View clinical trials related to Polycystic Kidney.
Filter by:The aim of the study is to assess the improvement of health in patients affected by CKD when they are exposed to non-pharmacological treatment strategies as nutritional program (NP), physical activity program (PA) and mindfulness program (MP), when they are conveyed to the patient by means of digital technologies or not. In the present study, non-pharmacological interventions conveyed by a digital technology (investigational arm) will be compared to a standard, paper-based approach (control arm).
Abdominal pain, sometimes severe, is a known symptom of polycystic kidney disease (PKD) related to the cystic expansion. This study will investigate whether the vasopressin V2 receptor antagonist lixivaptan can alleviate intractable pain in a pediatric PKD patient who cannot tolerate the related vasopressin V2 receptor antagonist tolvaptan.
Triptolide has been approve effective in animal model.
Positive data originating from two polycystic liver patients treated with somatostatin analogues, showed a volume reduction of 38.3% and 14.9%. These two patients had complicated polycystic livers and no other therapeutic options were available. Patients who participated in LOCKCYST trial are able to benefit from active treatment. Participants will be actively treated for 24 weeks.
Autosomal-Dominant Polycystic Kidney Disease (ADPKD) is the most common hereditary renal disease, characterized by the progressive development of fluid-filled cysts in the kidney leading to progressive loss of renal function and eventually to renal failure. It is responsible for 8% to 10% of the cases of end stage renal disease (ESRD) in Western countries. ADPKD progression is largely dependent on the development and growth of the cysts and secondary disruption of the normal tissue. Renoprotective interventions in ADPKD - in addition to achieve maximal reduction of arterial blood pressure and proteinuria and to limit the effects of additional potential promoters of disease progression such as dyslipidemia, chronic hyperglycemia or smoking - should also be specifically aimed to correct the dysregulation of epithelial cell growth, secretion, and matrix interactions characteristic of the disease. Genetically in the ADPKD three different genes are implicated (PKD1 85% of the cases, PKD2 15% and probably PDK3 not yet identified). PKD1 gene encodes a protein named polycystin-1 (PC1). Defect in PC1 lead to aberrant activation of the enzyme mTOR in the epithelial cells of the renal tubules which eventually leads to abnormal proliferation of these cells and cysts generation. Sirolimus (Rapamycin) is an immunosuppressant mostly used for the management of kidney transplant recipients. This drug by very specifically and effectively inhibiting mTOR, exerts antiproliferative and growth inhibiting effects and could be extremely important for the inhibition of cyst progression in ADPKD. Animal models of ADPKD have shown that short-term treatment with sirolimus resulted in dramatic reduction of kidney size, prevented the loss of kidney function, and lowered cyst volume density. Similarly, retrospective observations from kidney transplant recipients have documented that sirolimus treatment reduced kidney volumes by 25%, whereas there was no effect in patients not given the drug. Overall, these findings provide the basis for designing a prospective study in ADPKD patients aimed to document the efficacy of sirolimus treatment in preventing further increase or even reducing the total kidney volume and the renal volume taken up by small cysts, eventually halting kidney disease progression. It is a 6 month treatment with sirolimus compared to conventional therapy in adult patients with ADPKD and normal renal function or mild to moderate renal insufficiency.