The pathobiology of polycystic kidney disease from a metabolic viewpoint.

Autosomal dominant polycystic kidney disease (ADPKD) affects an estimated 1 in 1,000 people and slowly progresses to end-stage renal disease (ESRD) in about half of these individuals. Tolvaptan, a vasopressin 2 receptor blocker, has been approved by regulatory authorities in many countries as a therapy to slow cyst growth, but additional treatments that target dysregulated signalling pathways in cystic kidney and liver are needed. Metabolic reprogramming is a prominent feature of cystic cells and a potentially important contributor to the pathophysiology of ADPKD.

Systems biology of polycystic kidney disease: a critical review.

The proliferation and diminishing costs of 'omics' approaches have finally opened the doors for small and medium laboratories to enter the 'systems biology era'. This is a welcome evolution that requires a new framework to design, interpret, and validate studies. Here, we highlight some of the challenges, contributions, and prospects of the 'cyst-ems biology' of polycystic kidney disease.

Murine Models of Polycystic Kidney Disease.

Polycystic diseases affect approximately 1/1000 and are important causes of kidney failure. No therapies presently are in clinical practice that can prevent disease progression. Multiple mouse models have been produced for the genetic forms of the disease that most commonly affect humans.

N-acetylcysteine attenuates the progression of chronic renal failure.

Background: Lipid peroxidation impairs renal function. Aldosterone contributes to renal injury in the remnant kidney model. This study aimed to determine the effects of the antioxidant N-acetylcysteine (NAC) on renal function and aldosterone levels in chronic renal failure.