Diabetes is one of the leading causes of chronic kidney disease (CKD), and multiple underlying mechanisms involved in pathogenesis of diabetic nephropathy (DN) have been described. Although various treatments and diagnosis applications are available, DN remains a clinical and economic burden, considering that about 40% of type 2 diabetes patients will develop nephropathy. In the past years, some research found that hypoxia response and hypoxia-inducible factors (HIFs) play critical roles in the pathogenesis of DN. Hypoxia-inducible factors (HIFs) HIF-1, HIF-2, and HIF-3 are the main mediators of metabolic responses to the state of hypoxia, which seems to be the one of the earliest events in the occurrence and progression of diabetic kidney disease (DKD). The abnormal activity of HIFs seems to be of crucial importance in the pathogenesis of diseases, including nephropathies. Studies using transcriptome analysis confirmed by metabolome analysis revealed that HIF stabilizers (HIF-prolyl hydroxylase inhibitors) are novel therapeutic agents used to treat anemia in CKD patients that not only increase endogenous erythropoietin production, but also could act by counteracting the metabolic alterations in incipient diabetic kidney disease and relieve oxidative stress in the renal tissue. In this review, we present the newest data regarding hypoxia response and HIF involvement in the pathogenesis of diabetic nephropathy and new therapeutic insights, starting from improving kidney oxygen homeostasis.

Background: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease in humans. It is a multisystemic disorder characterized by progressive cystic dilatation of both kidneys, with variable extrarenal manifestations in the gastrointestinal tract (hepatic cysts), cardiovascular system, reproductive organs and brain. An important issue of patients with hepatorenal cystic disease is the fact that complications can arise due to the growing of the cysts: local kidney complications (intracystic infection, intracystic hemorrhage) and local liver complications (portal hypertension as a result of portal vein compression by cysts, bile duct compression, ruptures and bleedings of the cysts, obstruction of the liver veins).Objective: The main purpose of our case presentation is to emphasize the fact that ADPKD can be an aggressive disease with multiple complications, which requires an early diagnosis in order to properly avoid possible complications.Material and Method: We present the case of a 61 years old male, known with polycystic hepatorenal disease, chronic kidney disease (CKD) in chronic hemodialysis since 2010, renal hypertension, hypertensive cardiomyopathy, renal anemia and stage 1 chronic lymphatic leukemia. The patient was diagnosed with hepatorenal polycystic disease 20 years ago and 9 years ago he started undergoing renal replacement therapy by hemodialysis. Three months ago, the patient presented a suddenly installed ascitic syndrome for which an MRI was performed. The imagistic investigation revealed multiple kidney and liver cysts, with secondary compression of the portal vein and a tumoral mass that may suggest an adenocarcinoma.Results: The investigations performed confi rm the diagnosis of portal hypertension secondary to compression due to cystic formations.Conclusions: Hepatorenal polycystic disease has numerous clinical variations, so it needs to be followed in a multidisciplinary way with rapid therapeutic measures to prevent complications. Further investigations are needed when dealing with suspicious cystic formations with an uncertain substrate.