COVID-19-associated acute kidney injury

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Main article: COVID-19

For COVID-19 frequently asked inpatient questions, click here

For COVID-19 frequently asked outpatient questions, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sogand Goudarzi, MD [2], Nasrin Nikravangolsefid, MD-MPH [3]

Synonyms and keywords: COVID-19-associated AKI

Overview

COVID-19 can involve many organs leading to organ failure, one of which is kidneys that manifest with mild proteinuria to advanced acute kidney injury (AKI).

Historical Perspective

• Early reports from China revealed that COVID-19 rarely involves the kidneys, as acute renal failure was not seen among COVID-19 hospitalized patients and mild BUN or creatinine rise [10.8%] and mild proteinuria [7.2%] occurred.

• However, recent study found 75.4% of hospitalized patients with COVID-19 pneumonia developed hematuria, proteinuria, and AKI. But, these findings are not significantly different from other critical diseases.

Classification

• COVID-19-associated AKI may be classified into 3 subtypes:
  • Prerenal AKI
  • Rhabdomyolysis-induced AKI
  • Intrinsic AKI is the most common subtype of AKI.

Pathophysiology

• Angiotensin-converting enzyme 2 (ACE2), which is a primary receptor for SARS-CoV-2 entry into cells, mostly presents in renal tubular epithelial cells as well as lungs and heart.
• Despite kidney injury following COVID-19 infection is less frequent than severe lung injury, ACE2: ACE ratio is higher in the kidneys compared to the respiratory system. (1:1 in the kidneys VS 1:20 in the respiratory system)
• After SARS-CoV-2 enters through the nasal cavity, it may travel to the kidneys and enters the bloodstream leading to severe inflammatory response activation and cytokine storm.
  • Cytokine induced AKI may occur due to intrarenal inflammation, hyperpermeability of vessels, hypovolemia and cardiomyopathy, leading to cardiorenal syndrome type 1 that is characterized by third space volume overload such as pleural effusion, edema and intravascular volume loss (hypovolemia) and hypotension.
    • cardiomyopathy and COVID-19-associated myocarditis can lead to hypotension and reduction in renal perfusion.
  • The major cytokine is IL-6, which induces inflammation and lung endothelial cell injury, leading to ARDS and hypoxia that subsequently cause renal tubular cell injury and AKI.

• Other Cytokine releasing factors in critically ill patients with COVID-19 include:
  • Extracorporeal membrane oxygenation (ECMO)
  • Mechanical ventilation
  • Continuous renal replacement therapy

• To conclude, COVID-19-associated AKI can occur as a result of:
  • Sepsis and cytokine storm
  • Hypovolemia and Hypotension
  • Hypoxemia
  • Blood clots formation due to hypercoagulable state, leading to impaired blood flow in the renal arterioles.

Causes

• SARS-CoV-2 may have a Kidney tropism. As a recent study found SARS-CoV-2 antigens in renal tubules which suggests the direct damage of SARS-CoV-2 on the kidneys. https://www.medrxiv.org/content/10.1101/2020.03.04.20031120v4.
  • Angiotensin-converting enzyme 2 (ACE2), which is a primary receptor for SARS-CoV-2 entry into cells, mostly presents in Kidneys as well as lungs and heart.
    • High expression of ACE2 was found in the renal proximal tubular cells and rarely in podocytes.

Epidemiology and Demographics

• AKI is frequently seen among patients with COVID-19 hospitalized in ICU, with prevalence of 0.6-29% in China "Acute Kidney Injury in COVID-19 Patients | COVID-19". and 22.2% in the USA.
• Approximately 43% of critically ill patients with COVID-19 developed AKI during the admission period.
• The incidence of AKI in critcally ill patients with COVID-19 is estimated between 27-85%. "Acute Kidney Injury in COVID-19 Patients | COVID-19".

Age

• AKI is more commonly observed among elderly patients.(Mean age: 57.1)

Gender

• Men are more likely to be affected and have higher risk of COVID-19 complications.
• 57.1% of AKI cases following COVID-19 were male.

Race

• There is no racial predilection for COVID-19 associated AKI.

Risk Factors

• The most potent risk factors in the development of COVID-19 associated AKI include :
  • Elderly
    • Age>60 years
  • Comorbidities
    • Hypertension
    • Coronary artery disease
    • Chronic kidney disease
    • Liver disease
    • Diabetes
    • History of AKI

Natural History, Complications, and Prognosis

Natural History

• AKI is more likely to develop in the late stages of COVID-19 in critically ill patients.
• Severe COVID-19 pneumonia and severe acute respiratory distress syndrome are associated with developing AKI.

