Nephrotic syndrome pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The | ===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.<ref name="pmid13412057">{{cite journal| author=BROWN E, HOPPER J, WENNESLAND R| title=Blood volume and its regulation. | journal=Annu Rev Physiol | year= 1957 | volume= 19 | issue= | pages= 231-54 | pmid=13412057 | doi=10.1146/annurev.ph.19.030157.001311 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13412057 }} </ref><ref name="pmid14114444">{{cite journal| author=YAMAUCHI H, HOPPER J| title=HYPOVOLEMIC SHOCK AND HYPOTENSION AS A COMPLICATION IN THE NEPHROTIC SYNDROME. REPORT OF TEN CASES. | journal=Ann Intern Med | year= 1964 | volume= 60 | issue= | pages= 242-54 | pmid=14114444 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14114444 }} </ref> 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.<ref name="pmid6848563">{{cite journal| author=Ichikawa I, Rennke HG, Hoyer JR, Badr KF, Schor N, Troy JL et al.| title=Role for intrarenal mechanisms in the impaired salt excretion of experimental nephrotic syndrome. | journal=J Clin Invest | year= 1983 | volume= 71 | issue= 1 | pages= 91-103 | pmid=6848563 | doi= | pmc=PMC436841 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6848563 }} </ref> 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.<ref name="pmid496101">{{cite journal| author=Meltzer JI, Keim HJ, Laragh JH, Sealey JE, Jan KM, Chien S| title=Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling. | journal=Ann Intern Med | year= 1979 | volume= 91 | issue= 5 | pages= 688-96 | pmid=496101 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=496101 }} </ref><ref name="pmid474584">{{cite journal| author=Dorhout EJ, Roos JC, Boer P, Yoe OH, Simatupang TA| title=Observations on edema formation in the nephrotic syndrome in adults with minimal lesions. | journal=Am J Med | year= 1979 | volume= 67 | issue= 3 | pages= 378-84 | pmid=474584 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=474584 }} </ref><ref name="pmid6128546">{{cite journal| author=Brown EA, Markandu ND, Sagnella GA, Squires M, Jones BE, MacGregor GA| title=Evidence that some mechanism other than the renin system causes sodium retention in nephrotic syndrome. | journal=Lancet | year= 1982 | volume= 2 | issue= 8310 | pages= 1237-40 | pmid=6128546 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6128546 }} </ref> 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.<ref name="pmid10215332">{{cite journal| author=Vande Walle JG, Donckerwolcke RA, Koomans HA| title=Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 2 | pages= 323-31 | pmid=10215332 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10215332 }} </ref> The disequilibrium creates a state of uncompensated hypovolemia when COP becomes < 8 mmHg.<ref name="pmid10215332">{{cite journal| author=Vande Walle JG, Donckerwolcke RA, Koomans HA| title=Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 2 | pages= 323-31 | pmid=10215332 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10215332 }} </ref> The drooping pressure temporarily stimulates aldosterone and other sodium-handling indices to retain sodium.<ref name="pmid10215332">{{cite journal| author=Vande Walle JG, Donckerwolcke RA, Koomans HA| title=Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 2 | pages= 323-31 | pmid=10215332 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10215332 }} </ref><ref name="pmid4022206">{{cite journal| author=Koomans HA, Kortlandt W, Geers AB, Dorhout Mees EJ| title=Lowered protein content of tissue fluid in patients with the nephrotic syndrome: observations during disease and recovery. | journal=Nephron | year= 1985 | volume= 40 | issue= 4 | pages= 391-5 | pmid=4022206 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4022206 }} </ref><ref name="pmid3784303">{{cite journal| author=Koomans HA, Braam B, Geers AB, Roos JC, Dorhout Mees EJ| title=The importance of plasma protein for blood volume and blood pressure homeostasis. | journal=Kidney Int | year= 1986 | volume= 30 | issue= 5 | pages= 730-5 | pmid=3784303 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3784303 }} </ref> Following sodium retention, a steady-state is reached and sodium is no longer actively retained.<ref name="pmid7603230">{{cite journal| author=Vande Walle JG, Donckerwolcke RA, van Isselt JW, Derkx FH, Joles JA, Koomans HA| title=Volume regulation in children with early relapse of minimal-change nephrosis with or without hypovolaemic symptoms. | journal=Lancet | year= 1995 | volume= 346 | issue= 8968 | pages= 148-52 | pmid=7603230 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7603230 }} </ref><ref name="pmid8941579">{{cite journal| author=Van de Walle JG, Donckerwolcke RA, Greidanus TB, Joles JA, Koomans HA| title=Renal sodium handling in children with nephrotic relapse: relation to hypovolaemic symptoms. | journal=Nephrol Dial Transplant | year= 1996 | volume= 11 | issue= 11 | pages= 2202-8 | pmid=8941579 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8941579 }} </ref><ref name="pmid6486860">{{cite journal| author=Bohlin AB, Berg U| title=Renal sodium handling in minimal change nephrotic syndrome. | journal=Arch Dis Child | year= 1984 | volume= 59 | issue= 9 | pages= 825-30 | pmid=6486860 | doi= | pmc=PMC1628730 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6486860 }} </ref> 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. <ref name="pmid10215332">{{cite journal| author=Vande Walle JG, Donckerwolcke RA, Koomans HA| title=Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 2 | pages= 323-31 | pmid=10215332 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10215332 }} </ref> | |||
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.<ref name="pmid10215332">{{cite journal| author=Vande Walle JG, Donckerwolcke RA, Koomans HA| title=Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. | journal=J Am Soc Nephrol | year= 1999 | volume= 10 | issue= 2 | pages= 323-31 | pmid=10215332 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10215332 }} </ref> | |||
==References== | ==References== | ||
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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.