Interventions for preventing the progression of autosomal dominant polycystic kidney disease

Citation: Bolignano D, Palmer SC, Ruospo M, Zoccali C, Craig JC, Strippoli GFM. Interventions for preventing the progression of autosomal dominant polycystic kidney disease. Cochrane Database of Systematic Reviews 2015, Issue 7. Art. No.: CD010294. DOI: 10.1002/14651858.CD010294.pub2.

Which therapies are the most effective to prevent the progression of autosomal dominant polycystic kidney disease?

Current clinical care for people who have autosomal dominant polycystic kidney disease (ADPKD) focuses on controlling future risks for need for dialysis and symptom management, mainly pain and bleeding. Newly discovered molecules that may slow kidney cys t growth has recently switched attention from care and treatment toward preventing disease progression and symptom control. In this review, we aimed to analyse the benefits and harms of in terventions directed at preventing progression of ADPKD.

The literature was searched to 5 June 2015. We found 30 studies (involving 2039 participants) that tested 11 different treatments. Interventions for preventing the progression of autosomal dominant polycystic kidney disease.

Reported outcomes were mostly limited to kidney function and volume. In evidence largely limited to children, it was found th at ACEi (angiotensin converting enzyme inhibitor) medicines significantly reduced diastolic blood pressure but had uncertain effects on kidney volumes and how well the kidneys work (tested by measuring the glomerular filtration rate (GFR) and serum creatinine level in patients’ blood).

In adults, ACEi did not show different effects on GFR an d the amount of a protein called albumin in the urine (albuminuria) when compared with beta blockers, or serum creatinine when compared with drugs known as ARBs (angiotensin II receptor blockers).

Evidence from a single study was inconclusive concerning the effects of vasopressin receptor 2 antagonists on kidney function an d volumes; however, these drugs made patients thirsty and caused dry mouth.

Compared with no treatment, the group of medicines known as mTOR inhibitors (mammalian target of rapamycin inhibitors) had uncertain effects on kidney function and volume but caused soft tissue swelling, mouth ulcers, infections and diarrhoea. Drugs known as somatostatin analogues slightly improved serum creatinine and total kidney volume but had no definite effects on GFR and caused diarrhoea. Data for other drugs were sparse an d inconclusive.

There is currently insufficient evidence to show that drugs used for people with ADPKD can protect kidney function to delay needing dialysis or a kidney transplant.

Further evidence from large , well-designed clinical studies is needed to inform healthcare decision making before these drugs can be chosen routinely to achieve better health outcomes for people with ADPK