Background. IgA nephropathy is considered the most common cause of glomerulonephritis. Traditionally it presents with gross hematuria after an upper airway infection. However, there is a considerable population presenting asymptomatic microscopic hematuria. Patients with SpA are believed to be more affected by IgA nephropathy than the general population, as the two conditions share common etiopathogenic pathways. This mechanism might involve the decreased expression of the receptor responsible for the clearance of IgA 1 and its immune complexes on the surface of monocytes and neutrophils. Another frequent association for patients with systemic inflammatory diseases is renal amyloidosis. Case report. Male patient B, 49 y.o., was admitted to the Republican Clinical Hospital in Apr 2017 with hypotension (75/50 mmHg), profuse edema of lower limbs up to inguinal area and confusional state. Patient was known with a history of Ankylosing Spondylitis since the age of 14, with IV x-ray stage of sacroiliitis, coxofemural and spine involvement. Since 1991 the patient followed regularly NSAIDs and intermittently corticosteroids in small doses. For a period of 6 years intermittent microscopic hematuria and mild proteinuria were noticed. The patient repeatedly tested with increased levels of serum IgAs, however refused kidney biopsy. In December 2016 he was admitted with fever, myalgia and arthralgia and HTA to a local intensive care unit. Upon that admittance the patient displayed oliguria, microscopic hematuria, mild proteinuria, and accelerated ESR, with a creatinine of 249 mcmol/L. Musculoskeletal complaints prompted increased doses of NSAIDs and corticosteroids (Prednisone 40 mg, and Aceclofenac 100mg x 2 /day), considering his main disease, despite the modified pattern of myalgia and peripheral arthralgia. A week after he was discharged he developed profuse edema that consequently led to his admittance to the republican hospital. Hematology revealed severe anemia, leucocytosis and accelerated ESR. Urinalysis showed normal SD, with leucocyturia up to 27 HPF, microscopic hematuria up to 80 RBCs HPF, with a proteinuria of 30 g/24h. Serum chemistry showed hypoproteinemia (32 g/L) and hypoalbuminemia (8.6 g/L), and elevated creatinine – 409 mcmol/L. Kidney biopsy was performed revealing moderate amyloid deposits. Despite initiated hemodyalisis, the patient died within 1 month from multiorgan insufficiency. Conclusions. long standing AS favored the development of IgA nephropathy in the given patient; most likely the co-occurrence of newly depicted high levels of creatinine, with hematuria and modified pattern on musculoskeletal complaints spoke about acute tubulointerstitial nephritis due to use extensive use of NSAIDs precipitating loss of kidney function particularly considering pre-existing amyloid deposits.