Skip to main content
SpringerLink
Log in

Mechanismen der postobstruktiven polyurie

Mechanisms of post-obstructive polyuria

  • Zum Geleit
  • Published:
Klinische Wochenschrift Aims and scope Submit manuscript

Summary

Postobstructive diuresis occurs after relief of bilateral ureteral obstruction despite the persistent decrease in renal cortical perfusion and glomerular filtration rate (GFR). After an initial transient rise in renal blood flow (RBF) during acute ureteral obstruction, tubular damage and progressive vasoconstriction with decreased RBF, especially of medullary perfusion, are observed with chronic obstruction. These are associated with an activation of the renin-angiotensin system and of renal prostaglandin (PG) synthesis with enhanced production of the vasoconstrictor thromboxane A2. Azotemia and extracellular fluid volume (ECFV) expansion result from impaired renal function. Mechanisms of polyuria following relief from bilateral chronic obstruction include enhanced PGE-mediated medullary blood flow, structural and functional tubular damage with decreased sodium reabsorption and (vasopressin-resistent) impaired renal concentrating ability, osmotic diuresis, activation of natriuretic factors following ECFV-expansion, and sometimes iatrogenic excessive fluid replacement. The resulting loss of fluid and electrolytes represents a major hazard in patients after surgical correction of congenital or acquired urinary tract obstruction.

Zusammenfassung

Eine postobstruktive Polyurie wird nach Entlastung der beidseitigen Harnstauungsniere beobachtet. Nach anfänglicher passagerer Zunahme der Nierendurchblutung bei akuter Obstruktion stellt sich bei chronischer Obstruktion neben der strukturellen und funktionellen Tubulusschädigung eine zunehmende Vasokonstriktion mit erheblich eingeschränkter Nierendurchblutung vor allem des Nierenmarks ein. Sie ist mit einer Aktivierung des Renin-Angiotensin Systems und der renalen Prostaglandin (PG)-Synthese, insbesondere des vasokonstriktorischen Thromboxan A2, vergesellschaftet. Die Störung der exkretorischen Nierenfunktion führt zu Azotämie und Expansion des Extrazellularvolumens (EZV). Zu den Mechanismen, die trotz weiterhin stark eingeschränkter Nierenrindenperfusion und glomerulärer Filtration nach Entlastung der gestauten Niere zur Polyurie führen, gehören die erhöhte Nierenmarkdurchblutung bei gesteigerter medullärer PGE-Synthese, strukturelle und funktionelle Tubulusschädigung mit Hemmung der tubulären Natrium-Resorption und (Vasopressin-resistenter) Störung des renalen Konzentrationsvermögens, osmotische Diurese, Aktivierung natriuretischer Faktoren durch die Expansion des EZV sowie schließlich die iatrogene Überwässerung. Die daraus resultierenden Elektrolyt- und Wasserverluste stellen eine potentielle Gefahr bei der Korrektur der angeborenen oder erworbenen beidseitigen Harnabflußstörung dar und verlangen eine exakte Überwachung der Patienten.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

Literatur

  1. Better OS, Tuma S, Kedar S, Chaimowitz C (1975) Increased tubular reabsorption of phosphate following relief of unilateral ureteral obstruction in man. Arch Intern Med 135:245–248

    Google Scholar 

  2. Carmines PK, Tanner GA (1983) Angiotensin in the hemodynamic response to chronic nephron obstruction. Am J Physiol 245:F75-F82

    Google Scholar 

  3. Cadnapaphornchai P, Bondar NP, McDonald FD (1982) Effect of imidazole on the recovery from bilateral ureteral obstruction in dogs. Am J Physiol 243:F532-F536

    Google Scholar 

  4. Chander M, Stacy WK, Haden HT, Falls WF (1973) The influence of extracellular fluid volume expansion on postobstructive diuresis in the dog. Invest Urol 11:114–120

    Google Scholar 

  5. Chaudhari A, Kirschenbaum MA (1982) Decreased renal prostaglandin metabolism in ureteral obstruction. Biochim Biophys Acta 713:10–15

