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J. Adan Ganel, MD
Sacramento, Calif

JAMA. 1976;235(19):2079.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

Nephrotic patients with membranous glomerulonephritis have a very high incidence of renal vein thrombosis, as high as 40%.¹ The patient reported by Luft et al (234: 1158,1975) had this type of renal disease, and he also had another important predisposing factor for the development thrombosis—his extreme obesity.

Obese patients have a deficient fibrinolytic mechanism^2,3 that correlates with the degree of overweight.⁴ Obesity has recently been described in association with large amounts of fibrin in the glomeruli, mesangial IgM, C3, and a form of nephrotic syndrome that is reversible with weight reduction.⁵ It is conceivable that fibrin deposition in the glomeruli could limit the phagocytic action of the mesangial cells reducing their efficiency in the removal of immunocomplexes and other mediators of glomerular injury.

I share the view that nephrotic patients with massive obesity, as well as those with membranous glomerulonephritis, should be carefully . . . [Full Text PDF of this Article]

Footnotes
Edited by John D. Archer, MD, Senior Editor.

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