Institute for Medical Research and Occupational Health
Abstract
lznesen je problem toksičkog djelovanja olova na bubrege s obzirom na dosadašnje podatke u literaturi. Prikazana su vlastita zapažanja kod 54 od 56 bolesnika otrovanih olovom, koji su liječeni u Odjelu za profesionalne bolesti Instituta za medicinska istraživanja. Trajne promjene na bubrezima u obliku kronične progredijentne difuzne nefropatije opažene su samo kod 2 bolesnika. Oba su bila u dugoj i vjerojatno visokoj ekspoziciji olovu (20, odnosno 35 godina), a imali su višekratna manifestna otrovanja olovom. 28 bolesnika pokazivalo je oštećenja bubrežnih funkcija, koja su utvrđena pokusom koncentracije mokraće, PSP testom, Ucl testom i određivanjem ureje u krvi, a da kod toga u mokraći nije bilo patoloških promjena. Autori su mišljenja, da su funkcionalna oštećenja uvjetovana poremećajima u intrarenalnoj cirkulaciji, odnosno spastičkim djelovanjem olova na krvne žile bubrega i direktnim toksičkim ili indirektnim hipoksičkim efektom olova na tubule. Poremećenja parcijalnih funkcija bubrega bila su u pravilu tranzitorna. Krvni tlak je bio povišen samo kod 6 bolesnika, od kojih su 2 imala pogredijentnu organsku nefropatiju. Najvjerojatnije je, da se kod tih bolesnika radi o hipertenziji nefrogenog karaktera. U jednom slučaju povišeni krvni tlak bio je tipa esencijalne hipertonije, pa se uzročna veza između otrovanja olovom i hipertonije ne može sa sigurnošću pretpostaviti. Kod ostala 3 bolesnika hipertonija je bila prolazna i prisutna samo u vrijeme akutne manifestacije otrovanja. Autori su primijetili, da je pri ispitivanju parcijalnih funkcija bubrega neobično važno vrijeme, kada se pojedine pretrage vrše. Pokazalo se, da se eventualne lezije mijenjaju u prirodnom toku bolesti. Ako se to izgubi iz vida, mogu se dobiti prividno divergentni i protuslovni rezultati. Na temelju spomenutih nalaza autori zaključuju, da ekspozicija olovu i otrovanje olovom mogu izazvati prolazna bubrežna oštećenja funkcionalne prirode. Čini se, da su u iznimnim slučajevima vrlo duge i visoke ekspozicije i opetovanih otrovanja moguće i organske lezije bubrega.The problem of the toxic effect of lead upon the kidney, in spite of numerous studies, has not as yet been fully solved. The report presented deals with the clinical observations of 54 lead poisoned patients. Lasting kidney changes in the form of chronic, progredient and diffuse nephropathy were observed in only 2 patients with an exposure to high lead concentrations during a period of 20 and 35 years respectively, and repeated lead poisonings. These two patients had no history of previous kidney disorders, and kidney injuries progressed with repealed lead poisonings. It may, therefore, be assumed that the lesions observed were due to lead action. 24 patients showed functional kidney alterations which were proved by the test of urine concentration, the phenolsulphthalein test, the urea clearance test, and the urea value in the blood. Urine showed no abnormality in these cases. In the authors\u27 opinion these functional changes mostly consist in altered intrarenal circulation due to the spastic effect of lead upon the blood vessels of the kidney and the direct toxic and indirect hypoxic effect of lead upon the tubules. The injuries of partial renal functions were as a rule reversible. In only 6 patients the blood pressure was increased. 2 patients with hypertension were those with progredient organic nephropaty. It seems most probable that in these two cases hypertension was nephrogenic in character. In one case high blood pressure was of the type of essential hypertension, but the relation between lead poisoning and hypertension in this case cannot be assumed with certainty. In other 3 patients hypertension was transitory in type, lasting only during the acute manifestations of lead poisoning. Functional kidney alterations tend to change according to the natural course of the disease. This is why it is not the same in which phase of the poisoning functional kidney tests are carried out. If this fact is neglected, divergent and contradictory results may be obtained. On the basis of these clinical findings the authors conclude that lead exposure and lead poisoning may cause kidney injuries. However, these changes are not uniform and cannot therefore be considered a clinical and nosologic entity usually called nephropathia saturnina. In the exceptional cases of a very long and high exposure to lead and repeated poisoning, progressive organic kidney changes may be expected. Otherwise, possible renal alterations and changes in the blood pressure are functional and reversible
