Anuria

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definition

As anuria is referred to in the adult human , a urine ( Greek οὖρα. Oura "urine") of less than 100 ml in 24 hours; In paediatrics as well as in veterinary medicine , different volumes apply (depending on age, size and species ) . A distinction is made between real renal anuria caused by kidney damage and prerenal anuria, as well as false , postrenal anuria when the urinary tract is blocked. This false anuria is also called urinary obstruction , urinary retention , urinary retention or ischuria .

history

The problem of the anuric kidney has not been conclusively resolved for a long time. Since around 1965, after extensive research (including by François Reubi ), there is no longer any doubt about the "total reabsorption of the glomerular filtrate " in the tubules (independent of the glomerular filtration). This statement applies to both unilateral and bilateral anuria (unless the opposite is proven if one kidney is completely destroyed). Nevertheless, this knowledge is not yet a general doctrine . In a current standard work this problem is not mentioned with any syllable; the word anuria is found only once (in acute kidney failure ). This question is also not addressed in another textbook ; here, too, the anuria is found only once (with the drug dosage during anuria). In the standard work of Harrison's internal medicine , tubular necrosis is mentioned as a possible cause of anuria, without going into the increased tubular reabsorption which has the opposite effect. In The Merck Manual only prerenal and post-renal causes of anuria be mentioned, but not the tubular function.

In 1976 Volkmar Heinze described in detail the Thurau hypothesis with the Thurau mechanism from 1971 as an explanatory model for anuria: Nephrotoxins damage the kidneys and cause tubular lesions and glomerular damage. The “energetic potential” of the tubular apparatus deteriorates. The glomerular filtration is "reduced or even completely stopped." This leads to "oliganuria". Then the tubular epithelia are repaired with restoration of their "reabsorption capacity". The glomerular filtration is released again. Heinze leaves open how the "only minor pathological-anatomical changes" and the "missing morphological correlate" can be brought into agreement with this speculative hypothesis. In affected patients he described intact glomerules and unchanged tubules; "the acute renal parenchymal damage is absent". Heinze does not go into Reubi's representations, although he mentions him three times in the bibliography . - The above presentation by François Reubi (also from 1971 in the same book as Thurau's work) seems much more plausible than Klaus Thurau's hypothesis : The glomeruli and tubules are hardly damaged by the body's own nephrotoxins. The tubules (independently of the glomeruli) increase their resorption rate in a compensatory manner. This is how it comes to anuria or oliguria (summarized as oliganuria ).

Pathophysiology

A prerequisite for renal anuria is not a decrease in glomerular filtration to zero. Rather, the anuria is achieved by an increase in tubular reabsorption from an average of about 99% by only one percentage point to 100%. The urinary substances (such as creatinine ) continue to be produced and can no longer be excreted through the kidneys; so they are completely reabsorbed together with the plasma water. Creatinine-based estimation formulas for the GFR can therefore not provide reliable values. Such formulas would erroneously calculate glomerular filtration rates that are too small; because all of these formulas assume that creatinine is not (or only slightly) absorbed in a tubular manner. Likewise, the clearance formulas can not be used in anuria because of the lack of urine.

The increase in the tubular resorption rate can be understood pathophysiologically as an intended and necessary prevention of further fluid loss in shock or extreme physical stress. Until the contrary is proven, every anuria is therefore a necessary compensation of the cardiovascular system . In shock, the actual GFR can even increase in parallel with the CO. In circulatory shock needs to cardiology guidelines , the cardiac output (CO, English CO is the cardiac output ) can be determined; in healthy kidneys, the actual GFR is around two percent of the CO. Otherwise, if there is a suspicion of severe bilateral kidney disease in anuria in intensive care medicine, only the nuclear medicine provisions of the GFR come into question; here, however, there is a risk of additional iatrogenic contrast medium- induced kidney failure . But in the case of anuria, the result is only the filtration ratio of the two individual kidneys to each other with the total of 100% without specifying the actual GFR.

The extrarenal clearance of any partially urinary substance is equivalent to the total plasma clearance in anuria.

See also

Individual evidence

  1. ↑ Gerd Harald Herold : "Internal Medicine 2019", Cologne 2018, ISBN 978-3-9814660-8-9 , p. 599. He does not go into the pathomechanism .
  2. ↑ François Reubi ., Chr Vorburger, R. Sander: renal blood flow and renal Cr51 EDTA and NA24-distribution spaces in acute anuria of man , in: (ed.) Karl Klütsch, Ernst Wollheim, Hans-Jürgen Holt Meier: The kidney in circulation , Georg Thieme Verlag, Stuttgart 1971, ISBN 3-13-468201-X , pp. 86-89.
  3. ↑ Ulrich Kuhlmann, Joachim Böhler, Friedrich C. Luft , Mark Dominik Alscher , Ulrich Kunzendorf (eds.): Nephrology . 6th edition. Georg Thieme Verlag, Stuttgart / New York 2015, ISBN 978-3-13-700206-2 , p. 473.
  4. ↑ Helmut Geiger, Dietger Jonas, Tomas Lenz, Wolfgang Kramer (eds.): Kidney Diseases , Schattauer Verlag , Stuttgart / New York 2003, ISBN 3-7945-2177-3 , p. 512.
  5. ^ Harrison's Internal Medicine , 19th edition, Volume 1, McGraw-Hill, Berlin 2016, ISBN 978-3-88624-560-4 , p. 354.
  6. ^ The Merck Manual. 20th edition. Kenilworth 2018, ISBN 978-0-911910-42-1 , pp. 2077 and 2138 f.
  7. ↑ Klaus Thurau : Intrarenal Mechanisms for Adjusting the NaCl Excretion , in: Karl Klütsch, Ernst Wollheim, Hans-Jürgen Holtmeier (Ed.): The kidney in circulation , Georg Thieme Verlag, Stuttgart 1971, ISBN 3-13-468201-X , Pp. 70-79.
  8. ↑ Volkmar Heinze: Acute kidney failure , in: Hans Joachim Sarre : Kidney diseases , 4th edition, Georg Thieme Verlag, Stuttgart 1976, ISBN 3-13-392804-X , pp. 425–469, here 432–435.
  9. ↑ The total reabsorption (back diffusion) leads to anuria. Source: Hans Joachim Sarre : Kidney Diseases , 4th edition, Georg Thieme Verlag, Stuttgart 1976, ISBN 3-13-392804-X , p. 434, Figure 42.3.
  10. ↑ Ulrich Gessler, K. Schröder: Experimental contribution to the pathogenesis of acute anuria , in: Karl Julius Ullrich , Klaus Hierholzer (Ed.): Normal and pathological function of the renal tubule , Verlag Hans Huber , Bern, Stuttgart 1965, p. 349.
  11. ^ Heinrich Knauf, Ernst Mutschler : Diuretika , Urban & Schwarzenberg, 2nd edition, Munich / Vienna / Baltimore 1992, ISBN 3-541-11392-8 , p. 177.