Measurements of bone lead concentrations in the tibia, wrist, sternum, and calcaneus were performed in vivo by x ray fluorescence on active and retired lead workers from two acid battery factories, office personnel in the two factories under study, and control subjects. Altogether 171 persons were included. Lead concentrations in the tibia and ulna (representative of cortical bone) appeared to behave similarly with respect to time but the ulnar measurement was much less precise. In an analogous fashion, lead in the calcaneus and sternum (representative of trabecular bone) behaved in the same way, but sternal measurement was less precise. Groups occupationally exposed to lead were well separated from the office workers and the controls on the basis of calculated skeletal lead burdens, whereas the differences in blood lead concentrations were not as great, suggesting that the use of concentrations of lead in blood might seriously underestimate lead body burden. The exposures encountered in the study were modest, however. The mean blood lead value among active lead workers was 1-45 pmol l1 and the mean tibial lead concentration 21 1 pg (g bone mineral)-'. posure. Calcaneal lead concentration, by contrast, was strongly dependent on the intensity rather than duration of exposure. This indicated that the biological half life of lead in calcaneus was less than the seven to eight year periods into which the duration of exposure was split. Findings for retired workers clearly showed that endogenous exposure to lead arising from skeletal burdens accumulated over a working lifetime can easily produce the dominant contribution to systemic lead concentrations once occupational exposure has ceased.Lead is a widely used toxic metal that accumulates in the body. It is concentrated in bone, which contains over 90% of the body burden in adults.' Occupational exposure to lead is routinely monitored by determination of blood lead concentrations, which largely reflect recent average exposure as the half life of lead in blood is of the order of 35 days.2 Blood lead concentration has been shown to be associated with indicators of adverse effects on haem synthesis, such as free erythrocyte protoporphyrin,' and with neurophysiological4 and psychological effects.56The relation between blood lead concentration and exposure is, however, not necessarily linear7 and, in particular, it has been recognised that in a model of a skeletal subcompartment, the lead should be considered readily exchangeable and constitute an intrinsic source of lead input to the blood.

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Pre- and postoperative kidney size and kidney function were studied in 46 living kidney donors aged 20-74 years. Kidney size was measured by planimetry and by estimation of a renal index. Kidney function was assessed by endogenous creatinine clearance and serum creatinine. Planimetry was superior to the renal index for expressing changes in renal size. Compensatory renal hypertrophy took place in donors up to the age of 74, but the greatest changes in renal size were observed in donors of under 40. Total renal function decreased postoperatively to about 77% of the initial level; this change in renal function was inversely correlated with age, but in all subjects studied the function remained within normal limits.

ABSTRACT. Adult onset Fanconi syndrome with medullary cystic kidney was diagnosed in a 30‐year‐old male with muscular weakness, hypokalemia, normal BP, hyperreninemia, and secondary aldosteronism. He also had non‐specific aminoaciduria, lysozymuria, and β2‐microglobulinuria. Urinary concentrating and acidifying capacity was impaired, and both sodium and potassium were lost into the urine. I. v. pyelography revealed medullary cystic kidney. Renal biopsy showed juxtaglomerular hyperplasia, heavy subintimal deposits and C3 and IgG in preglomerular arteriolar walls, and degenerative changes in the tubules, including loss of brush border and “macula densa‐like” lesions. Polycythemia with elevated serum erythropoietin levels, and raised blood ACTH values with features of cortisolism were also present. Indomethacin therapy decreased plasma renin activity (PRA), plasma aldosterone, and urinary loss of potassium and sodium, while serum potassium approached normal levels. Metoprolol, a β‐adrenergic blocking agent, caused similar effects. Insensitivity to the pressor effect of angiotensin II was reversed by indomethacin treatment. Somatostatin infusion lowered PRA and aldosterone without affecting BP. Several biochemical aberrations of this patient resemble Bartter's syndrome, including the effect of indomethacin.

Reconstruction of a stenotic renal artery was done on 5 hypertensive renal transplant recipients, all of whom had deterioration of renal function when the stenosis was detected. After reconstruction renal function improved in 4 of the patients. The blood pressure was easier to control in all 5 patients, with 3 becoming normotensive. A high preoperative plasma renin activity returned to normal postoperatively in 4 patients. No recurrences were observed after a followup of more than a year.