Secondary hyperparathyroidism in an Andean mummy • 295 



many extrarenal tissues are expected but were absent in our 

 subject. Oxalosis appears to be a most improbable explana- 

 tion for our findings. 



Idiopathic h ypercalciuria must be considered a serious 

 possibility. In this hereditary condition a poorly defined met- 

 abolic aberration causes increased urinary excretion of 

 calcium which may precipitate as calcium oxalate or phos- 

 phate. It most frequently affects adults in the fourth and fifth 

 decades, but has been reported in children (Potts 1983: 1929- 

 1943). Nephrocalcinosis may also occur. 



Renai. tubular acidosis is an inherited defect in which 

 the distal renal tubule is unable to maintain normal pH control 

 resulting in excretion of an excessively basic urine causing 

 diffuse precipitation of calcium phosphate (nephrocalcino- 

 sis). The disease, however, is rare, usually requires a much 

 longer time to destroy the kidneys, and produces discrete 

 calculi (of predominantly calcium phosphate structure) only 

 in older patients. This, too, would seem an unlikely solution to 

 our diagnostic problem. 



Primary hyperparathyroidism is an obvious considera- 

 tion. In this rather common condition — 1:1000 — neoplasia 

 causes excessive production of parathyroid hormone. The 

 neoplastic lesion is usually a benign adenoma, rarely a car- 

 cinoma, of one or more parathyroid glands, or sometimes 

 primary hyperplasia of all four glands. One of this hormone's 

 principal effects is bone decalcification. Unregulated hor- 

 mone production by the tumor Hoods the kidney with 

 calcium to be excreted which often then precipitates as 

 calcium phosphate. It may do so in the form of diffuse 

 nephrocalcinosis or as discrete macrocalculi (but usually not 

 both in the same individual). The hormone's effect on the 

 bones, some forms of which are more or less unique, may be 

 detected radiologically. These include subperiosteal resorp- 

 tion (especially evident in phalanges), erosion of the lamina 

 dura adjacent to the teeth, and cystic-appearing lesions in 

 long bones rellecting the presence of osteoclastic "tumors." 

 However, these are often most obvious in rather late or ad- 

 vanced conditions and simple osteoporosis may be the only 

 identifiable radiological abnormality in many. Most clinical 

 diagnoses ai^e made on individuals in the third to sixth de- 

 cades. In our subject calcium phosphate is neither the princi- 

 pal nor the central component of the renal calculi. He is 

 younger than most persons with this diagnosis and has none 

 of the radiological stigmata of primary hyperparathyroidism 

 except the relatively nonspecific presence of diffuse os- 

 teopenia. 



There is, however, another form of hyperparathyroid- 

 ism — that secondary to hypocalcemia. The most 

 common condition producing a low blood calcium level is 

 chronic renal failure. In this state, the failing kidney's in- 

 ability to excrete phosphates results in a relentless rise in 

 blood phosphorus content and, because of calcium's recipro- 

 cal relationship to phosphorus, the blood calcium drops to 

 subnormal levels. Hypocalcemia thus provides a perpetual, 

 pathophysiological stimulus to parathyroid hormone produc- 



/Uinrch Paleopathology Symp I9SS 



tion. The consequent release of calcium by parathyroid hor- 

 mone from the skeleton raises and may even restore the nor- 

 mal blood calcium level. The tissue concentrations of 

 calcium and phosphorus frequently are then in a supersatura- 

 tion range and soft tissue precipitates of calcium phosphate 

 occur. The kidney itself is particularly vulnerable to such an 

 event (diffuse nephrocalcinosis), but commonly it also oc- 

 curs in other soft tissues. While such minute calcifications 

 are distributed diffusely through both kidneys, the condition 

 itself does not normally generate urinary calculi; any such 

 renoliths are usually the product of the original renal disease 

 which destroyed the kidneys. In children the chronic, de- 

 structive, primary renal condition leading to secondary hy- 

 perparathyroidism is by far most commonly chronic pyelone- 

 phritis (Kissane and Smith 1969:755). 



Other conditions causing nephrocalcinosis seem most im- 

 probable. The hypercalcemia of sarcoidosis is almost invar- 

 iably accompanied by infiltrations in other organs, absent in 

 our subject (Longcope and Freiman 1952). Renal cortical 

 necrosis spares the medulla, which was also destroyed in this 

 mummy's kidneys. Medullary sponge kidney spares the cor- 

 tex, again not consistent with the total kidney destruction 

 present in the Cabuza's kidneys (Heptinstall 1983). His 

 bones also revealed no discrete osteolytic lesions (car- 

 cinoma; blood dyscrasias). Milk alkali syndrome is caused 

 by excessive alkali ingestion for peptic ulcer disease: it may 

 produce mild renal insufficiency. As a presumed shaman 

 (large ear lobe perforations) he undoubtedly indulged in ritu- 

 al practice of coca leaf chewing accompanied with alkali to 

 enhance the leaf's alkaloid extraction, but it is not probable 

 this would have involved sufficient alkali ingestion to dupli- 

 cate the effect of the milk alkali syndrome. There is no reason 

 to suspect hypervitaminosis D. 



The composition of this mummy's renal calculus is of 

 special interest. While calcium oxalate is certainly the domi- 

 nant crystal present (nearly 30% of the stone's weight), sig- 

 nificant amounts of stru vite and carbonate apatite (each 1 0%) 

 are also noted and seem to be distributed diffusely through 

 the calculus. In addition it is important to emphasize that half 

 of the calculus was composed of blood, proteins, and 

 calcified tissue. More so than in purely metabolic conditions, 

 this calculus appears to have been initiated by precipitation of 

 renal salts within necrotic, hemorrhagic tissue debris (a "ma- 

 trix" stone). 



It appears to us that, while several of the discussed condi- 

 tions are possible, the nature of the calculus together with the 

 pattern of renal destruction in this age group imply that the 

 initiating event was a probably primary, bilateral renal dis- 

 ease with calculus formation resulting from local tissue ne- 

 crosis. Gradual onset of progressive renal failure produced a 

 uremic state causing fibrinous pericarditis as well as second- 

 ary hyperparathyroidism. The latter complication is then re- 

 sponsible for the observed diffuse, bilateral nephrocalcinosis 

 via the mechanism outlined above, as well as for the diffuse 

 osteoporosis. 