    Google Scholar 

  6. Currie MG, Davis BB, Needleman P (1981) Localization of exaggerated prostaglandin synthesis associated with renal damage. Prostaglandins 22:933–944

    Google Scholar 

  7. Düsing R, Nicolas V, Glänzer K, Kipnowski J, Kramer HJ (1982) Prostaglandins participate in the regulation of NaCl absorption in the diluting segments of the nephron in vivo: Effects of furosemide. Renal Physiol (Basel) 5:115–123

    Google Scholar 

  8. Folkert VW, Schlöndorff D (1981) Altered prostaglandin synthesis by glomeruli from rats with unilateral ureteral ligation. Am J Physiol 241:F289-F299

    Google Scholar 

  9. Fradet Y, Simard J, Grose JH, Lebel M (1980) Enhanced urinary prostaglandin E2 in postobstructive diuresis in humans. Prostaglandins and Medicine 5:29–30

    Google Scholar 

  10. Francisco LL, Hoversten LG, DiBona GF (1980) Renal nerves in the compensatory adaptation to ureteral occlusion. Am J Physiol 238:F229-F234

    Google Scholar 

  11. Gerzer R (1985) Das Herz, ein endokrines Organ: Die Entdeckung eines neuen Hormons. Klin Wochenschr 63:529–536

    Google Scholar 

  12. Ichikawa I, Brenner BM (1979) Local intrarenal vasoconstrictor-vasodilator interactions in mild partial ureteral obstruction. Am J Physiol 236:F131-F140

    Google Scholar 

  13. Kawasaki A, Needleman P (1982) Contribution of thromboxane to renal resistance changes in the isolated perfused hydronephrotic rabbit kidney. Circ Res 50:486–490

    Google Scholar 

  14. Klahr S (1983) Pathophysiology of obstructive nephropathy. Kidney Int 23:414–426

    Google Scholar 

  15. Kramer HJ (1981) Natriuretic Hormone — a circulating inhibitor of sodium-and potassium-activated adenosine triphosphatase. Its potential role in body fluid and blood pressure regulation. Klin Wochenschr 59:1225–1230

    Google Scholar 

  16. Kramer HJ, Glänzer K, Düsing R (1981) Role of prostaglandins in the regulation of renal water excretion. Kidney Int 19:851–859

    Google Scholar 

  17. Kramer HJ, Heppe M, Wiler E, Bäcker A, Liddiard C, Klingmüller D (1985) Further characterization of the endogenous natriuretic and digoxin-like immunoreacting activities in human urine: Effects of changes in sodium intake. Renal Physiol. (Basel) 8:80–89

    Google Scholar 

  18. Kramer HJ, Neumark A, Schmidt S, Klingmüller D, Glänzer K (1983) Renal functional and metabolic studies on the role of preventive measures in experimental acute renal failure. Clin Exp Dialysis and Apheresis 7:77–99

    Google Scholar 

  19. McNamara DB, Boineau FG, McMullen-Laird M, Lippton HL, She HS Lewy JE, Kadowitz PJ (1982) Prostaglandin endoperoxide metabolism by microsomes of whole kidneys from normal, congenital unilateral hydronephrotic and unlateral ureteral obstructed rats. Prostaglandins 24:585–605

    Google Scholar 

  20. Michaelson G (1974) Percutaneous puncture of the renal pelvis, intrapelvic pressure and the concentrating capacity of the kidney in hydronephrosis. Acta med Scand Suppl 559:1–26

    Google Scholar 

  21. Morrison AR, Benabe JE (1981) Prostaglandins and vascular tone in experimental obstructive nephropathy. Kidney Int 19:786–790

    Google Scholar 

  22. Nichikawa K, Morrison AR, Needleman P (1977) Exaggerated prostaglandin biosynthesis and its influence on renal resistance in the isolated hydronephrotic rabbit kidney. J Clin Invest 59:1143–1150

