Ten years ago we reported a case of acute kidney injury (AKI) with occlusive red blood cell (RBC) tubular casts in a patient on warfarin therapy, who had high international normalized ratio (INR). We termed this condition warfarin related nephropathy (WRN). Later, we and others demonstrated that WRN is a part of the broader syndrome, when patients on other anticoagulants may develop AKI. This new syndrome is referred nowadays as anticoagulant related nephropathy (ARN). We developed an animal model that reproduces the main histologic findings of ARN in humans. Renal pathology database was searched for kidney biopsies from patients on anticoagulant therapy. Cases with acute kidney injury were analyzed. Rtas were used to create 5/6 n4phrectomy model. Based on our renal pathology database, among 8636 native kidney biopsies reviewed at our institution, there were 47 (0.54 %) patients in whom deterioration in the kidney function could not be explained by kidney biopsy findings alone if anticoagulation was not taken into the equation. Thirty five of those patients (74%) were on warfarin therapy, five (11%) were on anti-platelet medications (including two on heparin, two on enoxaparin and one on Plavix/aspirin) and one (2%) on Factor Xa inhibitor (apixaban). Six (13%) did not have records of anticoagulation therapy, but they had acute coagulopathy (such as disseminated intravascular coagulation syndrome) at the time of deterioration of kidney function and their biopsy findings suggested of ARN. In addition to acute tubular necrosis (ATN) and numerous RBC casts, these patients had underlying glomerular changes, but the severity of that glomerular disease was out of proportion to the number of RBC casts and/or hematuria in these patients. Among these glomerular changes, the most common was mild glomerular immune complex deposits without significant proliferative lesions (23 cases, 49%), followed by mild focal pauci-immune crescentic glomerulonephritis (7 cases, 15%), diabetic glomerulosclerosis (5 cases, 11%) and focal segmental glomerular sclerosis (FSGS, 5 cases, 11%). We demonstrated that 5/6 nephrectomy in rats is a suitable models to study ARN. Thus, 5/6 nephrectomy rats had increase in serum creatinine and RBC tubular casts in the kidney when treated with high dose of warfarin or dabigatran (direct thrombin inhibitor). We demonstrated that the mechanisms of ARN include oxidative stress that plays a significant role in the acute tubular injury, but not in the glomerular filtration barrier injury. Anticoagulant-treated animals developed hypertension with more pronounced increase in the systolic blood pressure than in diastolic blood pressure. ARN is an uncommon diagnosis in renal pathology practice, but it should be considered when there is a disproportion between the severity of glomerular changes and the number of RBC casts and/or hematuria in a kidney biopsy in patients on anticoagulant therapy or who presented with acute coagulopathy. The glomerular changes in patients with suspected ARN are insufficient to explain the occurrence of substantial blood in tubules. Animal model of 5/6 nephrectomy in rats reproduces the main clinical and pathologic features of ARN.