrating myoglobin cast nephropathy—to add to the limited literature on coronavirus disease 2019-related acute kidney injury and rhabdomyolysis. 

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Case presentation: A 67-year-old Caucasian man presented to our hospital with 3 weeks of malaise and decreased oral intake and several days of abnormal taste, poor appetite, decreased urine output, gastrointestinal symptoms, and myalgias, and was ultimately diagnosed with coronavirus disease 2019. His hospital course was complicated by acute kidney injury and, upon workup of his renal failure, was diagnosed with myoglobin cast nephropathy due to coronavirus disease 2019-mediated rhabdomyolysis. Ultimately, his renal function improved following hydration back to his baseline 6 weeks after his initial diagnosis of coronavirus disease 2019. Conclusions: Given our limited knowledge of the manifestations of coronavirus disease 2019, it is important to have a more in-depth understanding of the spectrum of disease of coronavirus disease 2019, which can affect various organ systems, including the kidney, and the manifestations of end-organ damage associated with it. We present this case to highlight a rarely reported funding of myoglobin cast nephropathy due to coronavirus disease 2019-mediated rhabdomyolysis. 

Keywords: COVID-19, SARS-CoV-2, Acute kidney injury, Rhabdomyolysis, Myoglobin cast nephropathy, Case report

Background

Coronavirus disease 2019 (COVID-19) may present with a wide range of clinical manifestations, affecting various organ systems, including the kidney. Acute kidney injury in patients with COVID-19 is frequently multifactorial and evidence of direct viral invasion of renal tissue as a major etiology is lacking. Myoglobin cast nephropathy causing acute kidney injury may occur due to COVID-19-associated rhabdomyolysis. 

Case reports of COVID-19-related rhabdomyolysis have been described, but rarely have demonstrated associated renal biopsy histopathology findings, and we report this case to emphasize that myoglobin cast nephropathy can occur rarely due to COVID-19-mediated rhabdomyolysis and lead to severe, though reversible, renal failure.

Case presentation 

History 

The patient was a 67-year-old Caucasian man with a past medical history of low-grade, non-invasive papillary urothelial carcinoma treated by transurethral resection of the bladder tumor, atrial fibrillation on warfarin, critical aortic stenosis corrected surgically with biologic prosthetic aortic valve replacement, coronary artery disease (CAD) status post coronary artery bypass graft (CABG), and severe emphysematous chronic obstructive pulmonary disease, who presented to our hospital from home in mid-March 2021 with symptoms of malaise and decreased oral intake for 3  weeks. For several days prior to admission, he had noted an abnormal sense of taste and poor appetite. He had symptoms of generalized fatigue, and myalgias, as well as nausea, vomiting, and diarrhea. Notably, he was eating and drinking very little during this timeframe and had produced no urine for 3 days prior to admission. Due to severe fatigue that progressed to requiring a walker to ambulate, he presented to the emergency department for evaluation. He denied fevers, chills, cough, dyspnea, headache, abdominal pain, dyspnea, and extremity edema.

Of note, he lived at home with his wife, son, and daughter-in-law as well as three grandchildren who were all healthy, none of whom had COVID-19 symptoms. He was retired and worked for an aircraft manufacturer company the past 3 years prior. He had no reported family history of renal disorders.

Of note, 3 months prior, he had been hospitalized for over a month for critical aortic stenosis requiring biologic aortic valve replacement and had CABG for CAD. At that time, his course was complicated by atrial fibrillation with rapid ventricular rate during which he developed hypotension and shock, chronic obstructive pulmonary disease exacerbation, and malnutrition secondary to severe dysphagia. Remarkably, he had been discharged to a short-term rehabilitation facility and had been home for a few weeks. He had a 30-pack-year smoking history having quit 9  years prior but otherwise denied a current history of any substance or alcohol use. Additionally, the patient had received one dose of the messenger RNA (mRNA)-1273 COVID-19 vaccine approximately 1 month prior to his presentation.

