DOI: https://doi.org/10.21203/rs.3.rs-2342570/v1
The coronavirus disease outbreak of 2019 (COVID-19) has quickly turned into a pandemic around the world [1]. Acute kidney injury, which can occur in anywhere between 0.5% and 80% of hospitalized COVID-19 patients, is frequent [2]. Hematuria, proteinuria, and an acute kidney injury are signs of kidney involvement in the context of COVID-19, and these symptoms are linked to higher death rates and more serious infections [3]. Cardiorenal syndrome, which results in kidney damage, can be brought on by fluid loss, fever, and clinical signs of prerenal azotemia [4]. Severe blood loss and low blood pressure associated with major abdominal or heart surgery, severe infections like sepsis, and injuries are all potential causes of prerenal acute kidney injury [5]. Patients with COVID-19 frequently come with fever, and pre-hospital fluid resuscitation is infrequently used; therefore, volume depletion upon admission may be prevalent in these patients [6]. To avoid acute kidney injury in these situations, hypovolemia should be treated. This case study indicates that the middle-aged patient was newly diagnosed with prerenal acute kidney injury in a COVID-19 infection.
A middle-aged black African male carpenter (age 60) who had been experiencing difficulties breathing and a dry cough for three days was taken to the emergency room on September 2, 2022. The hospitalized patient had a two-day history of weakness, dizziness, and malaise. He had never before used any nephrotoxic medications. He had no prior history of sepsis, heart failure, shock, cirrhosis, or bilateral renal artery stenosis. The patient who was hospitalized had a history of medicines and medical conditions. He didn't come from a medically or pharmaceutically inclined household. He did not exhibit any signs of recent intense exercise, alcohol consumption, or urine urgency or dysuria. Five days prior to being admitted, he had a history of using public transportation to travel outside of the city to another town to visit his siblings while not wearing a face mask. He had never before experienced a COVID-19 infection or a chronic renal condition. He had previously had stage-I hypertension three years prior and had been treated with amlodipine 5 mg orally once daily and hydrochlorothiazide 25 mg orally once daily. Before being admitted, he had taken his antihypertensive medications consistently.
When he arrived at the emergency room, he had two days' low urine output, weight loss, cold intolerance, dehydration, stress, fever, and blood in his urine. Seven days before being admitted, he was in good health low urine output, weight loss, cold intolerance, dehydration, stress, fever, and blood in his urine. Seven days before being admitted, he was in good health. His vital signs at the emergency room were 38.8°C body temperature, 79 kg weight, 1.75 m height, 25.8 kg/m2 body mass index, 102 beats per minute peripheral pulse, 144/97 mmHg blood pressure, 20 breaths per minute respiratory rate, and 87% oxygen saturation on ambient air.
His blood chemistry done upon his admission in emergency department showed blood urea nitrogen of 41 mg/dl, fasting blood glucose of 117 mg/dL, a 2-hour postprandial blood glucose of 156 mg/dL, serum sodium of 121 mEq/L, serum potassium of 7.1 mEq/L, Hb 12.7 g/dL, leukocytes of 4,340/µL, polymorphonuclear leucocytosis with 1850 neutrophils per microliter of blood (normal value: 2,500-7,000 neutrophils per microliter of blood), platelets of 139,800/µL, neutrophils 70%, pH arterial blood of 7.07 (normal value: 7.32-7.43), anion gap level of 23 mEq/L (normal value: 3-10 mEq/L), partial pressure of carbon dioxide of 32 mmHg (normal value: 38-42 mmHg), serum bicarbonate level of 20.0 mEq/L (normal value: 22-29 mEq/L), plasma creatinine of 2.7 mg/dL, glomerular filtration rate of 32.5 mL/min, serum phosphate level of 2.6 mg/dL (normal value: 2.8-4.5 mg/dL), white blood cell count of 18750 cells/mm3 (normal value: 4500-11000 cells/mm3), serum chlorine level of 94 (normal value: 96-106 mEq/L), an aspartate aminotransferase level of 61 units/L (normal value: 0 - 35 units/L), an alanine aminotransferase level of 79 units/L (normal value: 0 - 35 units/L), an erythrocyte sedimentation rate of 15 mm/hour (normal value: 0 - 20 mm/hr), 45% hematocrit (normal value: 39% - 49%), lymphocytes 17%, urine volume of 1450 mL per day, troponin T level was normal, and urine analysis was positive for urine ketones of 2+. After being admitted, he received five liters of intranasal oxygen per minute for three hours before being transported to an intensive care unit.
The results of his neurological test showed a Glasgow coma scale of 10/15. The first chest radiograph revealed multifocal, patchy airspace illness, which was suggestive of atypical pneumonia or viral infection, specifically COVID-19.A sinus tachycardia was discovered on his electrocardiogram, with an ST-segment of 0.06 seconds and a heart rate of 110 beats per minute (normal range: 60-100 beats per minute) (the normal range of the ST-segment is ordinarily around 0.08 second). He has never made prior, approved COVID-19 contact. routine reverse transcription polymerase chain reaction (RT-PCR) COVID-19 testing in the emergency room; the results were positive, and he was subsequently hospitalized in the critical care unit.
