ANALGESIC NEPHROPATHY - A SODA AND A POWDER

Analgesic nephropathy has long been considered a potentially preventab le cause of renal disease, Early reports were described in patients wh o consumed analgesics containing phenacetin. In recent data, the remov al of phenacetin from analgesic preparations resulted in a reduction i n analgesic-induced end stage renal disease in Europe and Australia, H owever, a reduction in the incidence of analgesic nephropathy has not occurred uniformly, suggesting that phenacetin is not the sole cause, Current data raise concerns regarding adverse renal effects of acetami nophen and nonsteroidal antiinflammatory drugs, Aspirin taken alone ma y be of least concern, The diagnosis of analgesic nephropathy is sugge sted in subjects with chronic renal failure, a history of daily consum ption of analgesic preparations, small bumpy kidneys, and renal papill ary necrosis or chronic interstitial nephritis, However, the spectrum of disease may be changing, because these agents also may increase the risk of cardiovascular disease and chronic renal disease due to nephr osclerosis, glomerulonephritis, and diabetes mellitus, Potential patho genetic mechanisms in analgesic nephropathy include direct cellular in jury induced by analgesics, prostaglandin inhibition with reduction or redistribution of renal blood flow, and interesting new concepts rega rding the role of caffeine in increasing oxygen demand and reducing ox ygen supply in the medulla, The primary goal of therapy is discontinua tion of analgesic consumption: Because of the association between anal gesic intake and uroepithelial tumors, surveillance of patients for ne oplasm is suggested.