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Войти в исследования Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 1996
Occult lead intoxication as a cause of hypertension and renal failure.
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Sánchez-Fructuoso A I, Torralbo A, Arroyo M, Luque M, Ruilope L M, Santos J L, Cruceyra A, Barrientos A
Аннотация
BACKGROUND: The true incidence of lead (Pb) overload as a cause of chronic renal failure (CRF) is unknown. Also, it is unclear if CRF per se could generate an increment in the body Pb burden. Most studies of chronic Pb intoxication have been performed on cohorts or patients with a past history of occupational exposure. Therefore we studied the body Pb burden in CRF of known aetiology versus those patients with CRF with gout and hypertension of unclear aetiology without a past history of Pb exposure. In addition we studied patients diagnosed with essential hypertension.
METHODS: We studied 296 patients lacking a past history of Pb exposure, who were subdivided into four groups: group I (n = 30), normal control subjects; group II (n = 104), patients with 'essential' hypertension and normal renal function; group III (n = 132), patients with CRF of uncertain aetiology in association with hypertension and/or gout, and group IV (n = 30), patients with CRF of known aetiology. The blood and urine Pb levels were assessed before and after an EDTA test.
RESULTS: No abnormal test results were obtained for patients in groups I and IV. The EDTA test was abnormal in 16 patients (15.4%) in group II and in 74 patients (56.1%) in group III. A positive correlation was observed between plasma creatinine levels and post-EDTA urinary Pb in group III, but not in group I. No correlation regarding plasma creatinine and the duration of hypertension or gout were demonstrated. The bone Pb levels, measured in 12 patients with pathological EDTA test results, were positively correlated to the plasma creatinine levels.
CONCLUSIONS: A high percentage of patients with gout, hypertension, and CRF have an excessive Pb burden, and about 15% of the patients diagnosed as 'essential' hypertensives also show high Pb burdens. It is remarkable that a history of overt Pb exposure was lacking in the whole study population.
METHODS: We studied 296 patients lacking a past history of Pb exposure, who were subdivided into four groups: group I (n = 30), normal control subjects; group II (n = 104), patients with 'essential' hypertension and normal renal function; group III (n = 132), patients with CRF of uncertain aetiology in association with hypertension and/or gout, and group IV (n = 30), patients with CRF of known aetiology. The blood and urine Pb levels were assessed before and after an EDTA test.
RESULTS: No abnormal test results were obtained for patients in groups I and IV. The EDTA test was abnormal in 16 patients (15.4%) in group II and in 74 patients (56.1%) in group III. A positive correlation was observed between plasma creatinine levels and post-EDTA urinary Pb in group III, but not in group I. No correlation regarding plasma creatinine and the duration of hypertension or gout were demonstrated. The bone Pb levels, measured in 12 patients with pathological EDTA test results, were positively correlated to the plasma creatinine levels.
CONCLUSIONS: A high percentage of patients with gout, hypertension, and CRF have an excessive Pb burden, and about 15% of the patients diagnosed as 'essential' hypertensives also show high Pb burdens. It is remarkable that a history of overt Pb exposure was lacking in the whole study population.