After spending thirty hours in the emergency room and testing positive for SARS-CoV-2 virus, he was transferred to an intensive care unit with prior diagnoses of managed stage I hypertension, new onset prerenal acute kidney damage, and recently confirmed COVID-19 infection.
As part of the procedure for managing SARS-CoV-2 at the time of his admission, he began oxygen saturation with five liters of oxygen administered through a nasal cannula. He received a bolus of 1 L of ringer lactate upon admission to an intensive care unit, followed by 400 mL/hour of maintenance lactated ringer. He was anuric for the first day. On the second day after the initial 24 hours, his urine production climbed to 800 mL over 12 hours. He did not require continuous renal replacement therapy because his kidney indices were stable and his urine output increased to near-normal levels within 24 hours. He was given frusemide 40 mg/2 mL intravenously twice a day for three days to increase urine output, flow, and debris flushing. He was given subcutaneous enoxaparin 80 mg 12 hours a day for her confirmed COVID-19. To reduce hospital-acquired infections, he was given a broad-spectrum antibiotic such as 500 mg of azithromycin once a day for five days and 1 g of intravenous ceftriaxone daily for three days in a row. He was given 500 mg of acetaminophen as needed to reduce COVID-19 infection-related fever.
Outcome and follow-up
He managed his blood pressure effectively with antihypertensive drugs and dietary changes after nineteen days in the hospital. The Cockcroft-Gault equation was used to assess her estimated glomerular filtration rate prior to discharge, which resulted in a relative glomerular filtration rate of 61 mL/min/1.73 m2. On September 21, 2022, the patient was discharged from the hospital after two consecutive negative throat swab tests for COVID-19 infection. He was released while still on his original antihypertensive medications. He was advised to continue monthly follow-ups at the ambulatory clinic.
The coronavirus 2019 (COVID-19) pandemic has been linked to an increase in mortality globally [6]. The COVID-19 virus, which causes diffuse alveolar destruction, can cause an acute respiratory distress syndrome [7]. Other organs, especially the kidneys, may be damaged in addition to the lungs [8]. According to this study, COVID-19 infection damages not only the respiratory system but also the renal system through local and systematic inflammatory and immunological responses, endothelial injury, activation of coagulation pathways, and the renin-angiotensin system.
SARS-CoV-2 can infect the renal tubular epithelium and podocytes directly via an angiotensin-converting enzyme-2-dependent route, resulting in mitochondrial dysfunction, acute tubular necrosis, protein reabsorption vacuoles, collapsing glomerulopathy, and protein leakage in Bowman's capsule [9].Acute renal damage is a frequent COVID-19 consequence that is linked to considerably higher mortality [10]. COVID-19 was shown in this study to generate tiny clots in the circulation, which can block the tiniest blood vessels in the kidney and impede its function. This patient suffered from fever, fluid loss, and dehydration, all of which are symptoms of prerenal acute kidney damage.
Renal involvement with SARS-CoV-2 infection spans the entire range of kidney impairment, including blood creatinine increases and urine abnormalities [11]. The presence of hematuria and proteinuria is strongly related to an elevated risk of mortality in COVID-19 patients admitted to the hospital [12]. The patient in this study exhibited high serum creatinine, which is a biomarker of acute renal injury, as well as blood in his urine, indicating that the patient's kidney was injured.
Acute kidney damage is a well-known COVID-19 consequence, occurring in 36.6% of SARS-CoV-2 infections [13]. Approximately 5% of COVID-19 hospitalized patients develop AKI, with up to 40% admitted to the ICU [14]. In this study, the patient was brought to the ICU owing to shortness of breath caused by the presence of COVID-19 and acute renal damage, as well as low oxygen saturation in ambient air. He was taken to the intensive care unit to get mechanical ventilation.
COVID-19-related kidney dysfunction manifests itself in a variety of ways, including (1) prerenal AKI from volume depletion or cardiorenal syndrome, (2) acute tubular injury in the context of circulatory collapse, (3) thrombotic microangiopathy secondary to hypercoagulation, and (4) myoglobin-cast nephropathy due to rhabdomyolysis [15]. When compared to the methods and manifestations of COVID-19-related acute kidney damage, the patient in this study had prerenal acute kidney injury due to fluid loss and fever, as well as hypercoagulation caused by COVID-19 blocking blood in tiny blood vessels.
Implementing the Kidney Disease: Improving Global Outcomes (KDIGO) supportive care guidelines in critically ill patients with kidney involvement (e.g., avoidance of nephrotoxins, regular monitoring of serum creatinine and urine output, consideration of hemodynamic monitoring) is likely to reduce the occurrence and severity of AKI in COVID-19 [16]. He was admitted to an intensive care unit and given a bolus of 2 L of lactated ringer before being put on maintenance lactated ringer at 400 mL/hour.
The reason for renal involvement in COVID-19 is likely multifaceted, with cardiovascular comorbidities and predisposing conditions (eg, sepsis, hypovolaemia, and nephrotoxins) playing major roles.
Consent for publication
Written informed consent was obtained from the patient for publication of this case report.
Funding
None
Competing interests
The author has no financial or proprietary interest in any of the materials discussed in this article.