Glomerular feedback

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The tubuloglomeruläre feedback (also in the masculine as tubuloglomerulärer Feedback designated; tubuloglomerulärer feedback mechanism ) describes a ( neurohumoral controlled) mechanism with which the filtration of a single nephron in the kidney and thus the water supply to be regulated. The glomerulotubular balance should not be disturbed. Sometimes the renin-angiotensin-aldosterone system is also used as tubuloglomerular feedbackdesignated. Because of the importance of the sodium concentrations, one spoke earlier of the sodium feedback theory . Georg Schütterle and others spoke of the "so-called autoregulation of the kidney circulation".

physiology

According to this theory, the filtrative function of the glomeruli (German: kidney balls ) is to be influenced by the resorptive function of the tubules (German: kidney tubules ). It remains unclear whether this feedback works in both directions or only from the tubules to the glomeruli. That is why the terms glomerulotubular feedback or glomerulotubular balance are common . Franz Volhard already thought about the division of labor of the glomeruli and tubules .

If the glomerular filtration rate (GFR) is too high, the amount of sodium chloride (NaCl, common salt) in the primary urine exceeds the absorption capacity of the tubule. This leads to an increase in the NaCl concentration in the tubule, which is registered by the sensor function of the macula densa , part of the juxtaglomerular apparatus , via an ion transporter (Na + / K + / 2Cl symporter; NKCC). This measurement is made indirectly by measuring the speed of the transport.

At high NaCl concentrations, adenosine is secreted from the cells of the macula densa , which leads to the contraction of the smooth muscles in the vas afferens . When the NaCl content in the distal tubule (middle section) increases, the glomerular filtration rate of the same nephron is reduced. This reduces the flow of urine through the loop of Henle , more ions can be reabsorbed and the ion concentration in the distal tubule decreases again.

The opposite effect occurs with hypoosmolar primary urine. The tubules regulate the water balance ; the glomeruli filter the plasma in proportion to cardiac output .

Prostaglandins, on the other hand, provide increased blood flow to the kidneys, which leads to increased NaCl and water excretion, i.e. a stronger GFR. Nonsteroidal anti-inflammatory drugs ( NSAIDs ) lower the GFR as a result of their inhibition of prostaglandin synthesis.

history

These speculations go back to the Danish physiologist Poul Kristian Brandt Rehberg. Building on his work from the 1920s, tubuloglomerular feedback and tubuloglomerular balance were further developed. Originally this now abandoned, but sometimes still learned, hypothesis goes back to Homer William Smith ( glomerulo-tubular balance ). Thereafter, the decrease in GFR up to the glomerular shutdown is caused by the decrease in the tubular reabsorption rate. The neurohumoral regulation of the (in wide areas) opposing development (tending to be reciprocal proportionality ) of the two parameters primary urination and secondary urination or the proportionality of glomerular filtration and tubular resorption are overlooked. The purpose of this autonomous regulation is to avoid unnecessary water loss, especially during high physical exertion with a corresponding increase in CO and GFR.

Numerical example

In the average adult with acute kidney failure, a decrease in the tubular resorption rate by, for example, 10% with an induced decrease in the GFR also by 10% (according to the now obsolete feedback theory ) only insignificantly reduces the GFR from 150 l / d to 135 l / d, but the daily amount of urine increases from 1.5 l / d (= 1% of 150 l / d) to 13.5 l / d (= 10% of now 135 l / d ). That would be an extreme polyuria (compensatory "forced polyuria") and thus exactly the opposite of the postulated oliguria. The specialist literature even reports a polyuria of 70 l / d after successful treatment of acute postrenal kidney failure. The authors Klaus Thurau and John W. Boylan call for "further research"; they are currently calling their theory about the failure of the feedback mechanism of the juxtaglomerular apparatus "speculative". According to this theory, halving the tubular re-absorption function would reduce urine production to 60 ml / min [sic!] (= 86.4 l / d ). enlarge.

criticism

It remains unclear whether tubuloglomerular feedback (TGF) postulates an inverse or a proportional relationship between primary urine formation (= GFR) and secondary urine formation (= urine). Presumably both are correct:

  • With increased cardiac output, primary urine and secondary urine behave in opposite directions. Those who drink a lot and sweat a lot while exercising hardly urinate.
  • With increased cardiac output without sweating , primary urine and secondary urine behave in the same direction. People who drink a lot urinate often.
  • When the cardiac output is reduced, the primary urine and secondary urine behave in the same direction in order to save water if you die of thirst or in a coma .

It should be noted that the glomerular filtration rate and creatinine clearance can only be validly determined in optimally hydrated organisms (without a cardiorenal syndrome ) . In all other cases, the compensatory increased tubular function changes the concentration of urinary substances in the blood and urine.

