Muriel MacDowell

RENAL LESIONS AND DISTURBANCE OF RENAL FUNCTION IN RATS WITH MAGNESIUM DEFICIENCY

Magnesium (Mg) deprivation in the rat results in the following biochemical alterations: hypomagnesemia, hypercalcemia, and azotoemia,l-“ as well as a coexisting small but significant decrement in muscle potassium content.44 The renal morphologic counterpart of these biochemical abnormalities has in past investigations been described by the general term “nephrocalcinosis,” affecting various regions of the renal ti~sues.7-l~ Microdissection studies have been carried out to define more precisely the morphologic characteristics and location of the renal lesion induced by Mg depletion.12J3 Initially, microliths appear in the thin limb of Henle’s Loop sometime during the second week of depletion (FIGURE 1 ) . These laminated microliths react positively with para-aminosalicylic acid (PAS), von Kossa and alizarin stains, indicating the presence of calcium as well as organic matrix. With repeated formation and accretion of new microliths, the lumen of the tubule becomes filled and distended by this composite mass, an intranephronic calculus (FIGURE 2). The structural disturbances exerted by these intraluminal aggregates are manifested locally as well as more generally. First, the local effects are illustrated in FIGURE 3. Note that a microspherolith has lodged in the “hairpin” turn of this portion of the loop. Proximal to the microlith the lumen is filled with PAS positive, von Kossa and Alizarin negative, material. Throughout the entire length of the proximal convolution up to the glomerulus, the epithelium of this first portion of the nephron appeared normal; specifically there was no dilatation of the tubule or Bowman’s Space. Distal to the calculus, scattered debris from erosion of the epithelial wall lies within the tubular lumen and extends throughout the remainder of the thin ascending limb and into the thick ascending portion of Henle’s Loop. This cellular debris, staining deeply with iron hematoxylin, was in part negative to alizarin. A conglomerate of calcareous salts was noted in the large scattered masses of cellular debris which distended and compressed the tubular wall (FIGURE 4); there was no evidence of the periodic pattern of mineral deposition (Liesegang rings) that characterized the original calculus. With increase of this amorphous accumulation, not only is the normal contour of the tubule destroyed but neighboring broad ascending tubules are similarly affected through lateral compression exerted by the enlarging calcareous mass (FIGURE 5) . The terminal portion of the