Difficulties in the differential diagnosis of granulomatous interstitial nephritis; [Трудности дифференциальной диагностики гранулематозного тубулоинтерстициального нефрита]

Granulomatous tubulointerstitial nephritis (GTIN) is the rarest form of acute tubulointerstitial nephritis (ATIN) and, therefore, may present with acute kidney injury (AKI). GTIN accounts for only 0.5-0.9% of cases in the spectrum of native kidney biopsies, 0.6% in graft biopsies, and 6% in nephrobiopsies in interstitial nephritis. Identification of this morphological variant of ATIN obliges the physician to conduct a differential diagnosis between diseases characterized by the development of granulomatous inflammation in different organs, which is often associated with significant difficulties. The presented observation of GTIN in a 57-year-old patient without a history of chronic kidney disease (CKD), with newly diagnosed type 2 diabetes mellitus and developed AKI after the start of therapy with modern hypoglycemic drugs from the group of sodium-glucose cotransporter-2 inhibitors (iSGLT-2) – dapagliflozin and the glucagon-like peptide-1 receptor agonist (GLP-1 RA) – semaglutide examination which led to the diagnosis of sarcoidosis with lesions of the lungs, intrathoracic and intra-abdominal lymph nodes, illustrates the complexity of the diagnostic search in such cases. The granulomas found during the morphological examination of the kidney biopsy did not have signs of caseous necrosis and were combined with diffused eosinophilic infiltration of the renal interstitium, which made it even more difficult to differentiate between GTIN of drug-induced etiology and sarcoidosis kidney damage. The key feature of the disease was the unresolved AKI after the discontinuation of antidiabetic drugs by the patient, and newly diagnosed sarcoidosis, both of which served as the reason for determining the leading cause of GTIN in the presence of two likely triggers – drug-induced kidney injury and systemic granulomatous disease. A thorough analysis of the clinical and morphological manifestations of the disease led to the conclusion that granulomatous lesions of the interstitium have combined genesis. The features of the course of GTIN in sarcoidosis and drug-induced kidney injury are also discussed. It is noted that the presented observation is the first description of the GTIN case when using a combination of drugs from the iSGLT-2 and GLP-1 RA groups. In connection with the simultaneous appearance of AKI and signs of sarcoidosis, the possibility of developing a drug-induced sarcoidosis-like reaction is discussed. Difficulties in isolating the leading factor in the development of the disease, in this case, did not prevent the initiation of pathogenetic therapy with systemic corticosteroids with the achievement of a rapid effect: a decrease in blood creatinine and a positive clinical and radiological dynamics of the pulmonary process were noted. © 2023 JSC Vidal Rus. All rights reserved.