294 -J. Blackman. M.J. Allison, A.C. Aufderheide, N. Oldroyd, and R.T. Steinbock 



calcium oxalate monohydrate (20%), calcium oxylate dihy- 

 drate (9%). cagnesium ammonium phosphate hexahydrate 

 (10%), carbonate apatite ( 10%), ammonium hydrogen urate 

 (1%), and proteins, calcified tissue, and degenerated blood 

 (50%). 



NECK masses: Transmission electron microscopy revealed 

 no residual evidence of intact cellular structure. Immu- 

 noperoxidase studies demonstrated no reactivity of any mate- 

 rial in the neck masses with antibodies against either thyroid 

 or parathyroid hormone. 



lungs: Polarized light study of microscopic sections re- 

 vealed many minute, crystalline structures. Electron micro- 

 probe analysis demonstrated an elemental pattern identical 

 with that of soil from the tomb: silicon, aluminum, calcium, 

 chlorine, sulfur and potassium. 



Discussion 



The diagnostic problem to be resolved is identification of one 

 or more conditions capable of producing bilateral renal 

 nephrocalcinosis with atrophy, bilateral mildly dilated ure- 

 ters, right renal calculi of a mixed crystalline structure, 

 fibrinous pericarditis, and mild osteoporosis in an 18-year- 

 old male. 



Nonbacterial, fibrinous pericarditis most probably reflects 

 a terminal, uremic status secondary to the renal pathology. 



The ureters were not dilated to the extreme degree ex- 

 pected in either congenital hydroureters or long-standing, 

 acquired obstruction, yet were two to three times wider than 

 normal with a normal wall structure histologically. Transient 



obstruction by a calculus, expelled from the kidney and 

 passed subsequently, would appear to be the most likely 

 explanation of this finding. 



Principal candidates for explanation of this constellation 

 of findings are listed in Table 1 . It includes conditions which 

 produce renal calculi either ( I) as a complication of a primary 

 renal disease, or (2) by causing increased excretion of 

 calcium or oxalate through a normal kidney with resulting 

 precipitation of the calcium salt and secondary renal damage 

 by the calculus (infection or obstruction). 



The chemical structure of the renal calculi produced varies 

 in the different conditions under consideration . In evaluating 

 these diseases it must be kept in mind that a calculus of 

 almost any structure may eventually cause renal parenchy- 

 mal damage by obstructing urine flow or by bacterial infec- 

 tion secondary to erosion of the renal pelvic mucosa. The 

 urea-splitting action of the organisms commonly producing 

 kidney infections will then usually cause precipitation of 

 struvite (magnesium ammonium phosphate) regardless of the 

 original chemical and crystalline structure of the calculus. 

 Such a sequence of events, however, is often revealed by 

 separate chemical examinations of the stone's various layers, 

 the innermost ones reflecting the original chemical milieu at 

 the time of the calculus" origin. 



Oxalosis is characterized by an excessive level of oxalate 

 in the blood, tissues and urine. It occurs as a congenital 

 metabolic defect or as an acquired condition with excessive 

 absorption secondary to intestinal pathology. The insoluble 

 salt, calcium oxalate, precipitates in the urine. It is a rare 

 disease. A much higher content of calcium oxalate would be 

 expected in the calculus than was seen in this Cabuza subject. 

 Furthermore, since the oxalate is distributed by the blood 

 throughout the body, widespread calcium oxalate deposits in 



Zitf;reh PaU'ttpathology Symp. 1988 



