Shang-Der Shieh

A Prospective Study of Calcium Metabolism in Exertional Heat Stroke with Rhabdomyolysis and Acute Renal Failure

Intensive training in a humid and warm environment can cause exertional heat stroke (ExHS) and rhabdomolysis (RBD) in military recruits. To investigate the role of vitamin D and monomeric calcitonin (CT) on the calcium metabolism in ExHS with RBD and acute renal failure (ARF), we studied 21 recruits with ExHS (mean age 21.4 years), 7 of which had ARF. Another 11 age-matched recruits with heat exhaustion (HE) and 11 healthy subjects were selected as controls. Our results showed that in 14 ExHS patients without ARF, mean serum creatinine (Cr) levels were significantly higher (151.16 vs. 106.08 mumol/l, p < 0.01), whereas serum osteocalcin (OC) levels were significantly lower (2.22 vs. 4.65 micrograms/l, p < 0.01) than in healthy controls. In 7 patients with ExHS and ARF, the mean serum Cr (774.38 vs. 105.20 mumol/l, p < 0.01), phosphorus (P) (2.26 vs. 1.26 mmol/l, p < 0.05), creatine phosphokinase (CPK) 274,143.97 vs. 85.78 IU/l, p < 0.05), intact parathyroid hormone (I-PTH) (299.81 vs. 18.66 ng/l, p < 0.05) and CT (13.58 vs. 6.63 ng/l, p < 0.01) levels on admission were significantly higher while the mean ionized calcium (iCa) levels were significantly lower than the healthy controls (0.9 vs. 1.18 mmol/l, p < 0.01). The mean serum 25-hydroxyvitamin D [25(OH)D] levels were not significantly different from healthy controls. However, mean serum 1,25-dihydroxyvitamin D [1,25(OH)2D] levels and the ratio of 1,25(OH)2D to 25(OH)D were significantly lower than healthy controls throughout the whole course of ARF. None of the 7 patients with ExHS and ARF developed hypercalcemia during the diuretic phase. Their mean serum I-PTH levels decreased significantly from 299 to 18 ng/l during the recovery phase (p < 0.05). Our study seems to suggest that the abnormal calcium metabolism in this unique patient group is in part caused by persistently decreased renal production of 1,25(OH)2D, although increased monomeric CT levels were associated with hypocalcemia. However, whether or not a causal relationship exists merits further investigation.

Fatal aeromonas hydrophila bacteremia in a hemodialysis patient treated with deferoxamine

A 49-year-old woman undergoing long-term hemodialysis and treated with deferoxamine (DFO) 1.5 g twice weekly for aluminum bone disease developed fever and bilateral calf pain caused by myonecrosis with gas gangrene. She had a rapidly fatal outcome. The cultures of blood and aspirates from both calf muscles demonstrated Aeromonas hydrophila. No obvious entry point could be traced. The in vitro growth of the patients strain was found to be stimulated by the deferoxamine-iron complex in an iron-deprived medium. It is suggested that high-dose DFO therapy in this patient was responsible for promoting a bacterial infection by this microorganism.

Rapid correction of metabolic acidosis in chronic renal failure: Effect on parathyroid hormone activity

To investigate the effect of rapid correction of chronic metabolic acidosis on circulating intact parathyroid hormone (I-PTH) activity by free calcium clamp in chronic renal failure, 18 patients were enrolled in this study. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was clamped at the preinfusion level throughout the entire procedure. The plasma pH, bicarbonate, total CO2, sodium, serum total calcium and 1,25(OH)2 vitamin D3 levels increased significantly while serum concentrations of I-PTH, alkaline phosphatase and albumin showed significant decreases after bicarbonate infusion. The plasma ionized calcium, potassium, serum magnesium and inorganic phosphorus levels showed no significant difference before and after bicarbonate infusion. These results demonstrate that rapid correction of metabolic acidosis attenuates circulating PTH activity in chronic renal failure and may underline the importance of maintaining normal acid-base homeostasis particularly in the presence of secondary hyperparathyroidism.

Influence of rapid correction of metabolic acidosis on serum osteocalcin level in chronic renal failure.

Metabolic acidosis induces a combination of inhibited osteoblastic and stimulated osteoclastic activity. To determine the role of alkali therapy in osteoblast function in chronic renal failure, serum bone isoenzyme of alkaline phosphatase (BAP) and osteocalcin were assessed before and after bicarbonate infusion. Eighteen patients with mild to moderate metabolic acidosis, none of whom had received dialysis therapy, were enrolled in this study. Metabolic acidosis was corrected by continuous bicarbonate infusion while plasma ionized calcium was monitored at 5 min intervals and held at the preinfusion level by calcium solution infusion during the entire procedure. The end-point of the study was reached when the plasma bicarbonate was approximately 24 mmol/l or pH was approximately 7.4 and plasma ionized calcium was clamped at the preinfusion level with only a 0.01 mmol/l fluctuation. The plasma pH (7.31 +/- 0.04 vs. 7.40 +/- 0.03, P < 0.001), bicarbonate (18.46 +/- 2.49 vs. 23.66 +/- 2.72 mmol/l, P < 0.001), serum total calcium, and osteocalcin (15.61 +/- 6.45 vs. 18.79 +/- 6.71 mg/l, P < 0.05) levels were significantly increased, whereas serum concentrations of alkaline phosphatase and albumin levels were significantly decreased after bicarbonate infusion. The serum BAP (1.85 +/- 1.29 vs. 1.79 +/- 1.18 mukat/l, P = 0.252), and inorganic phosphorus levels showed no significant differences before and after bicarbonate infusion. These results demonstrate that rapid correction of metabolic acidosis improves osteoblast function and may underline the importance of maintaining normal acid-base homeostasis in chronic renal failure.

