Improved model systems to predict drug efficacy, interactions, and drug-induced kidney injury
(DIKI) are crucially needed in drug development. Organ-on-a-chip technology is a suitable …

Cystinosis is the major cause of inherited Fanconi syndrome, and should be suspected in
young children with failure to thrive and signs of renal proximal tubular damage. The diagnosis …

Renal proximal tubules are highly sensitive to ischemic and toxic insults and are affected in
diverse genetic disorders, of which nephropathic cystinosis is the most common. The …

Reabsorption of filtered solutes from the glomerular filtrate and excretion of waste products
and xenobiotics are the main functions of the renal proximal tubular (PT) epithelium. A human …

Drug-induced nephrotoxicity still hampers drug development, because current translation
from in vitro or animal studies to human lacks high predictivity. Often, renal adverse effects are …

Recent evidence implies that impaired metabolism of glutathione has a role in the
pathogenesis of nephropathic cystinosis. This recessive inherited disorder is characterized by …

Proximal tubule epithelial cells (PTEC) are susceptible to drug-induced kidney injury (DIKI).
Cell-based, two-dimensional (2D) in vitro PTEC models are often poor predictors of DIKI, …

Drug-transporter interactions could impact renal drug clearance and should ideally be detected
in early stages of drug development to avoid toxicity-related withdrawals in later stages. …

Receptor-mediated endocytosis, involving megalin and cubilin, mediates renal proximal-tubular
reabsorption and is decreased in Dent disease because of mutations of the chloride/…

The renal proximal tubule epithelium is responsible for active secretion of endogenous and
exogenous waste products from the body and simultaneous reabsorption of vital compounds …