    Google Scholar 

  23. Okegawa T, DeSchryver-Kecskemeti K, Needleman P (1983) Endotoxin induces chronic prostaglandin and thromboxane synthesis from ureter-obstructed kidneys: Role of inflammatory cells. J Pharmacol exp Therap 225:213–218

    Google Scholar 

  24. Oliw E (1978) Acute unilateral ureteral occlusion increases plasma renin activity and contralateral urinary prostaglandin excretion in rabbits. Europ J Pharmacol 53:95–102

    Google Scholar 

  25. Purkerson ML, Rolf DB, Chase LR, Slatopolski E, Klahr S (1974) Tubular reabsorption of phosphate after release of complete ureteral obstruction in the rat. Kidney Int 5:326–336

    Google Scholar 

  26. Schubert G, Staudhammer R, Rolle K, Kneissler U (1975) Tubular dimensions and juxtaglomerular granulation index in rat kidneys after unilateral obstruction of the ureter, a study of morphogenesis of hydronephrosis. Urol Res 3:115–122

    Google Scholar 

  27. Sigel A, Chlepas S, Ernstberger W (1979) Natrium-und Wasserdiurese, ein Schlüssel zur Pathophysiologie und Klinik der bilateralen obstruktiven Nephropathie. Urol int 34:237–259

    Google Scholar 

  28. Smith WL, Bell TG, Needleman P (1979) Increased renal tubular synthesis of prostaglandins in the rabbit kidney in response to ureteral obstruction. Prostaglandins 18:269–277

    Google Scholar 

  29. Strand JC, Edwards BS, Anderson ME, Romero JC, Knox FG (1981) Effect of imidazole on renal function in unilateral ureteral-obstructed rat kidneys. Am J Physiol 240:F508-F514

    Google Scholar 

  30. Tannenbaum J, Purkerson ML, Klahr S (1983) Effect of unilateral ureteral obstruction on metabolism of renal lipids in the rat. Am J Physiol 245:F245-F262

    Google Scholar 

  31. Übelhör R (1962) Die Entleerungsstörungen der Blase. VIII. Der Rückstauungsschaden der Nieren. In: Alken CE, Dix VW, Weyrauch HM, Wildbolz E (Hrsg) Handbuch der Urologie, Bd. VIII, Springer, Berlin, S 303–320

    Google Scholar 

  32. Whinnery MA, Shaw JO, Beck N (1982) Thromboxane B2 and prostaglandin E2 in the rat kidney with unilateral ureteral obstruction. Am J Physiol 242:F220-F225

    Google Scholar 

  33. Wilson DR (1980) Pathophysiology of obstructive nephropathy. Kidney Int 18:281–292

    Google Scholar 

  34. Wilson DR, Honrath U (1976) Cross-circulation study of natriuretic factors in postobstructive diuresis. J Clin Invest 57:380–389

    Google Scholar 

  35. Wilson DR, Honrath U, Sole MJ (1983) Tissue catecholamines in obstructive nephropathy and acute uremia in the rat. Can J Physiol Pharmacol 61:131–136

    Google Scholar 

  36. Wilson DR, Knox WH, Sax JA, Sen AK (1978) Post-obstructive nephropathy in the rat: Relationship between Na-K-ATPase activity and renal function. Nephron 22:55–62

    Google Scholar 

  37. Yarger WE, Schocken DD, Harris RH (1980) Obstructive nephropathy in the rat. Possible roles for the renin-angiotensin system, prostaglandins, and thromboxanes in postobstructive renal function. J Clin Invest 65:400–412

    Google Scholar 

  38. Zimskind PD, Mannes HA (1974) Clinical aspects of ureteral peristalsis. Urol Clin North Am 1:413–420

    Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Medizinische Poliklinik der Universität Bonn, Germany

    H. J. Kramer

Authors
  1. H. J. Kramer
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Kramer, H.J. Mechanismen der postobstruktiven polyurie. Klin Wochenschr 63, 934–943 (1985). https://doi.org/10.1007/BF01738148

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/BF01738148

Key words

Schlüsselwörter

Search

Navigation