In the United States, 726,331 patients were treated for end-stage renal disease (ESRD) in 2016 at an annual cost near $50 billion in Medicare expenditures. 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 (CKD) secondary to occupational and environmental exposures in the United States is unknown. However, these exposures represent potentially preventable causes of CKD. 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. The kidneys receive approximately 20% of cardiac output and a fraction is filtered; this amount represents 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 common renal lesion is acute tubular necrosis, and the clinical presentation is dominated by the extrarenal manifestations of these exposures with renal recovery as the rule if the other organ systems recover. CKD or ESRD also may develop after certain exposures. The common renal lesion in these cases is chronic interstitial nephritis, and lead nephropathy is a prime example. However, a rare presentation is a glomerular lesion 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 help differentiate between acute and chronic kidney disease. In acute kidney injury, the urine sediment typically is diagnostic of acute tubular necrosis with evidence of tubular damage. Most CKDs associated with exposure to agents such as lead or cadmium present with chronic interstitial nephritis characterized by tubular proteinuria (usually < 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 as to organic ...