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| Minimal Change Disease |
| Etiology •The etiology in the majority of cases of minimal change disease is unknown. •The disease however is believed to have an immune basis because of association of some cases with lymphomas such as Hodgkins disease, previous or concomitant infections, recent immunizations, and because of the response of the disease to steroid therapy. |
| Pathogenesis •See etiology. •There is presumably an alteration in the electrical charge of the glomerular basement membranes that makes some proteins, especially albumin permeable. The glomerular capillaries (though structurally intact) are no longer able to retain albumin in the vascular space and so albuminuria results. •The urine loss of albumin results in hypoalbuminemia which leads to diminished oncotic pressure and movement of water into the extravascular space resulting in tissue edema. •Additionally, the hypoalbuminemia triggers the liver to produce lipoproteins and there is resultant hyperlipidemia., |
| Epidemiology •Although minimal change disease may be seen in all ages, it is more commonly seen in children. •In the pediatric population, most cases are seen below the age of 6 with a peak incidence betwen ages 2 and 4 years. •In children the male:female ratio is 2:1. •Immunogenetics: DR7. |
| General Gross Description •The kidneys in minimal change disease show no gross abnormalities that reflect the pathologic process. |
| General Microscopic Description •Although the diseased structures in minimal change disease are the glomeruli, there are no histologic abnormalities of note. •The pathologic alteration is a change in the electrical charge barrier of the capillary wall which cannot be visualized. •Direct immunofluorescence studies show negative findings. •Electron microscopy shows effacement of foot processes of the visceral epithelial cells, cytoplasmic swelling and surface pseudomembranous transformation. •The tubular epithelial cells may show cytoplasmic hyaline droplets due to protein reabsorption and may also show lipid vacuoles due to lipiduria. These tubular alterations however are secondary to the primary glomerular pathology. |
| Clinical Correlation •Patients with minimal change disease manifest heavy proteinuria (3.5 gm or more per 24 hours) and the consequence of protein loss (hypoalbuminemia, hyperlipidemia, edema). •Additional complications of heavy proteinuria include increased vulnerability to infections, increased risk of thrombotic and thromboembolic diseases. |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 950-952. •Rose B. Renal Pathophysiology the essentials. Baltimore: Williams and Wilkins. 1994. Ch. 9. |
| Minimal Change Disease |
| Synopsis by: Harold Yamase M.D. (T71200M00001)[211] |
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