In the United States, 594,374 patients were treated for end-stage renal disease (ESRD) in the year 2010 at a yearly cost of well over $47 billion. Both the number of patients and the associated costs continue to grow annually. The etiology of the kidney injury in a significant percentage of these patients is never fully elucidated, and the diagnosis of renal disease of occupational origin is rarely considered. The true incidence of chronic kidney disease secondary to occupational and environmental exposures in the United States is unknown. However, these exposures represent potentially preventable causes of chronic kidney disease. Even if occupational and environmental exposures account for only a small percentage of the causes of ESRD in the United States, the significant morbidity, mortality, and costs associated with renal replacement therapy potentially could be prevented.
The kidney is especially vulnerable to occupational and environmental exposures. Approximately 20% of the cardiac output goes to the kidneys, and a fraction of this then is filtered; this is represented by the glomerular filtration rate (GFR). The GFR is normally 125 mL/min, or 180 L/d. Along the nephron, this filtrate is largely reabsorbed and then concentrated and acidified. Thus, occupational and environmental toxins can be highly concentrated in the kidney, and as the pH of the filtrate changes, some toxins can exist in certain ionic forms. These factors help to explain the pathophysiologic mechanisms involved in certain toxins. For example, lead and cadmium cause much of their renal ultrastructural damage in the proximal tubule, where two-thirds of the filtered load is reabsorbed.
Following relatively high-dose exposure to certain organic solvents, metals, or pesticides, acute kidney injury may develop within hours to days. The renal lesion usually is acute tubular necrosis. The clinical picture usually is dominated by the extrarenal manifestations of these exposures, and if the other organ systems recover, renal recovery is the rule. Chronic kidney disease (CKD) or ESRD also may develop after certain exposures. The renal lesion in these cases usually is chronic interstitial nephritis, and lead nephropathy is a prime example. However, glomerular lesions are also seen after selected exposures such as to organic solvents or silicosis; in general, glomerular lesions after occupational or environmental exposures are very uncommon.
The renal evaluation of patients thought to have renal disease associated with an environmental or occupational exposure should be guided by the history, physical examination, and clinical presentation of the renal disease. The time course will separate acute from chronic kidney disease. In acute kidney injury, the urine sediment usually is diagnostic of acute tubular necrosis. Most chronic kidney diseases associated with exposure to agents such as lead or cadmium present with chronic interstitial nephritis characterized by tubular proteinuria (usually less than 2 g/24 h) and a urine sediment usually lacking any cellular elements. A nephritic urine sediment is suggestive of a proliferative renal lesion and has been associated with only a few exposures, such ...