Benjamin Vervaet defended his PhD thesis in april 2010, entitled: The tubular epithelium and intratubular nephrocalcinosis.
Intratubular nephrocalcinosis is a kidney pathology characterized by deposition of calcium phosphate and/or oxalate crystals within the lumen of the renal tubular system. Depending on the extent of crystal deposition, nephrocalcinosis can either be left unnoticed, lead to acute and/or chronic renal failure or evolve towards kidney stones (nephrolithiasis).
Like any other bio-mineralization process its initiation and progression is determined by a complex interplay between physicochemistry and cell biology. As intratubular nephrocalcinosis is characterized by the intimate contact of crystals with the tubular epithelial cell layer, the question “What is the role of the tubular epithelium in nephrocalcinosis?” has intrigued researchers for decades.
In this thesis this cell biological issue was addressed in vivo during the initiation, the course and the recovery of intratubular nephrocalcinosis.
The major finding was that, in addition to a causal role in initiating renal crystal retention, the tubular epithelium also is involved in an active crystal clearing mechanism. Based on this dual role for the tubular epithelium, it can be suggested that kidneys undergoing crystal deposition at an extent, duration or rate above a certain threshold might deteriorate, whilst below this threshold the kidney may (continuously) clear the adhered crystal deposits and secure renal function.