Kidney damage in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can occur even in patients with no underlying kidney disease. Signs of kidney problems can progress to a state that demands dialysis and hampering recovery. Although not without controversy, emerging evidence implicates direct infectivity of SARS-CoV-2 in the kidney. At the early stage of the pandemic, consideration was mainly on the well-recognized angiotensin-converting enzyme 2 (ACE2) receptor as being the site for viral interaction and subsequent cellular internalization. Despite the abundance of ACE2 receptors in the kidneys, researchers have expanded beyond ACE2 and identified novel viral entry pathways that could be advantageously explored as therapeutic targets. This review presents the potential involvement of toll-like receptor 4 (TLR-4), kidney injury molecule-1/T cell immunoglobulin mucin domain 1 (KIM-1/TIM-1), and cluster of differentiation 147 (CD147) in SARS-CoV-2-associated renal damage. In this context, we address the unresolved issues surrounding SARS-CoV-2 renal infectivity.