Role of plasma catecholamines, autonomic, and left ventricular function in normotensive and hypotension prone dialysis patients

The current study looked at plasma catecholamines, clinical autonomic function tests, and hemodynamic parameters in 10 ESRD patients (five men and five woman, aged 56.4 ± 3.6) with dialysis hypotension and 10 patients (five men and five women, aged 58.6 ± 4.2) without dialysis hypotension. Catecholamines were measured using high performance liquid chromatography—electrochemical detection (HPLCECD). Dialysis led to a significant decrease in mean arterial pressure (MAP) in the hypotensive group as compared with the normotensive group. Significantly higher basal (predialysis) plasma norepinephrine (NE) and dopamine levels (DA) were found in the hypotensive uremic group as compared with the normotensive group. Levels of plasma epinephrine (EP) were not significantly different between the normotensive and hypotensive groups. In response to postural stimulation, blood pressure fell in both groups, but the fall in the hypotensive group was significantly greater. Percentage increments of plasma catecholamines in response to postural stimulation in both groups were similar, however. Among the measured hemodynamic parameters, including total peripheral vascular resistance and left ventricular function (cardiac index and fractional shortening), only the cardiac index showed significantly lower values in the hypotensive group after dialysis, as compared with the normotensive group. Results of four tests of autonomic function indicated that although both groups responded similarly to hand-grip and cold-pressor tests, impaired responses to orthostasis and Valsalva maneuver after dialysis were observed in the hypotensive group. The MAP changes in dialysis in the hy-potension prone group correlated inversely with predialysis plasma NE, but not with EP and DA. The MAP changes after dialysis in both groups also correlated positively with orthostatic pressure changes, cold-pressor changes, and Valsalva maneuver results. These data suggest that impaired autonomic and left ventricular function may both contribute to dialysis induced hypotension.

Milk-Alkali Syndrome in an Aged Patient with Osteoporosis and Fractures

Shih-Hua Lin, MD, Division of Nephrology, Department of Internal Medicine, Tri-Service General Hospital, No. 8, Sect. 3, Ting-Chow Road, Taipei (Taiwan) Dear Sir, Milk-alkali syndrome is caused by the excessive intake of calcium and absorbable alkali and is characterized by the triad of metabolic alkalosis, hypercalcemia and renal failure. With the development of better 7⁄8 blockers and antacids, the number of cases of milk-alkali syndrome has markedly decreased in the past two decades. Recently reported cases have been limited to new and variable etiologies of this hypercalcemic disorder [1,2]. We present a case of milkalkali syndrome resulting from the use of calcium carbonate and calcitriol for the treatment of osteoporosis and bony fractures. A 70-year-old Asian female with no pertinent medical history sustained accidental fractures of her pelvis and right humerus 1 month prior to admission. At that time, closed reduction of the pelvis and right humerus was performed. X-rays revealed severe osteoporosis, and the patient was started on calcium carbonate, 1,250 mg three times daily and Rocaltrol, Roche [ 1,25-dihydroxycholecalciferol, calcitriol, 1,25(OH)2D3]0.25 μg twice daily to enhance bone formation. On admission, the patient presented with anorexia, nausea, lethargy and an altered level of consciousness. On physical examination, her supine blood pressure was 114/70 mm Hg and her heart rate was 100/min. Skin turgor was reduced, oral mucosa was dry, and the jugular veins were not distended. Slow and shallow respiration was observed. Cardiac, pulmonary and abdominal examinations were unremarkable. Neurological examination revealed decreased alertness, slow recall, and bilateral hyporeflexia. Laboratory data showed normal peripheral blood pictures. Urinalysis showed pH 8.0, granular cast and trace proteinuria. Biochemistry indicated sodium 155mEq/l, potassium 3.1 mEq/1, chloride 114mEq/l, total calcium was 15.9mg/dl, free calcium 7.7 mg/dl, inorganic phosphate 1.9mg/dl, glucose 88 mg/dl, albumin 3.3 g/dl, uric acid 14.8 mg/dl, blood urea nitrogen 77 mg/dl, creatinine 3.7 mg/dl. Arterial blood gas showed metabolic alkalosis with pH7.51, PC02 52.0 mm Hg, P02 66.4 mm Hg, and HCO3 40.6 mEq/1. Chest roentgenography and KUB were normal without soft tissue calcification. Abdominal sonography showed normal kidney size without nephro-calcinosis. At this point milk-alkali syndrome was diagnosed. Hypercalcemia, metabolic alkalosis and renal failure completely resolved within 1 week after withdrawal of calcium carbonate and Rocaltrol, coupled with fluid supplementation consisting of normal saline and 5% glucose.