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      Development of the Idea of Chronic Renal Failure

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          Ancient literature contained suggestions of references to people whom we might now speculate suffered from chronic renal failure; however, the first glimmerings of an understanding of the subject arose out of the clinico-pathological correlations that a number of 18th and 19th century observers drew. The concurrent studies by chemists of circulating and urinary levels of urea, creatinine, urate, phosphate, potassium, sodium and hydrogen ions expanded those correlations to a pathophysiological domain, especially in the late 19th and early 20th centuries. With the subsequent development of ideas about circulating hormones and the development of techniques for their measurement during the 20th century, the contemporary idea of chronic renal failure developed. The development of methods for quantifying tests of renal function enhanced that undertaking. Then, in the latter half of the 20th century, the development of effective dialytic techniques for the treatment of patients who suffer from chronic renal failure brought a renewed focus upon the mechanisms involved and problems posed by existing ideas. Nevertheless, the continuing high morbidity and mortality of patients who require such treatment suggest that existing ideas remain quite imperfect.

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          Most cited references 4

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          These experiments indicate that, in dogs at least, ischemia localized to the kidneys is a sufficient condition for the production of persistently elevated systolic blood pressure. When the constriction of both main renal arteries is made only moderately severe in the beginning, the elevation of systolic blood pressure is unaccompanied by signs of materially decreased renal function. In this respect the hypertension in these animals resembles the hypertension which is associated with so called benign nephrosclerosis in man. Subsequent increase of the constriction of the main renal arteries does not materially damage renal function, probably because of adequate development of accessory circulation. More delicate methods for detecting a change may yet prove that some damage does occur. Almost complete constriction of both main renal arteries, from the beginning, results in great elevation of systolic blood pressure which is accompanied by severe disturbance of renal function and uremia. This resembles the type of hypertension which is associated with so called malignant nephrosclerosis, in the sense of Fahr (17). In several of the animals with persistent elevation of systolic blood pressure, anatomical changes were observed in the glomeruli, vessels and parenchyma of the kidneys which are most probably directly referable to the ischemia. It is hoped that these investigations will afford a means of studying the pathogenesis of hypertension that is associated with renal vascular disease.
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            Hyposthenuria: Sándor Korányi’s Concept of Renal Insufficiency

             S Sonkodi (1999)
            Around the turn of the 19th century, the Hungarian physiologist and clinician, Sándor Korányi, started to use physicochemical methods to estimate renal function. In parallel with the deterioration of renal function, he found characteristic changes in the freezing point depression of urine, which he termed hyposthenuria. On the basis of these findings, he was the first to introduce the functional concept of renal insufficiency.
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              The Contribution of French-SpeakingScientists to the Origins of Renal Physiologyand Pathophysiology (1790–1910)

              Some contributions: (1) urinary urea, its chemical composition and physiological meaning, Fourcroy and Vauquelin (1790–1808); (2) in binephrectomized animals blood urea is high and chemically identical to that of urine, Prevost and Dumas (1821); (3) urea level in renal vein blood is 50% of that in the arteries, Picard (1856); (4) retained potassium is the uremic poison, Feltz and Ritter (1881); (5) polyuria induced by intravenous injections of sugars or urea, Richet and Moutard Martin (1880); is the kidney in command of the concentration of the blood? Using cryoscopy, Hédon got the clue, the osmotic load (1900); (6) methylene dye excretion measures the global renal function and thus the degree of renal failure, Achard and Castaigne (1897); (7) the disentanglement of chronic uremia and edema, Widal and Achard (1900–1910); (8) evaluation of the global renal function by the ratio plasma urea/urine urea output, Ambard’s Constant (1905), initial step of the concept of clearance; (9) a circulating nephropoietic factor in one-kidney animals, Carnot (1910). In bled animals he also disclosed a hemopoietic factor which later became the renal erythropoietin.

                Author and article information

                Am J Nephrol
                American Journal of Nephrology
                S. Karger AG
                July 2002
                27 June 2002
                : 22
                : 2-3
                : 231-239
                Concord Hospital, Sydney, and Unit for the History and Philosophy of Science, University of Sydney, Australia
                63767 Am J Nephrol 2002;22:231–239
                © 2002 S. Karger AG, Basel

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                Page count
                References: 61, Pages: 9
                Self URI (application/pdf):
                History of Diseases of the Kidney


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