• Approximately half of the new AKI cases following COVID-19 is mild with good short-term prognosis.

• If no improvement occurs during follow-up, it is contributed to higher mortality.

Diagnosis

Symptoms

• Patients in the early stages of kidney failure may be asymptomatic. If left untreated, patients may progress to develop Azotemia and Uremia, which occur due to the buildup of waste materials in the blood.

• Symptoms of kidney injury include :
  • Nausea and Vomiting
  • Weakness
  • Fatigue
  • Weight loss
  • Loss of appetite

Physical Examination

• Physical examination of patients with AKI is usually remarkable for:
  • Signs of dehydration, such as tachycardia, tachypnea, hypotension, and dry mucosa
  • Fluid retention, leading to edema and swelling of periorbital and extremities
  • Confusion due to severe dehydration and electrolyte imbalances
  • Decrease in urine output:Oliguria or Anuria
  • cardiac arrhythmia due to electrolyte imbalances such as high level of Potassium

Laboratory Findings

• Laboratory findings of COVID-19-associated AKI include:
  • Elevated BUN level
    • Plasma BUN-creatinine ratio> 20 in prerenal AKI
    • Plasma BUN-creatinine ratio< 15 in intrinsic AKI or acute tubular necrosis
  • Based on KDIGO definition for the diagnosis of AKI:
    • Elevated serum Creatinine by ≥0.3 mg/dl (≥26.5 μmol/l) within 48 hours; or
    • Elevated serum Creatinine to ≥1.5 times baseline within the previous 7 days; or
    • Urine volume < 0.5 ml/kg/h for >6 hours
  • Fractional excretion of sodium (FENa)
    • (FENa)< 1% in prerenal AKI
    • (FENa)> 2% in intrinsic AKI or acute tubular necrosis
  • Urinary sediment
    • Hyaline casts in prerenal AKI
    • Granular or Muddy brown casts in intrinsic AKI or acute tubular necrosis
  • Several biomarkers have been found to diagnose and predict AKI that include :
    • neutrophil gelatinase-associated lipocalin (NGAL)
    • kidney injury molecule 1 (KIM-1)
    • liver-type fatty acid-binding protein
    • interleukin 18 (lL-18)
    • insulin-like growth factor-binding protein 7
    • tissue inhibitor of metalloproteinase 2 (TIMP-2)
    • calprotectin
    • urine angiotensinogen (AGT)
    • urine microRNA

Electrocardiogram

• There are no specific ECG findings associated with AKI. However, electrolyte disturbances such as hyperkalemia might lead to various ECG abnormalities.

Treatment

Medical Therapy

• Management of AKI following COVID-19 includes antiviral therapies, identifying electrolyte disorders, and intravenous fluid resuscitation.
  • Early diagnosis and treatment of AKI in patients with COVID-19 can avoid the progression of AKI into ESRD and reduce mortality.

• Treatment of AKI following COVID-19 includes:
  • Correction of hypovolemia and hypotension by the administration of adequate intravenous fluid
    • Isotonic crystalloid is recommended among all patients who develop AKI.
  • Correction of electrolyte disorders
  • antiviral therapy:
    • Recently, Remdesivir has been found effective against COVID-19.
  • Anticoagulants in hypercoagulable conditions
  • Loop diuretics
    • In volume overload conditions
    • Diuretics should not be used regularly as they predispose patients to volume depletion.

Interventions

• renal replacement therapy
  • If AKI is unresponsive to conservative therapy
  • In volume overload conditions
  • Modality of choice in unstable hemodynamic status and ESRD, severe metabolic acidosis, severe hyperkalemia
  • renal replacement therapy is associated with hypercoagulation.
• Sequential extracorporeal therapy
  • It removes cytokines, which reduces systemic inflammation and subsequent organ failure.

Prevention

• Patients with COVID-19 should be evaluated for intravascular volume status based on physical examination and fluid balance.
  • BUN, serum creatinine, and electrolytes such as sodium, potassium and bicarbonate should be monitored frequently every 48 hours or more in high risk patients.
  • Isotonic saline is recommended as a prevention strategy for patients who are at increased risk for AKI by expanding intravascular volume.

References

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