Edema and uremia from 1827 to 1905: the first faltering steps of renal pathophysiology.
After Richard Bright's studies, both edema and uremia were thought to be due to a renal retention of urinary substances; but if so why were they so rarely associated with each other? To solve this dilemma, a few clinicians turned to physics and chemistry. In 1897, Korànyi measured the freezing point depression (FPD) of the urine during water restriction. He found that in advanced renal disease it was lower than normal, approaching that of plasma, a phenomenon which he named isothenuria. He introduced the concept of renal insufficiency when, whatever the lesions, urinary excretory function does not adapt to the needs of the body. In the same year Achard and Castaigne found that in uremia, the excretion of methylene blue into the urine was delayed. In contrast, the dye was normally excreted in edematous patients with proteinuria. In 1902 Strauss and Widal, using a new steel needle to obtain blood, each studied the chemistry of plasma and performed water, chloride and nitrogen balances. They revealed that in advanced nephritis without edema there was a retention of nitrogen metabolites but not of chloride, whereas in proteinuric edematous patients the blood urea was normal, and there was a retention of chloride and then of water. Physical chemistry and its objective results had been introduced into renal medicine. Modern renal pathophysiology was now launched.
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D004487:Edema / Q000266:history* / Q000503:physiopathology; D049672:History, 19th Century; D049673:History, 20th Century; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D014511:Uremia / Q000266:history* / Q000503:physiopathology