This paper presents a study of renal function in I02 patients with lead poisoning admitted to the Occupational Diseases Clinic in Bucharest during the past IO years; nearly half the patients had no history of lead colic. Every possible cause of renal damage, other than lead, was excluded by a careful differential diagnosis.Renal function was investigated by repeated determinations of blood urea, creatinine and uric acid, urea clearance, and endogenous creatinine clearance tests.Significant decreases of the clearance values (less than 50 ml./min. urea clearance and less than 8o ml./min. creatinine clearance), persistent high blood urea (more than 50 mg./Ioo ml.), and high blood creatinine (more than I-2 mg./ioo ml.) were found in a significant number of cases. These signs of impaired renal function were more frequent in the group of patients with chronic lead poisoning who had had several episodes of colic and an occupational exposure of more than IO years. A high blood pressure was also found more frequently in this group of patients.Undercompensated and decompensated renal failure was found in I7 patients, most of whom had been exposed to lead for more than IO years and had a history of several attacks of colic. Arterial hypertension accompanied the chronic renal failure in 13 patients, the renal impairment generally preceding the rise in blood pressure by several years.The duration of occupational lead exposure, the high absorption in the past, and the long period of observation of these patients, most of whom were repeatedly hospitalized, may explain the relatively high incidence (17 cases) of nephropathy with chronic renal failure in the present group. Impairment of urea clearance seems to be the earliest sign, at a time when the creatinine clearance is still normal. As the duration of exposure lengthens and the patient is subjected to active episodes of poisoning the creatinine clearance also deteriorates. Persistent urea retention and high creatininaemia may follow in time, accompanied rather frequently by arterial hypertension. A study of some of the cases followed for several years demonstrated this progressive evolution of lead nephropathy.A functional and transitory impairment of renal function is very probably caused by an impairment of intrarenal circulation, resulting from marked vasoconstriction of the renal vessels, forming part of the generalized vasoconstriction of lead poisoning. Prolonged exposure and frequently recurring episodes of acute poisoning may lead to progressive impairment of renal function and to the development of organic lesions.Special attention should be paid to renal function tests in all cases with prolonged exposure to lead in order to prevent the development of severe lead nephropathy.The question whether lead poisoning can cause certain pathological states earlier than has been a chronic nephropathy is of interest at the present possible hitherto. time not only in occupational medicine but also inIn the past, many authors have held that chronic paediatrics, general medicin...
SUMMARY Four case reports are presented of patients who ate the meat of a hog inadvertently fed seed treated with fungicides containing ethyl mercury chloride. The clinical, electrophysiological, and toxicological, and in two of the patients the pathological data, showed that this organic mercury compound has a very high toxicity not only for the brain, but also for the spinal motoneurones, peripheral nerves, skeletal muscles, and myocardium.
Lead in urine has been determined by an ashing technique to give total lead and by a standard coprecipitation technique to give precipitable lead. In 44 normal subjects values obtained by both methods were the same. In 72 subjects exposed to lead, of whom 57 had clinical lead poisoning, the precipitable lead was significantly less than the total lead. As much as 40 % of urinary lead can escape determination by the coprecipitation methods of estimation. Preliminary findings suggest that the non-precipitable lead may be present as a natural chelate. The significance of these observations is discussed. The danger is stressed that cases of threatened lead intoxication may be overlooked if only coprecipitation methods of estimating lead in urine are used.
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