Comments submitted for publication must be typed doublespaced. Text length must not exceed 500 words, and no more than five references may be used. Complete references must be furnished, as specified in "Information for Authors" (page 1-6). Specific permission to publish should be appended as a postscript. Publication depends on availability of space: we give preference to comment on recent content and to new information. Letters for this section should be concise—the Editor reserves the right to shorten them and make changes that accord with our style. Secondary Hyperparathyroidism in Acute Renal Failure from Rhabdomyolysis TO THE EDITOR: The recent paper by Koffler, Friedler, and Massry (Ann Intern Med 85:23-28, 1976) attributes hypercalcemia in the diuretic phase of acute renal failure to either secondary hyperparathyroidism, immobilization, or remobilization of previously deposited calcium in damaged muscle. A patient we have recently seen who presented with acute renal failure from alcoholic rhabdomyolysis had clearly elevated plasma parathyroid hormone levels throughout his course and well into the diuretic phase without the development of hypercalcemia (Table 1). The parathyroid hormone level was inappropriately elevated in relation to the serum calcium or magnesium level and suggests loss of normal feedback control. However, it is clear from the observations in this patient and those of Massry and associates (1) that skeletal resistance to parathyroid hormone often occurs in acute renal failure, as shown by a failure of rise in serum calcium with infusion of parathyroid hormone extracts. In the absence of hypomagnesemia this suggests reduced availability of 1,25-dihydroxycholecalciferol. These observations suggest that in patients who are hypercalcemic during the diuretic phase of acute renal failure, availability of 1,25-dihydroxycholecalciferol may be of greater importance in the genesis of hypercalcemia than the absolute parathyroid hormone levels. Future studies should direct their attention to vitamin D metabolism in acute renal failure and evaluate its role in hypercalcemia. JACOB D. BITRAN, M.D.

The Pritzker School of Medicine The University of Chicago Chicago, IL 60637 REFERENCE 1. MASSRY SG, ARIEFF AI, COBURN JW, et al: Divalent ion metabolism in patients with acute renal failure: studies on the mechanism of hypocalcemia. Kidney Int 5:437-445, 1974

Dialysis and Triglycerides TO THE EDITOR: According to the recent paper of Dr. Cattran and colleagues ( 1 ) , peritoneal dialysis leads to more severe and sustained hypertriglyceridemia than hemodialysis. Since higher values of triglycerides may further accelerate cardiovascular disease ( 2 ) , they are justifiably concerned about the "increasing number of children and adults maintained on chronic peritoneal dialysis." We were unable, however, to confirm their findings. We have recently examined the fasting serum triglyceride levels in a group of 21 patients on chronic peritoneal dialysis for 6 to 65 months (average, 25.6 months) and 15 patients on chronic hemodialysis for 1 to 73 months (average, 19.5 months). As shown in Table 1, we could not confirm any difference between the mean triglyceride levels in the two groups. Although most of our patients on peritoneal dialysis were receiving 1000 units of heparin in two litres of dialysate, significantly more than Dr. Cattran's patients, we do not think that the use of the anticoagulant was responsible for the lower triglyceride concentrations, because serum triglyceride levels measured in another group of 13 patients preperitoneal and postperitoneal dialysis did not change (average preperitoneal level, 197.2 mg/dl; postperitoneal, 190.4 mg/dl). In contrast to our centre where chronic peritoneal dialysis is often the treatment of first choice for new patients with chronic renal failure, in most other centres chronic peritoneal dialysis is reserved for older patients and those with cardiovascular complications. The higher mean age of the peritoneal dialysis group in Dr. Cattran's study indicates that such a selection may have taken place in allocating his patients to the two groups. If this were the case, some of his patients may have had elevated tri-

Table 1. Clini cal and Laboratory D;ata Date

13 Jan 27 Jan 3 Feb 10 Feb 28 Feb

Blood Urea Nitrogen


148 70 44 28 24

16.2 6.5 3.5 2.0 1.2


,„ mg/dl

P0 4


8.5 5.0 3.5 3.3 4.5

2.8 2.6 1.9 2.0 1.9


3.5 9.6 9.0 9.4 9.5

Parathyroid Hormone (Normal,

Secondary hyperparathyroidism in acute renal failure from rhabdomyolysis.

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