The virus responsible for COVID-19, SARS-CoV-2, causes disease that extends far beyond the respiratory system. The infection triggers a complex, body-wide response that affects nearly every major organ, including the kidneys. This systemic involvement makes the kidneys a vulnerable target, often leading to serious complications during the acute phase of illness. The kidney’s functional unit, which filters waste and regulates fluid balance, is susceptible to both direct viral attack and the body’s inflammatory reaction.
Acute Kidney Injury During COVID Infection
The most immediate and severe kidney complication observed during the acute phase of COVID-19 is Acute Kidney Injury (AKI). AKI is the sudden loss of kidney function, causing waste products to build up in the blood. Studies show AKI is frequent in hospitalized patients, with incidence rates often reported between 28% and 36% of all admitted cases.
The risk for AKI increases significantly in the most severely ill patients, particularly those requiring intensive care and mechanical ventilation. For patients admitted to the Intensive Care Unit (ICU), the prevalence of AKI can be as high as 46%. This drop in filtering capacity can be life-threatening and may require temporary support.
In the most severe cases, roughly 9% of all hospitalized patients need renal replacement therapy, commonly known as dialysis, to clean toxins from their blood while the kidneys recover. Dialysis is necessary when the kidneys cannot manage fluid and waste, which can lead to swelling, dangerous electrolyte imbalances, and confusion. Many patients who receive this support during acute infection eventually recover enough function to discontinue the treatment.
Biological Pathways of Kidney Damage
Kidney damage during COVID-19 results from a combination of three distinct biological processes. The first is direct viral invasion. The virus uses the angiotensin-converting enzyme 2 (ACE2) receptor, which is highly present on kidney cells, particularly the proximal tubules. Replication within these cells causes structural and functional lesions, directly contributing to injury.
A second major pathway is systemic inflammation, often referred to as a cytokine storm. The body’s immune response becomes excessively aggressive, releasing high levels of signaling proteins called cytokines. This inflammatory overreaction leads to widespread damage to healthy tissues, including the delicate filtering structures and blood vessels within the kidneys.
The third mechanism involves hypercoagulation and microvascular injury, meaning the blood has an increased tendency to clot. COVID-19 affects the lining of blood vessels, leading to endothelial dysfunction and widespread clotting. These small clots can block tiny vessels within the kidneys, restricting blood flow and causing localized tissue death. The virus’s interaction with the ACE2 receptor can also disrupt the renin-angiotensin system, promoting vasoconstriction and further damage to the renal blood supply.
Recognizing Kidney Distress
Identifying potential kidney issues is important for early detection and improved treatment outcomes. A primary sign of kidney distress is a noticeable reduction in urine output. Failure to manage fluid balance also leads to swelling, known as edema, often visible in the legs, ankles, feet, or around the eyes.
Other symptoms include unusual fatigue and shortness of breath. In advanced cases, the buildup of waste products can affect the central nervous system, leading to confusion. Doctors rely on laboratory tests to confirm distress, looking for elevated levels of creatinine and blood urea nitrogen. These indicators, along with protein or blood in the urine, signal compromised filtering capacity.
Long-Term Kidney Health Following Recovery
The consequences of COVID-19 often extend beyond the initial acute illness, raising concerns about the development of chronic kidney disease (CKD). Studies tracking patients for up to a year after infection reveal a significant decline in kidney function, even in those who did not experience severe AKI. This decline is measured by the estimated glomerular filtration rate (eGFR), which indicates how well the kidneys are filtering the blood.
For patients with long COVID, the eGFR decline over one year has been measured at approximately 2.96 milliliters per minute, significantly faster than the typical age-related decline. This accelerated loss of function increases the risk of developing CKD later in life. The long-term impact is pronounced for patients who were hospitalized or who have pre-existing conditions such as diabetes or hypertension.
Even when patients who experienced AKI initially recover, kidney function often does not return to its pre-infection baseline. This lasting reduction in kidney health underscores the need for continued monitoring and follow-up care with specialists after recovery, especially for those who were severely ill.