Renal failure processes

The primary goals of treatment are correction of the intraabdominal disease processes or injuries that have caused infection and drainage of collections of purulent material (abscess). A secondary objective is to resolve the infection without major organ system complications (e.g., pulmonary, hepatic, cardiovascular, or renal failure) or adverse drug effects. Ideally, the patient should be discharged from the hospital with full function for self-care and routine daily activities. 

The water-soluble and fat-soluble vitamins in the parenteral multivitamin mix are essential cofactors for numerous biochemical reactions and metabolic processes. Parenteral multivitamins are added daily to the PN. Patients with chronic renal failure are at risk for vitamin A accumulation and potential toxicity. Serum vitamin A concentrations should be measured in patients with renal failure when vitamin A accumulation is a concern. Previously, vitamin K was administered either daily or once weekly because intravenous multivitamin formulations did not contain vitamin K. However, manufacturers have reformulated their parenteral multivitamin products to provide 150 meg of vitamin K in accordance with FDA recommendations. There is a parenteral multivitamin formulation available without vitamin K (e.g., for patients who require warfarin therapy), but standard compounding of PN formulations should include a parenteral multivitamin that contains vitamin K unless otherwise clinically indicated. 

Foxall PJD, Bending MR, Gartland KI, et al. 1989. Acute renal failure following accidental cutaneous absorption of phenol Application of NMR urinalysis to monitor the disease process. Human Toxicol 9 491-496. 

Most estimates of diuretic binding to albumin assume that the protein itself is not altered as part of the disease process. In renal failure, however, the number of binding sites on the protein may change, which in turn affects the pharmacokinetics and dynamics of the response to an administered diuretic. Another setting associated with diminished effective diuretic concentrations occurs in nephrotic syndrome. In this disease, protein escaping from the glomerulus into the tubules binds the diuretic within the lumen. The bound drug is unavailable to exert its inhibitory effect on sodium transport. 

Traditionally, when searching for the etiology of AKI, the clinician s will subdivides the potential causes of a sudden decline of GFR into one of three general pathophysiologic processes pre renal failure, intrarenal failure or post renal failure [1]. Recently, Miet et al [ 52] in discussing drug-induce acute kidney injury detailed two additional mechanisms that need to be considered in addition to those outlined in Table 2. 

Melnikov VY, EcderT, Fantuzzi G, et al. Impaired IL-18 processing protects caspase-1-deficient mice from ischemic acute renal failure. J Clin Invest 2001 107 1145-1152. 

Nigam SKand Lieberthal W. Acute renal failure. III. The role of growth factors in the process of renal regeneration and repair. Am J Physiol Renal Physiol 279 F3-11, 2000. 

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