Acute tubular necrosis drug-induced

Tubular and interstitial diseases (e.g., analgesic nephropathy, drug-induced nephritis, oxalate nephropathy, radiation nephritis, acute tubular necrosis, and sarcoidosis)... 

It is worth emphasizing that the same drug is capable of inducing several types of renal injury, e.g. NSAIDs may lead to intrarenal hemodynamic disturbances as well as to acute tubular necrosis, acute interstitial nephritis with or without nephrotic syndrome, and sometimes to various glomerular and arteriolar diseases [50,51]. 

Acute tubular necrosis is the most common presentation of drug-induced kidney disease in hospitalized patients. The primary agents implicated are aminoglycosides, radiocontrast media, cisplatin, amphotericin B, foscarnet, and os-motically active agents. 

In an analysis of 131 biopsies of drug-induced ARE [6,16], acute tubular necrosis occurred in 61.1% of the cases while acute interstitial nephritis was the diagnosis in 16.8%. Most cases were due to aminoglycoside antibiotics, NSAIDs and analgesics. Interestingly, acute... 

ACE inhibitors have emerged as a major cause of drug-induced ARF [9,14, 31, 48, 49]. Only a minority of ACE-inhibitor related cases have associated renal artery stenosis [31]. However, these groups of patients are older than the usual patient with drug-induced ARF, and more frequently are afflicted with underlying chronic renal failure [49]. When a renal biopsy is performed, it shows either severe arteriosclerosis of small renal arteries or acute tubular necrosis [31]. ACE inhibition followed by ARF may sometimes result in severe irreversible renal damage [31, 49] and even death [31]. 

Nishijima T, Yazaki H, Hinoshita F, Tasato D, Hosimoto K, Teruya K, et al. Drug-induced acute interstitial nephritis mimicking acute tubular necrosis after initiation of tenofovir - containing antiretroviral therapy in patient with HFV-l infection. Intern Med... 

Tacrolimus causes acute reversible renal dysfunction in renal [661-663,667], hver [290,664-666,679,680], heart [681-683] and pulmonary [684, 685] transplant recipients and in patients with immunologically mediated diseases [686]. Tacrolimus-induced GFR and RBF decrease is associated with an important increase in renal vascular resistance, both in humans and rodents [63,679,687-692]. Calcium channel blockers improved renal function in TAC-treated liver transplant recipients [693] and in animal models of TAC nephrotoxicity [689,694-6%]. Tacrohmus acute nephrotoxicity, similar to CSA, shows normal renal histology or non-specific changes such as isometric cytoplasmic vacuolation in tubular epithelial cells, microcalcification, giant mitochondria and lysosomes, and necrosis and early hyahnosis of individual smooth muscle cells in the afferent arterioles, which revert with drug reduction or discontinuation [697-699]. 

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