More and more evidences indicate that the accumulation of intracellular lipids in the kidney will induce the pathogenesis of kidney disease. Lipid accumulation is observed in both genetic and non-genetic origins of kidney disease. Data from three different animal models of kidney disease indicate that hydroxypropyl-β-cyclodextrin can reduce intracellular renal lipids, prevent kidney structural damage, and restore function.
Dyslipidemia is common in patients with chronic kidney disease, including high blood cholesterol levels (hypercholesterolemia) and accumulation of cholesterol in the kidneys. Recent studies have shown that the increase in cholesterol in the kidney, rather than the increase in blood cholesterol, is the cause of the onset and progression of kidney disease.
Compared with untreated diabetic mice, hydroxypropyl beta-cyclodextrin significantly reduced renal cortex total cholesterol. This is related to a significant reduction in kidney damage. Using 2-HPβCD to reduce lipids in renal cells can prevent glomerular damage and renal insufficiency, suggesting that 2-HPβCD may become a treatment method for diseases. In vitro and in vivo studies on animal models representing three different types of kidney disease (diabetic nephropathy, FSGS, and Alport syndrome), the results are consistent.
The main drug candidate for the kidney is hydroxypropyl-β-cyclodextrin (HPβCD), which is a cholesterol efflux medium, which has been proven in preclinical studies to promote the elimination of cholesterol by podocytes (a component of the kidney filtration system) , Slow down the progression of podocyte damage and kidney disease.