Renal toxicity

This chapter describes toxicity of chemicals that target the renal system. Toxicants and toxins can produce their effects on the different anatomical locations of the kidneys by affecting the tubules, glomeruli, ducts, vessels, and interstitium. The majority of toxins manifest their effects by acute renal failure. The most important manifestation of acute renal failure is the decrease in glomerular filtration rate (GFR) that leads to an excess of urea or other nonprotein nitrogenous components in the blood (azotemia). The decrease in GFR can be due to prerenal, renal, or postrenal causes. Renal toxicity generally leads to renal or sometimes postrenal azotemia. Postrenal azotemia is usually observed in conditions of obstruction to renal outflow or postrenal leakage. The toxic effects of chemicals on the kidneys result in reduced GFR, leading to azotemia. Clinical signs of chronic renal failure primarily include: edema due to reduced renal perfusion leading to stimulation of the renin-angiotensin system, which stimulates aldosterone secretion leading to retention of sodium and water, hypocalcemia with compensatory parathyroid activity, and osteodystrophy, and reduced red blood cell counts due to decreased synthesis of erythropoietin as a result of damage to the juxtaglomerular cells. Urine analysis is one of the most important methodologies to evaluate renal function and to interpret injury to the various anatomical components of the kidneys. Urine analysis involves multiple physical and chemical parameters as well as sediment analysis.