Individual evidence

  1. ^ Hans Joachim Sarre : Kidney Diseases , 4th Edition, Georg Thieme Verlag, Stuttgart 1976, ISBN 3-13-392804-X , p. 63.
  2. ^ Hans Joachim Sarre : Kidney Diseases , 4th Edition, Georg Thieme Verlag, Stuttgart 1976, ISBN 3-13-392804-X , p. 212.
  3. ^ Claas Wesseler: Physiologie , Volume 1, 3rd edition, Medi-Learn, Marburg 2009, ISBN 978-3-938802-58-8 , p. 38.
  4. ^ Karl Klütsch, Ernst Wollheim, Hans-Jürgen Holtmeier (eds.): The kidney in circulation , Georg Thieme Verlag, Stuttgart 1971, ISBN 3-13-468201-X , p. 66.
  5. ↑ Georg Schütterle, Gert Müller-Berghaus, Klaus Müller, Gerhard Goubeaud, Walter Krause: Renal microcirculation in shock , in: Karl Klütsch, Ernst Wollheim, Hans-Jürgen Holtmeier (eds.): The kidney in circulation , Georg Thieme Verlag, Stuttgart 1971, ISBN 3-13-468201-X , p. 90.
  6. ↑ Harrison's Internal Medicine , Electronic Chapter 3 (332e).
  7. ↑ Franz Volhard : The bilateral hematogenous kidney diseases . In: Gustav von Bergmann , Rudolf Staehelin (Ed.): Handbook of Internal Medicine , 2nd edition, Springer-Verlag, Berlin, Heidelberg 1931, Volume 6, ISBN 978-3-662-42701-9 (reprint), pp. 64.
  8. ^ Heinrich Knauf, Ernst Mutschler : Diuretika , Urban & Schwarzenberg, 2nd edition, Munich / Vienna / Baltimore 1992, ISBN 3-541-11392-8 , p. 41 and p. 51-61.
  9. ↑ Heinz Lüllmann u. a .: pharmacology and toxicology . Georg Thieme Verlag, Stuttgart 2006, ISBN 3-13-368516-3 , p. 291.
  10. ↑ Poul Brandt Rehberg: About the determination of the amount of glomerular filtrate using creatinine as a kidney function test, along with some theories about urine preparation. In: Central sheet for internal medicine . Volume 50, 1929, pp. 367-377.
  11. ↑ Gerd Harald Herold : Internal Medicine. Self-published , Cologne 2019, ISBN 978-3-9814660-8-9 , p. 636.
  12. ^ Heinrich Holzgreve, Hans Bräuer: kidney, hypertension and edema. Picture atlas. Röhm Pharma , Weiterstadt without year, p. 65.
  13. ↑ Gert Mayer: The cardiorenal syndrome. Uni-Med-Verlag, Bremen / London / Boston 2013, ISBN 978-3-8374-1335-9 , p. 26.
  14. ↑ John W. Boylan, Peter Deetjen, Kurt Kramer : Kidney and water balance. Urban & Schwarzenberg, Munich / Berlin / Vienna 1970, ISBN 3-541-04911-1 , p. 32.
  15. ^ Klaus Thurau, John W. Boylan: Acute Renal Success - The Unexpected Logic of Oliguria in Acute Renal Failure. In: The American Journal of Medicine. Volume 61, September 1976, p. 313. On page 314, complete kidney failure is even referred to as bankruptcy .
  16. ^ J. Schnermann, FS Wright, JM Davis, W. von Stackelberg, G. Gill: Regulation of superficial nephron filtration rate by tubulo-glomerular feedback. In: Pflüger's archive . Issue 318, June 1970, pp. 147-175.
  17. ^ Heinrich Holzgreve, Hans Bräuer: kidney, hypertension and edema. Picture atlas. Röhm Pharma, Weiterstadt without year, p. 43.
  18. ↑ Hans Erhard Bock , KH Hildebrand, Hans Joachim Sarre (ed.): Franz Volhard : Recollections , Schattauer Verlag , Stuttgart, New York 1982, ISBN 3-7845-0898-X , p. 30.
  19. ^ Franz Volhard : Before the therapy, the gods put the diagnosis , Hoffmann-La Roche , Grenzach 1952, p. 9.
  20. ↑ Georg Sabin: The cardiogenic shock. Verlag W. Kohlhammer , Stuttgart / Berlin / Cologne / Mainz 1984, ISBN 3-17-008618-9 , p. 21.
  21. ↑ Marlys H. Witte, Floyd A. Short, Walter Hollander: Massive polyuria and natriuresis Following relief of urinary tract obstruction. In: The American Journal of Medicine. Volume 37, Issue 2, August 1964, pp. 320–326.
  22. ^ Klaus Thurau, John W. Boylan: Acute Renal Success - The Unexpected Logic of Oliguria in Acute Renal Failure. In: The American Journal of Medicine. Volume 61, September 1976, p. 314.
  23. ^ Klaus Thurau, John W. Boylan: Acute Renal Success - The Unexpected Logic of Oliguria in Acute Renal Failure. In: The American Journal of Medicine. Volume 61, September 1976, p. 311.