A six-year-old male castrated English Spaniel, presented to Cornell University Hospital for Animals (CUHA) emergency service November 17, 2012 on referral for azotemia. After a complete diagnostic work-up and history it is suspected that our patient’s infliction is Canine Lyme nephritis. Lyme disease causative agent is Borrelia burgdorferi that is transmitted by arthropod vectors, most notably the Ixodes ticks. 2,4,6 The most frequent presentation of canine Lyme disease is an acute monoarthritis or polyarthritis often without any systemic clinical signs. A presumptive diagnosis of Lyme disease can be made with a positive Lyme ELISA test that is followed with a positive quantitative C6 ELISA and/or a positive multiplex test after clinical signs and history raise suspicion of the disease.2,6 Over the last few years the atypical presentation of Lyme nephritis seems to be increasing in frequency. Lyme nephritis can presents as an acute renal injury evident by a protein-losing nephropathy.6,7 Acute renal injury clinical signs typically include: lethargy, polyuria, polydipsia, dehydration, and anorexia.6 Diagnostic tests usually reveal a severe azotemia, hyperphosphatemia, hypoalbuminemia, a metabolic acidosis, and positive Lyme ELISA and C6 quantitative ELISA tests.6 Renal biopsies combined with suggestive diagnostic tests, are necessary for definitive diagnosis of Lyme nephritis and reveal a glomerulonephritis, diffuse tubular necrosis therefore showing tubular casts, and interstitial lymphoplasmocytic inflammation.2 These pathologic changes are irreversible as well as the resulting renal failure, ultimately ending in death. A renal biopsy was not performed on in this case therefore a definitive diagnosis of Lyme nephritis is unable to be made. However, with all the other suggestive clinical signs and diagnostic tests it was highly suspected that our case was a case of Lyme nephritis.