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. He was a non-smoker and had no family history of renal disease. He worked as a plumber and his examination was entirely normal.
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. He was using it to fix joints and was regularly exposed to lead vapor. Even at this, his exposure was significantly less than it had been when he was younger before work practices changed.
Lead toxicity is an under-recognized cause of chronic kidney disease. 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.
The renal signs of lead toxicity depend on the duration and degree of exposure. Acute lead toxicity leads to proximal tubular inclusions and an acute fanconi syndrome. 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. Even low levels of lead exposure appear to be associated with a decline in GFR. A study 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. There is a chicken and egg issue here however, as a lower GFR can lead to decreased lead excretion.
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.
The treatment involves removing the sources of exposure and, in patients with substantial lead toxicity, chelation therapy. This is not entirely without risk and has been associated with acute renal failure in children. Chelation in the presence of ongoing exposure will actually increase toxicity as it will lead to an overall increase in blood levels.
We are in the process of getting the XFR scan for this patient and it may be that he does not have lead toxicity after all; but it is definitely one to think about in the future.
3 comments:
Hi Gearoid,
Nice post! The associated gout is often termed 'saturnine gout' because of the ancient association of the planet Saturn with lead and appears to result from decreased urate excretion. Another important source of lead in some regions is drinking moonshine, where the distilling equipment can contain lead. In the US, generally it is limited to the south, however, as a resident I had a patient who had migrated with much of his family to the northeast and had chronic lead nephropathy from past moonshine drinking (and some current, around the holidays and visits down south). Of course, the other interesting gout-CKD association is FJHN, written about by Albert Lam in the past I think.
Is there any utility to checking a lead level or a ZPP (the "hemoglobin a1c" of lead exposure) if he was still having ongoing exposure?
Best,
Ernest
Gearoid and Ernest,
Nice post and nice additional association.
I got another one, recently saw a retired gas station manager who had worked in the business for 40 plus years, no medical problems except for CKD with a bland urine sediment. Although lead has largely been phased out of gasoline now I understand it's addition was pretty commonplace prior to the 1970s. My patient did not have the history of gout so wasn't quite as classic as Gearoid's but I really couldn't find any other good reason for the man to have CKD.
I used to practice nephrology in Charleston, SC. We had a cadre of patients (particularly in the VA) with moderate CKD, florid tophaceous gout, and a tendency toward type IV RTA. The African American patients typically (but not always) had a history of unbonded liquor ingestion. Of note, in Charleston the house paint used to be mixed with lead acetate or carbonate in a proportion of 30% by weight - great paint, it never mildewed. As a result, there are places in peninsular Charleston where the soil is up to 1000 ppm lead. Children living in historic houses that were being renovated occasionally had to undergo chelation therapy.
I've moved to North Carolina, but recently saw a patient with the typical clinical picture described above. It turned out that he used to work in an auto body shop - before there was Bond-O and fiberglas, they used lead to fill in dents and dings. He described routinely melting elemental lead in a hubcap over an open flame in the shop.
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