In the emergency department, he was noted to be afebrile with a temperature of 97.6  °F, hypotensive to 86/44  mmHg, with a heart rate of 73 beats per minute. His oxygen saturation was 92% on room air. On examination, he was chronically ill-appearing, but in no acute distress. His oral mucosa appeared dry. A cardiovascular examination demonstrated a grade III/VI systolic murmur in the left upper sternal border. Pulmonary examination demonstrated diminished breath sounds bilaterally. He had severe right lower quadrant abdominal and suprapubic tenderness to palpation, as well as severe bilateral thigh tenderness to palpation. Extremities were warm and well perfused. He was alert, oriented to person, place, and time, and conversant. He had no focal defects, and sensation was intact to light touch in his bilateral upper and lower extremities. To assess strict input and output measurements, a Foley catheter was placed with 200  cc urine output initially

Investigations 

A severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ribonucleic acid (RNA) polymerase chain reaction (PCR) via nasopharyngeal swab on admission was positive (Cepheid GeneXpert, N2 cycle threshold of 38.7). Additional laboratory data were notable for decreased sodium of 130  mmol/L (136–144  mmol/L), potassium of 3.7  mmol/L (3.3–5.1  mmol/L), chloride of 95  mmol/L (98–107  mmol/L), and bicarbonate of 15  mmol/L (20–30  mmol/L), with elevated anion gap of 20 (7–17). His admission creatinine was 9.55  mg/dL, from a baseline of 1.04  mg/dL (0.40–1.30  mg/dL) when last checked in January 2021 (creatinine trend during hospitalization noted in Fig. 1). His blood urea nitrogen (BUN) was 57 mg/dL (8–23 mg/dL) with estimated glomerular filtration rate (eGFR) of 6  mL per minute per 1.73 m2 (>60 mL per minute per 1.73 m2 ). Creatine kinase level was 521 U/L (11–204 U/L). He had an albumin level of 2.1  g/dL (3.6–4.9  g/dL) and a protein level of 5.8  g/dL (6.6–8.7 g/dL). These investigations are noted in Table 1. His white blood cell count was elevated to 15.4×1000 cells/µL (4.0–11.0×1000 cells/µL), hemoglobin 12.3  g/ dL (13.2–17.1  g/dL), MCV (mean corpuscular volume) 78.8  fL (80.0–100.0  fL), platelets 584×1000 cells/µL (150–420×1000 cells/µL). AST (aspartate aminotransferase) was elevated to 78  U/L (10–35  U/L) and ALT was 34 U/L (9–59 U/L). ALP (alkaline phosphatase) was elevated to 200 U/L (9–122 U/L). D-Dimer was 0.51 FEU (fibrinogen equivalent unit) (≤0.67  mg/L FEU). High-sensitivity C-reactive protein was elevated to 114.6 mg/L (≤10 mg/L).

Urinalysis demonstrated turbid, orange urine with a pH of 6, specific gravity of 1.019 with proteinuria (2+ protein), 1+ blood, positive leukocyte esterase, and no nitrite on dipstick testing. Microscopy revealed 0–3 hyaline casts, many white blood cells (unquantified), 0–2 red blood cells per high-power field, and many bacteria. Additionally, urine chemistry demonstrated sodium of 118  mmol/L, potassium of 9  mmol/L, chloride of 82  mmol/L, creatinine of 62  mg/dL, urea nitrogen of 64 mg/dL, random protein of 9.39 g/L, random albumin of 3,782.6  mg/L, with an elevated albumin/creatinine ratio of 6,130.6 mg/g Cr (0–29 mg/g Cr). Urine osmolality was decreased to 298  mOsm/kg (300–900  mOsm/kg). Tese results are noted in Table 2. He underwent a chest x-ray on admission that showed no acute pathology but revealed chronic under-lying emphysematous changes. Computed tomography (CT) of the abdomen/pelvis without contrast demonstrated edema or wall thickening of the descending and rectosigmoid colon, suggestive of colitis, as well as a horseshoe kidney (Fig.  2), and a new irregular mass-like scarring lesion and speculation in the right lower lobe of the lungs and possible ground glass and nodular lesion in the right middle lobe (the latter of which was limited by motion degradation).

