Nephrotic syndrome pathophysiology
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Pathophysiology
Edema Formation
The pathophysiology of edema formation in nephrotic syndrome is still controversial. Earlier studies hypothesized that the "underfill" mechanism is responsible of edema formation due to loss of colloid oncotic pressure, followed by increased filtration from the intravascular space to the interstitial space.[1] Eventually, hypovolemia and renal hypoperfusion will lead to activation of the renin-angiotensin-aldosteron system (RAAS) and sodium retention.[1]
The Starling equation adequately explains the net fluid movement between the intravascular and the interstitial compartments:
Jv is the net fluid movement between compartments; Pc is the capillary hydrostatic pressure.; Pi is the interstitial hydrostatic pressure; σ is the reflection coefficient to proteins. It is a measure of vascular permeability; πc is the capillary oncotic pressure; πi is the interstitial oncotic pressure; Kf is the overall filtration permeability constant to volume flow; it is a product of the hydraulic conductance and capillary surface area. It is a measure of vascular permeability.
However, edema formation is not simply due to a sodium retention following a decrease in systemic volume and fall in plasma colloid pressure.[2][3] Tubular absorption is increased in patients with nephrotic syndrome due to unknown mechanism.[4] Additionally, a modest decrease in GFR and filtration fraction due to a decrease in effective circulating volume leads to volume retention.[5] 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.[6][7][8] 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.[4] The disequilibrium creates a state of uncompensated hypovolemia when COP becomes < 8 mmHg.[4] The drooping pressure temporarily stimulates aldosterone and other sodium-handling indices to retain sodium.[4][9][10] Following sodium retention, a steady-state is reached and sodium is no longer actively retained.[11][12][13] 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. [4]
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.[4]
References
- ↑ 1.0 1.1 Siddall EC, Radhakrishnan J (2012). "The pathophysiology of edema formation in the nephrotic syndrome". Kidney Int. 82 (6): 635–42. doi:10.1038/ki.2012.180. PMID 22718186.
- ↑ 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.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 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.
- ↑ 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.
- ↑ 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.