J.H.Noyes1)Enveloped virions are the OG #LipidNanoparticles. Under ideal conditions, lipid nanoparticles < 100nm pass through the kidneys into the urine. Those larger than 100nm can get trapped in the tissues of the kidney. #KidneyDisease --structural damage and/or inflammation--further reduces the efficiency of the kidney, and presumably this reduces the size of LNPs that can be excreted through urine.
2)SARS-CoV-2 virions range from 60nm-140nm, with the majority falling somewhere between 80-120nm. After NABs denature the S-protein, larger virions will accrue in the tissues of the kidneys. Local titers of C1-INH, C4BP, and Factor H will eventually be depleted resulting in dysregulated MAC deposition and ultimately lytic activation of the SARS-like inflammatory payload, the NP-native consensus motif #TGPEAXLPY.
3)Evidence supporting this interpretation can be found in the following paper detailing the correlation between the presence of SARS-like nucleocapsid protein in urine and disease severity.
SARS-CoV-2 nucleocapsid urine antigen in hospitalized patients with Covid-19
SARS-CoV-2 nucleocapsid antigen (N-Ag) can be detected in the blood of patients with Covid-19. We used a highly sensitive and specific assay to explore the presence of N-Ag in urine during the course of Covid-19, and explore its relationship with the ...
4)Here's another paper detailing the phenomenon. It notes that the Acute Kidney Injury / Nucleocapsid Protein signal is very strong whereas no corresponding ACE2/TMPRSS2 signal is present. Subjects are obviously pre-Omicron.
https://www.frontiersin.org/articles/10.3389/fmed.2021.644715/full
Urinary Levels of SARS-CoV-2 Nucleocapsid Protein Associate With Risk of AKI and COVID-19 Severity: A Single-Center Observational Study
Background: Acute kidney injury (AKI) is very common in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) disease 2019 (COVID-19) and considered as a risk factor for COVID-19 severity. SARS-CoV-2 renal tropism has been observed in COVID-19 patients, suggesting that direct viral injury of the kidneys may contribute to AKI. We examined 20 adult cases with confirmed SARS-CoV-2 infection requiring ICU supportive care in a single-center prospective observational study and investigated whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19.Objectives: The objective of the study was to evaluate whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19.Results: Urinary SARS-CoV-2 N measured at ICU admission identified patients at risk for AKI in COVID-19 (HR 5.9, 95% CI 1.4–26, p = 0.0095). In addition, the combination of urinary SARS-CoV-2 N and plasma albumin measurements further improved the association with AKI (HR 11.4, 95% CI 2.7–48, p = 0.0016). Finally, combining urinary SARS-CoV-2 N and plasma albumin measurements associated with the length of ICU supportive care (HR 3.3, 95% CI 1.1–9.9, p = 0.0273) and premature death (HR 7.6, 95% CI 1.3–44, p = 0.0240). In contrast, urinary ACE2 and TMPRSS2 did not corr...