Renal manifestations of septic shock include acute renal failure (ARF) with azotemia, oliguria, and active urinary sediment. Factors associated with the development of ARF in septic shock include hypotension, dehydration, aminoglycoside administration, and pigmenturia. Within the kidney, both vasoconstrictive and vasodilator mediators are generated and their balance dictates renal hemodynamics. If renal hypoperfusion predominates, renal ischemic injury occurs. Renal hypoperfusion is considered to be a major factor in the pathogenesis of ARF in sepsis. Toxic products resulting from neutrophil-endothelial interactions, endothelial damage by various mediators, reperfusion injury, and microvascular thrombosis in the kidney also contribute to renal dysfunction. In patients without septic shock, renal insufficiency may occur as a consequence of glomerulonephritis or interstitial nephritis. Glomerular disease in the setting of sepsis has been reported in subacute bacterial endocarditis, pyogenic visceral abscesses, and infections at other sites. Urine sediment in glomerular disease contains red blood cells, casts (red, white, or pigmented), and protein. Renal biopsy usually shows proliferative changes. Immune complex deposition with glomerular deposits of IgG, IgM, C3, bacterial antigens, and antibodies to these antigens has been reported. Tubulointerstitial disease has been associated with Streptococcus pneumoniae, Staphylococcus pyogenes, Legionella pneumophila, salmonellosis, brucellosis, and diphtheria infections. Acute interstitial nephritis secondary to allergic reaction to antibiotics (most commonly, methicillin) has also been reported; eosinophilia and eosinophiluria are usually present in this setting.
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