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Purpose: The aim of this study was to determine the incidence of treatment of hyperkalemia in hospitalized patients., Methods: This is a prospective chart review of adults in a tertiary care hospital with hyperkalemia (serum potassium [K] ≥5.1 mEq/L) over a 6-month period. The treatments and their effectiveness, causative factors and associated electrocardiographic (ECG) changes were examined., Results: There were 154 hyperkalemic episodes, 32 with K ≥6.5 mEq/L and 122 with K<6.5 mEq/L. Overall, 97% received treatment for an average K of 5.9 mEq/L. Sodium polystyrene sulfonate (SPS) was included in 95% of the regimens. Incremental doses of SPS monotherapy yielded potassium reductions between 0.7 and 1.1 mEq/L, and inadequate responses (K <0.5 mEq/L) were less frequent with higher doses. There were no differences in the effectiveness of SPS among dialysis-dependent, chronic kidney disease, or nonchronic kidney disease patients. Greater reductions in potassium were observed using a combination of treatments. ECGs were performed in 44% of patients, and 50% showed no ECG changes despite K being ≥6.5 mEq/L. The most common abnormality, peaked T waves, was associated with a higher frequency of calcium administration but not with the number of K+-lowering therapies., Conclusions: Almost all the patients were treated for hyperkalemia. Oral SPS monotherapy was the predominant treatment with the best response at the highest dose. Some combination therapies had greater K reductions but were used infrequently. An ECG was obtained in about 50% of the cases, but two thirds showed no K-related changes. Reduced kidney function was associated with 70% of hyperkalemic episodes. Angiotensin-converting enzyme inhibitors and trimethoprim were the most commonly implicated medications.

Secondary hyperparathyroidism is highly prevalent in patients with end-stage renal disease. After successful kidney transplantation, however, parathyroid glands gradually involute to normal size with subsequent normalization of intact parathyroid hormone (PTH), serum calcium, and phosphorous concentrations. This report describes a 48-year-old diabetic end-stage renal disease patient who underwent a successful cadaveric kidney transplant. Serum calcium and phosphorous concentrations normalized within 6 months. Three years later, he presented with complaints of proximal muscle weakness that was progressively worsening. Physical examination revealed temporal wasting and proximal muscle weakness. Detailed neurologic examination was unremarkable except for decreased vibratory sensation in both feet. Laboratory data showed stable allograft function (serum creatinine, 1.3 mg/dL), hypocalcemia, and hypophosphatemia with markedly elevated alkaline phosphatase level (726 IU/L) and intact PTH level (947 pg/mL). Further laboratory evaluation revealed poor nutritional status and severe deficiency of 25(OH)D (4.0 ng/mL). Past medical history included remote episodes of acute pancreatitis due to prior alcohol abuse. Computed tomography of the abdomen showed calcific atrophic pancreas, and steatorrhea was confirmed on stool studies. Decreased bone mineral density was noted by computed tomography bone density scan. Secondary hyperparathyroidism and osteomalacia had developed due to severe vitamin D deficiency, occurring as a result of previously unrecognized, minimally symptomatic pancreatic exocrine insufficiency. Treatment with vitamin D, calcium, and pancreatic enzyme replacement led to remarkable resolution of clinical symptoms and secondary hyperparathyroidism (intact PTH, 65 pg/mL after therapy) and resulted in significant improvement in bone mineralization. Factors associated with vitamin D deficiency in the chronic kidney disease and post-transplant patient population are reviewed.

The prevention and treatment of the secondary hyperparathyroidism of chronic renal failure by medical means relies on a number of different possible approaches, which should be tailored to each patient's individual needs. Schematically, prevention should start early during the course of chronic renal failure (ie, when plasma intact parathyroid hormone is normal or only slightly elevated). Small calcium supplements prevent the development of a calcium deficit and may prevent parathyroid hormone oversecretion. The various therapeutic options that are available at present include: oral or intravenous vitamin D and vitamin D derivatives, in particular the 1alpha-hydroxylated vitamin D compounds; oral calcium supplements (calcium carbonate and calcium acetate) to avoid calcium depletion and also to bind phosphate in the intestinal lumen; aluminum-containing phosphate binders, the use of which should be restricted; oral magnesium salts (magnesium carbonate and magnesium hydroxide), which often are not well tolerated; general measures, such as dietary restriction of phosphate intake; and, in the case of resistance to all these approaches, the possibility of attempting ultrasound-guided ethanol injection of grossly hyperplastic parathyroid glands. Finally, it is encouraging to know that new drugs are in development, including calcium-free, aluminum-free, nonabsorbable oral phosphate binders, potentially nonhypercalcemic vitamin D derivatives, and calcimimetics. Some of them already have entered the stage of clinical evaluation, and preliminary results are promising.

Calcium supplementation has long been regarded as a fundamental part of the prevention and treatment of postmenopausal osteoporosis, but it is only in recent years that clear evidence has emerged demonstrating its impact on bone mass. Calcium supplementation does not completely arrest postmenopausal bone loss but slows the rate of decline by 30 to 50%. The effect of calcium supplementation on fracture incidence in postmenopausal women has not been established. Vitamin D deficiency is common in the frail elderly, particularly in countries where fortification or food with this vitamin is not practiced. Treatment of vitamin D deficiency has been associated with significant reductions in the number of hip fractures. The role of the potent vitamin D metabolites, calcitriol and alphacalcidol, in the management of postmenopausal osteoporosis is not clear. Although some studies show substantial benefits in bone density or fracture rate from the use of these compounds, the published data are inconsistent. In general, hormone replacement therapy and the potent bisphosphonates produce greater effects on bone density and there is a greater consistency among the results of the published studies of these other interventions. Controlled trials of exercise interventions in postmenopausal women show that exercise can positively influence bone density by a few percent. Exercise interventions in the elderly have been reported to decrease fall frequency by 10%. This latter effect may have a greater impact on fracture frequency than the modest benefits of exercise on bone-density.

A 72-year old man presented with clinical signs of cervical myelopathy , a short neck, low posterior hairline, and limited neck movements. He also had a solitary kidney and anomaly of the third rib. Biochemical hypoparathyroidism with low parathyroid hormone level was discovered and secondary causes excluded. Treatment with alfacalcidol, calcium, and spinal decompression by complex laminectomy allowed complete recovery of symptoms. Klippel-Feil syndrome encompasses an increasing constellation of clinical features that affect most organs. The association with hypoparathyroidism, however, has not been described previously. This may be yet another syndrome with single pathology responsible for all the findings.

A patient with the hungry bone syndrome following parathyroidectomy for hyperparathyroidism developed congestive heart failure, probably due to the myocardial depressant effects of hypocalcemia and hypomagnesmia. Calcium and magnesium alone were instrumental in relieving his symptoms, decreasing his heart size, and clearing the pulmonary congestion. A mechanism for the pathogenesis of hypocalcemia and hypomagnesemia induced heart failure is proposed.