Kidney growth

Kidney growth is a physiological and pathological process involving the increase in renal mass and size through cellular hypertrophy (increase in cell size) and hyperplasia (increase in cell number) [12, 13]. It is essential during metanephric development and serves as a compensatory response to nephron loss, but pathological growth is a defining feature of diseases such as Autosomal Dominant Polycystic Kidney Disease (ADPKD) and diabetic nephropathy [1, 3, 5]. This process is regulated by a network of molecular drivers, including the mTOR signaling pathway, the vasopressin V2 receptor, and growth factors like insulin-like growth factor 1 (IGF-1) and epidermal growth factor (EGF) [12, 13, 3]. In the context of pharmacology, 'Kidney growth' is typically considered a biological endpoint or clinical phenotype rather than a discrete molecular target [1, 2]. Therapeutic strategies aim to attenuate this growth by targeting its underlying molecular drivers, such as using V2 receptor antagonists like tolvaptan or mTOR inhibitors like sirolimus to slow cyst expansion and preserve renal function [5, 6, 12]. Consequently, monitoring changes in Total Kidney Volume (TKV) has become a standardized biomarker for evaluating the efficacy of treatments designed to limit pathological renal enlargement in renal ciliopathies [1, 6].

Other names

Renal hypertrophyRenal hyperplasiaCompensatory renal growthKidney enlargementCystic kidney growthRenal mass increase

Kidney growth is modulated via diverse mechanisms depending on the therapeutic driver, including Vasopressin V2 receptor antagonism to reduce intracellular cAMP and cell proliferation [5, 6], mTOR inhibition to block hypertrophic protein synthesis [12], somatostatin receptor agonism to inhibit fluid secretion and cyst growth [4, 5], and tyrosine kinase inhibition to block EGF-mediated signaling pathways [3, 8].