Nephrotic syndrome pathophysiology
Nephrotic Syndrome Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Nephrotic syndrome pathophysiology On the Web |
American Roentgen Ray Society Images of Nephrotic syndrome pathophysiology |
Risk calculators and risk factors for Nephrotic syndrome pathophysiology |
Please help WikiDoc by adding more content here. It's easy! Click here to learn about editing.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
Edema Formation
The pathophysiology of edema formation is not simply due to a sodium retention following a decrease in systemic volume and fall in plasma colloid pressure.[1][2] Tubular absorption is increased in patients with nephrotic syndrome due to unknown mechanism.(0) Additionally, a modest decrease in GFR and filtration fraction due to a decrease in effective circulating volume leads to volume retention.[3] Recent evidence has shown that edema formation and sodium retention may be related to a primary intrinsic dysfunction of the renal handling of sodium followed by superimposing hypovolemia.[4][5][6] It is believed that excessive proteinuria, as seen in patients with minimal change disease, and depletion of serum alubmin creates a disequilibrium between plasma and extravascular stores of albumin in attempt to restore the plasma-to-interstitial difference in colloid oncotic pressure.[7] The disequilibrium creates a state of uncompensated hypovolemia when COP becomes < 8 mmHg.[7] The drooping pressure temporarily stimulates aldosterone and other sodium-handling indices to retain sodium.[7][8][9] Following sodium retention, a steady-state is reached and sodium is no longer actively retained.[10][11][12] If a stable steady-state is not reached in cases when COP cannot be maintained above 8 mmHg, massive proteinuria persists and patients have a worse clinical presentation. [7]
It is important to recognize that the pathology of edema formation is not homogeneous. On the contrary, it is different with different diseases and is thus not comparable.[7]
References
- ↑ BROWN E, HOPPER J, WENNESLAND R (1957). "Blood volume and its regulation". Annu Rev Physiol. 19: 231–54. doi:10.1146/annurev.ph.19.030157.001311. PMID 13412057.
- ↑ YAMAUCHI H, HOPPER J (1964). "HYPOVOLEMIC SHOCK AND HYPOTENSION AS A COMPLICATION IN THE NEPHROTIC SYNDROME. REPORT OF TEN CASES". Ann Intern Med. 60: 242–54. PMID 14114444.
- ↑ Ichikawa I, Rennke HG, Hoyer JR, Badr KF, Schor N, Troy JL; et al. (1983). "Role for intrarenal mechanisms in the impaired salt excretion of experimental nephrotic syndrome". J Clin Invest. 71 (1): 91–103. PMC 436841. PMID 6848563.
- ↑ Meltzer JI, Keim HJ, Laragh JH, Sealey JE, Jan KM, Chien S (1979). "Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling". Ann Intern Med. 91 (5): 688–96. PMID 496101.
- ↑ Dorhout EJ, Roos JC, Boer P, Yoe OH, Simatupang TA (1979). "Observations on edema formation in the nephrotic syndrome in adults with minimal lesions". Am J Med. 67 (3): 378–84. PMID 474584.
- ↑ Brown EA, Markandu ND, Sagnella GA, Squires M, Jones BE, MacGregor GA (1982). "Evidence that some mechanism other than the renin system causes sodium retention in nephrotic syndrome". Lancet. 2 (8310): 1237–40. PMID 6128546.
- ↑ 7.0 7.1 7.2 7.3 7.4 Vande Walle JG, Donckerwolcke RA, Koomans HA (1999). "Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease". J Am Soc Nephrol. 10 (2): 323–31. PMID 10215332.
- ↑ Koomans HA, Kortlandt W, Geers AB, Dorhout Mees EJ (1985). "Lowered protein content of tissue fluid in patients with the nephrotic syndrome: observations during disease and recovery". Nephron. 40 (4): 391–5. PMID 4022206.
- ↑ Koomans HA, Braam B, Geers AB, Roos JC, Dorhout Mees EJ (1986). "The importance of plasma protein for blood volume and blood pressure homeostasis". Kidney Int. 30 (5): 730–5. PMID 3784303.
- ↑ Vande Walle JG, Donckerwolcke RA, van Isselt JW, Derkx FH, Joles JA, Koomans HA (1995). "Volume regulation in children with early relapse of minimal-change nephrosis with or without hypovolaemic symptoms". Lancet. 346 (8968): 148–52. PMID 7603230.
- ↑ Van de Walle JG, Donckerwolcke RA, Greidanus TB, Joles JA, Koomans HA (1996). "Renal sodium handling in children with nephrotic relapse: relation to hypovolaemic symptoms". Nephrol Dial Transplant. 11 (11): 2202–8. PMID 8941579.
- ↑ Bohlin AB, Berg U (1984). "Renal sodium handling in minimal change nephrotic syndrome". Arch Dis Child. 59 (9): 825–30. PMC 1628730. PMID 6486860.