minimal change disease


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minimal change disease

 
subtle alterations in kidney function demonstrable by clinical albuminuria and the presence of lipid droplets in cells of the proximal tubules; abnormalities of foot processes of the glomerular epithelial cells are present but too subtle to be seen with light microscopy. It is seen primarily in children under 6 but sometimes in adults with the nephrotic syndrome and may or may not progress to glomerulosclerosis or glomerulonephritis.

minimal change disease

a kidney disorder characterized by subtle changes in renal function, including albuminuria and presence of lipid droplets in the proximal tubules. It mainly affects small children but also occurs in adults with idiopathic nephrotic syndrome. It may or may not progress to glomerulonephritis. Also called lipoid nephrosis, nil disease. See also idiopathic nephrotic syndrome.
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Minimal change disease

minimal change disease

Idiopathic nephrotic syndrome of childhood, lipoid nephrosis, minimal change nephrotic syndrome, nil disease Nephrology A cause of nephrotic syndrome, so named because, by LM, the glomeruli appear normal; by EM, characteristic glomerular changes are seen–eg, fusing of the epithelial layer; MCD is most common in children Etiology Unknown; risk is ↑ in those with immune disorders, recent immunizations, bee stings Prognosis MCD is not linked to oliguria or progressive renal failure. Cf Renal failure.

minimal change disease

The form of nephrotic syndrome most often found in children, in which renal biopsies reveal little if any pathological change under the light microscope. With electron microscopy, effacement of the foot processes of the glomerulus becomes evident.
See: nephrotic syndrome
References in periodicals archive ?
FSGS - Focal Segmental Glomerulosclerosis, MCD - Minimal Change Disease, TIN - Tubulointerstitial
Minimal change disease was first described as lipoid nephrosis.
Minimal change disease (MCD) is one such disease that results in glomerular injury.
One literature review revealed that minimal change disease was found in 33 of 134 cases of cancer-related nephrotic syndrome.
A hypercoaguable state may develop in minimal change disease for the following reasons: (a) increased platelet aggregation secondary to thrombocytosis and release of beta thromboglobulin for platelets; (b) increased procoagulant activity secondary to physical conditions of the nephrosis such as hemoconcentration and hyperviscosity; (c) increased production of factor V and factor VIII due to excessive urinary loss of protein S; (d) reduction of antithrombin III, which inhibits thrombin; and (e) hypertriglyceridemia can also lead to a hypercoaguable state.
The histopathological appearance of minimal change disease by light microscopy is completely normal.
IgM nephropathy is a subset of minimal change disease that may evolve into FSGS.
To comprehend the pathophysiology of minimal change disease and pregnancy outcomes, glomerular anatomy and physiology must be understood as a prerequisite.
Although minimal or no alterations are evident by light microscopy, electron microscopy reveals diffuse epithelial foot process effacement within the glomerulus of patients with minimal change disease (Brady et al.
The immunoglobulin and complement deposits with the mesangial hypercellularity are believed to be variations of minimal change disease rather than separate entities (Schnaper & Robson, 1997).
Several features of minimal change disease would support an immunological basis for the disease.
Minimal change disease is generally considered a disease of children, although adult onset cases do occur (Nakayama et al.

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