Nephrotic syndrome natural history, complications and prognosis
|
Nephrotic Syndrome Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Nephrotic syndrome natural history, complications and prognosis On the Web |
|
American Roentgen Ray Society Images of Nephrotic syndrome natural history, complications and prognosis |
|
FDA on Nephrotic syndrome natural history, complications and prognosis |
|
CDC on Nephrotic syndrome natural history, complications and prognosis |
|
Nephrotic syndrome natural history, complications and prognosis in the news |
|
Blogs on Nephrotic syndrome natural history, complications and prognosis |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Complications
Infections
Patients with nephrotic syndrome are at increased risk of infections due to several mechanisms:
- Urinary loss of immunoglobulins
- Delay in complement-dependent opsonisation of encapsulated organisms, such as S. pneumoniae[1]
- Reduction in factors B and I[1]
- Decrease of blood flow to mesenteric regions
Patients with nephrotic syndrome who complain of abdominal pain must always be assessed for peritonitis that requires paracentesis. The rate of spontaneous bacterial peritonitis is 2-6%[2] which contributed to 1-2% of mortality in these patients. Gram-negative bacterial organisms, such as E. coli, are especially important infectious agents in patients with nephrotic syndrome.[3] Urinary tract infections and skin infections are also common, such as cellulitis, erysipelas, and lymphangitis.[4] Since patients are often treated with immunosuppressants, the susceptibility to infections is further heightened in these patients.[5][1]
Thromboembolism
Several factors contribute to thromboembolism in nephrotic syndrome[6]:
- Increase in platelet aggregation
- Increase in concentration of fibrinogen
- Urinary Loss of antithrombin III
- Increase in blood viscosity
- Decrease in blood flow
Thromboembolism is considered the second most important cause of mortality in nephrotic syndrome. Thromboembolism may occur at any site; common locations include deep veins of the extremities, cerebral veins, renal veins, and pulmonary veins. Although arterial occlusion is much less common, its prognostic significance is much graver than venous thromboembolism and is associated with mortality.[6]
Growth Retardation
Urinary loss of insulin-like growth factor (IGF) binding proteins may cause a decrease in serum concentration of IGF-I and IGF-II. Corticosteroids, often used in the treatment of nephrotic syndrome, may also suppress growth.[6]
Prognosis
The prognosis depends on the cause of nephrotic syndrome. It is usually good in children, because minimal change disease responds very well to steroids and does not cause chronic renal failure. However, other causes such as focal segmental glomerulosclerosis frequently lead to end stage renal disease. Factors associated with a poorer prognosis in these cases include level of proteinuria, blood pressure control and kidney function (GFR).
References
- ↑ 1.0 1.1 1.2 Patiroglu T, Melikoglu A, Dusunsel R (1998). "Serum levels of C3 and factors I and B in minimal change disease". Acta Paediatr Jpn. 40 (4): 333–6. PMID 9745775.
- ↑ Feinstein EI, Chesney RW, Zelikovic I (1988). "Peritonitis in childhood renal disease". Am J Nephrol. 8 (2): 147–65. PMID 3293444.
- ↑ Tain YL, Lin G, Cher TW (1999). "Microbiological spectrum of septicemia and peritonitis in nephrotic children". Pediatr Nephrol. 13 (9): 835–7. PMID 10603131.
- ↑ Eddy AA, Symons JM (2003). "Nephrotic syndrome in childhood". Lancet. 362 (9384): 629–39. doi:10.1016/S0140-6736(03)14184-0. PMID 12944064.
- ↑ Goldstein SL, Somers MJ, Lande MB, Brewer ED, Jabs KL (2000). "Acyclovir prophylaxis of varicella in children with renal disease receiving steroids". Pediatr Nephrol. 14 (4): 305–8. PMID 10775074.
- ↑ 6.0 6.1 6.2 Roth KS, Amaker BH, Chan JC (2002). "Nephrotic syndrome: pathogenesis and management". Pediatr Rev. 23 (7): 237–48. PMID 12093934.