Drug-induced renal disease

Drug-induced renal disease by direct and indirect biochemical effects and by immunological effects... 

The estimated incidence of 18-33% drug-induced AKI in hospitalized patients contrasts with the extremely low incidence of drug-induced renal disease in outpatients as reported by Beard et al. [30], i.e., 1 300,000 person/year. This low incidence is in part due to the author s exclusion of chronic renal disease. On the other hand, acute iatrogenic renal disease developed in 1% of all patients admitted to a Canadian hospital and in as many as 5.6% of those admitted directly to the nephrology unit of the same inshtution [25] the AKI was due to multiple etiologies in 50% of... 

Swainson CP, Thompson D, Short AIK, Winney RJ. Plasma exchange in the successful treatment of drug-induced renal disease. Nephron 1982 30 244-249. 

Most instance of drug-induced renal disease are probably due to direct toxicity. Even cephalosporins such as cephalothin or cephaloridin, which can produce immunological reactions, more frequently damage the kidney directly (Parker 1979 a). 

Pearson J (2008) Drug-induced kidney disease. In Ashley C, Morlidge C (eds) Introduction to Renal Therapeutics. London Pharmaceutical Press, 139-144. 

Markowitz GS, Perazella MA. Drug induced renal failure a focus on tubulointerstitial disease. Clin Chim Acta 2005 351 31-47... 

Markowitz GS, Perazella MA Drug-induced renal failure a focus on tubulointerstitial disease. Clin Chim Acta 2005 351 31-47. Spanou Z, Keller M, Britschgi M, Yawalkar N, Fehr , Neuweiler , Gugger M, Mohaupt M, Pichler W Involvement of drug-specific cells in acute drug-induced interstitial nephritis. Am Soc Nephrol 2006 17 2919-27. 

Heroin nephropathy/clinical course Amyloidosis associated with intravenous drug abuse HIV nephropathy and its relationship to heroin nephropathy Acute kidney injury due to drug-induced rhabdomyolysis Cocaine-induced renal disease 598 599 601 603 605... 

Mechanisms of drug-induced kidney disease include immune-mediated toxicities (e.g., glomerulonephritis and allergic interstitial nephritis) and nonimmunologic-mediated toxicities which effect specialized characteristics of normal renal physiology. 

Pelletier L, Druet P. Immunologically-mediated toxin induced renal diseases. In Clinical nephrotoxins - renal injury from drugs and chemicals. De Broe ME, Porter GA, Bennett WM, Verpooten GA (editors). Kluwer Academic PubI, Dordrecht 1998 p. 31-... 

Contraindications Anuria, drug-induced or preexisting hyperkalemia, progressive or severe renal disease, severe hepatic disease... 

Biguanide drugs are contraindicated in patients with renal disease, alcoholism, hepatic disease, or conditions predisposing to tissue anoxia (eg, chronic cardiopulmonary dysfunction) because of an increased risk of lactic acidosis induced by biguanide drugs. 

When cardiac output is reduced by disease, the resultant changes in blood pressure and blood flow to the kidney are sensed as hypovolemia and thus induce renal retention of salt and water. This physiologic response initially expands the intravascular volume and venous return to the heart and may partially restore the cardiac output toward normal (see Chapter 13 Drugs Used in Heart Failure). 

Argatroban is a small molecule thrombin inhibitor that is FDA approved for use in patients with heparin-induced thrombocytopenia (HIT) with or without thrombosis and coronary angioplasty in patients with HIT. It, too, has a short half-life, is given by continuous intravenous infusion, and monitoring is done by aPTT. Its clearance is not affected by renal disease but is dependent on liver function. The drug requires dose reduction in patients with liver disease. Patients on argatroban will demonstrate elevated INRs because of test interference, rendering the transition to warfarin difficult. 

Pharmacokinetics Slow intravenous infusion is employed for treatment of systemic infections or for prophylaxis. Because vancomycin is not absorbed after oral administration, this route is only employed for the treatment of antibiotic-induced colitis due to Q difficile. Inflammation allows penetration into the meninges. Metabolism is minimal 90-100 % is excreted by glomerular filtration. [Note Dosage must be adjusted in renal failure since the drug will accumulate. Normal half-life is 6-10 hours compared to over 200 hours in end-stage renal disease.]... 

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