Methods of Pathological Changes in the Adrenal Gland in Rheumatoid Arthritis

Abstract

Relevance. In some cases, hemodynamic disorders are pronounced sharply and lead to acute tubular necrosis with acute renal failure. This can happen with an overdose of NSAIDs. when combined with alcohol intake, and in the elderly. Acute interstitial nephritis with NSAID treatment (mainly indomethacin and ibuprofen) develops in about 1-2 out of 10,000 people. The features of this pathology are more frequent development in women and the elderly, the rarity of systemic allergic reactions, as well as the possibility of massive proteinurpn with the formation of nephrotic syndrome, which requires the appointment of GCS. Morphologically, at the same time, a combination of acute interstitial nephritis with minimal glomerular changes is often found in the kidneys. Chronic interstitial nephritis against the background of long-term HI1B1I administration (analgesic nephropathy) is found in 10-30% of patients with RA and is characterized by a progressive course with frequent attachment of papillary necrosis and gradual development of CRF. Mixtures of analgesics, especially those containing phenacetin, are considered the most nephrotoxic, however, it is currently recognized that kidney damage can develop against the background of prolonged use of any analgesic or NSAID. The duration of taking analgesics or NSAIDs before the development of analgesic nephropathy is more than 5 years. and the total doses of drugs are above 1 kg. Pathological changes in the kidneys are caused by the direct toxic effect of NSAIDs on the tubular epithelium and interstitial tissue, suppression of the production of locally renal 11 g. the development of interstitial fibrosis. Morphological examination of patients with analgesic nephropathy reveals dystrophy and atrophy of the epithelium of the renal calculi. interstitial fibrosis. and the pages of the urinary scientist also contain sclerosis of the capillaries of the mucous membrane of the urinary tract (in 80-90% of patients), papillary necrosis (in 15-40% of patients). Signs of secondary focal segmental glomerulosclerosis are less common.