For initial management, he received almost 3.5  L of normal saline intravenous fluids administered at 1  L per hour and was initiated on piperacillin–tazobactam intravenously every 6 hours for two doses. He was subsequently de-escalated to metronidazole 500  mg intravenously once and ceftriaxone 1  g intravenously daily for 3  days (empirically for presumed infectious colitis with potential urinary tract infection) and was transferred to the medical floor as blood pressure responded to intravenous fuids. Antibiotics were changed the next day to piperacillin–tazobactam. When his urine culture eventually grew>100,000 colony-forming units (CFU)/ mL Escherichia coli, which was pan-susceptible to all antibiotics tested, he was transitioned to a course of cephalexin 500 mg orally for 4 days. Blood cultures demonstrated no growth. During the hospitalization, the nephrology service had been consulted and initially felt the etiology of his renal failure was pre-renal in the setting of volume depletion, but progressive renal failure and proteinuria unresponsive to volume resuscitation and repletion with 3.5  L of intravenous fluids raised concern that there was an intrinsic renal pathology. Nephrotoxic medications such as lisinopril 2.5  mg orally were held as was his home rosuvastatin 40  mg daily orally, as creatine kinase was elevated. He had strict monitoring of intake and output as well as frequent monitoring of post-void residuals. There was no evidence of a post-obstructive component of his renal failure. He continued to have poor oral intake during the hospital course. He remained on room air during the hospitalization, aside from episodes of apnea associated with hiccups, which were attributed to vagal nerve dysfunction in the setting of recent surgery, and improved with the administration of temporary supplemental oxygen at a flow rate of 1–2 L per minute via nasal cannula.

During the hospitalization, the nephrology service had been consulted and initially felt the etiology of his renal failure was pre-renal in the setting of volume depletion, but progressive renal failure and proteinuria unresponsive to volume resuscitation and repletion with 3.5  L of intravenous fluids raised concern that there was an intrinsic renal pathology. Nephrotoxic medications such as lisinopril 2.5  mg orally were held as was his home rosuvastatin 40  mg daily orally, as creatine kinase was elevated. He had strict monitoring of intake and output as well as frequent monitoring of post-void residuals. There was no evidence of a post-obstructive component of his renal failure. He continued to have poor oral intake during the hospital course. He remained on room air during the hospitalization, aside from episodes of apnea associated with hiccups, which was attributed to vagal nerve dysfunction in the setting of recent surgery, and improved with the administration of temporary supplemental oxygen at a rate of 1–2 L per minute via nasal cannula.

On the third day of hospitalization, in the setting of worsening anion gap acidosis, anuria, and worsening renal failure with creatinine reaching 11.5 mg/dL (0.40– 1.30  mg/dL), BUN increasing to 72  mg/dL (8–23  mg/ dL), and eGFR declining to 4 mL per minute per 1.73 m2 (>60  mL per minute per 1.73  m2 ), he was initiated on intermittent hemodialysis through a Quinton hemodialysis catheter placed into his right internal jugular vein. A workup, including human immunodeficiency virus (HIV) antigen/antibody, hepatitis B surface antigen, and hepatitis C antibody testing, was unrevealing. Of note, he did have elevated serum kappa and lambda light chains but no monoclonal spike. On hospital day 3, the SARS-CoV-2 nucleocapsid immunoglobulin (IgG) antibody was positive at 23.4 (<1)

On day 4 of hospitalization, he underwent a renal biopsy (Fig.  3). Light microscopy demonstrated a distorted kidney architecture. There was interstitial fibrosis with proportional atrophy involving 30% of the biopsy tissue. There was also a patchy interstitial infiltrate consisting of lymphocytes and plasma cells with rare neutrophils present. The tubules demonstrated acute tubular injury (Fig.  3a). Several intratubular pigmented casts were present. The glomeruli and vessels demonstrated no abnormalities. Ultrastructural findings show corrugation and foot process effacement which suggests hypertension-mediated injury. Immunohistochemistry for myoglobin was positive within casts in tubules (Fig.  3a, b), while hemoglobin A was negative. The kidney biopsy showed negative immunohistochemical staining using an antibody against the SARS-CoV-2 nucleocapsid protein (TermoFisher, mouse monoclonal antibody clone B46F, dilution 1:200).

Electron microscopy demonstrated patent capillary loops. Glomerular architecture demonstrated corrugation of basement membranes with an increase in lamina rara interna (Fig.  3c).  No subepithelial deposits and no intramembranous deposits were identified. There was cytoplasmic vacuolization of the podocytes. There was segmental effacement of foot processes (Fig.  3c). There were no subendothelial deposits. Mesangial electron-dense deposits were not identified. Electron microscopy did not show the presence of viral particles. Tubuloreticular inclusions were not noted. Immunofluorescent testing was not performed in this case in the setting of this being a specimen from a patient with COVID-19.

By day 15 of his hospitalization, his creatinine kinase level had decreased from 521  U/L on admission, to 64  U/L (11–204  U/L); his creatinine downtrended to 4.19 mg/dL toward the end of his hospitalization.

Thus, his acute renal failure was attributed to myoglobin cast nephropathy in the setting of COVID-19-mediated rhabdomyolysis. His proteinuria was attributed to extensive tubular injury.

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