TRIP

Lead Nephrotoxicity

Renal Fellow Network, 2012

I saw a patient in the clinic who was referred for evaluation by his PCP with CKD, a bland urine sediment and a history of hyperuricemia and gout.
He had no history of diabetes or hypertension and had no obvious (to me) reason for his CKD at first glance.
My attending came in and asked him if he was still using as much lead these days as he had in the past – apparently he was down to 4 times monthly.
Even at this, his exposure was significantly less than it had been when he was younger before work practices changed.
Commoner in the past when lead was ubiquitous and likely less important now as an environmental cause of renal disease, it should be suspected in people who still work with lead regularly (or had a significant past exposure).
Plumbers, fishermen (who make their own weights) and hunters (who make their own shot) continue to be at risk.
Chronic lead toxicity causes a chronic interstitial nephritis with a relatively bland urine sediment.
Patients typically have gout and this condition has sometimes been confused with uric acid nephropathy.
A in 1992 in the NEJM found that a 10-fold increase in blood lead concentration was associated with a 10-13mls/min decline in GFR in a population of asymptomatic patients.
The diagnosis is made by first determining if the patient has been exposed to significant amounts of lead and then measuring lead levels in the blood.
In patients with a historic exposure, this may not be reliable because of sequestration in the bone and x-ray fluorescence is more reliable.