http://www.faculty.umb.edu/pjt/epi/jick00.pdf

Statins and the risk of dementia.

Bone metabolism and disease in chronic kidney disease

https://www.amjmed.com/article/0002-9343(89)90297-0/pdf

Ethanol reduces bone formation and may cause osteoporosis

We studied the natural history of primary hyperparathyroidism in patients in whom the disease was discovered fortuitously by multichannel biochemical screening and who were selected for conservative management because they were asymptomatic, had no renal stone disease or radiographic osteitis fibrosa, and had serum calcium values below 3.00 mmol/L, serum creatinine levels below 133 mumol/L, and forearm bone density not more than 2.5 SD below the mean expected for age, sex, and race. One hundred and seventy-four patients meeting these criteria were encountered during a 10-yr period, of whom 80 (mean age, 61 yr) had adequate follow-up; they did not differ significantly in any initial characteristic from the remaining 94 patients. These 80 patients were followed for 1-11 yr (mean, 46 months; median, 38 months), during which there was no change, mean or individual, in any index of PTH secretion or any of its biochemical effects and no decline in forearm bone density apart from that expected from increased age. There were 4 deaths from causes unrelated to hyperparathyroidism, and the overall death rate was not increased. The data suggest that no change occurred in either the number of parathyroid cells or secretory set-point, the 2 principal determinants of basal PTH secretion. This implies a biphasic course, with a short period of disease progression followed by a long period of disease stability. Our data support the decision to withhold surgical intervention in such patients, but to establish this as the correct policy for all asymptomatic patients will require a controlled clinical trial.

Lack of biochemical progression or continuation of accelerated bone loss in mild asymptomatic primary hyperparathyroidism: evidence for biphasic disease course.

To examine the use of analgesics as a cause of chronic renal disease, we performed a multicenter case–control study of 554 adults with newly diagnosed kidney disease (serum creatinine, ≥130 μmol per liter [1.5 mg per deciliter]) and 516 matched control subjects selected randomly from the same area of North Carolina. Histories of use of analgesics (phenacetin, acetaminophen, and aspirin) were obtained by telephone interview with the patients or their proxies. Daily users of analgesics had significantly more renal disease than infrequent users (odds ratio, 2.79; 95 percent confidence interval, 1.85 to 4.21). The risk of renal disease was highest in daily users of phenacetin (odds ratio, 5.11; confidence interval, 1.76 to 14.9, after adjustment for the effects of other analgesics). The risk of renal disease was also increased in daily users of acetaminophen; after adjustment for the use of aspirin and phenacetin, the odds ratio was 3.21 (confidence interval, 1.05 to 9.80). There was no increased ris...

https://www.nejm.org/doi/pdf/10.1056/NEJM198905113201903?listPDF=true

Analgesic Use and Chronic Renal Disease

A radioimmunoassay is described for parathyroid hormone in human serum, in which commercially available reagents are used almost exclusively. This assay can be done by any laboratory with experience in radloimmunoassay. Thirty-two of thirty-three patients with surgically proven primary hyperparathyroidism had detectable concentrations of parathyroid hormone in their serum, and concentrations of the hormone exceeded the normal range in 24 of them. Significant positive correlations were found between pre-operative serum calcium, pre-operative serum parathyroid hormone, and the weight of parathyroid tissue removed at operation. These three parameters were also significantly correlated with severity of the skeletal changes as assessed by semiquantitative histological methods.

Parathyroid Hormone Assay in Primary Hyperparathyroidism: Experiences with a Radioimmunoassay Based on Commercially Available Reagents

A radioimmunoassay is described for parathyroid hormone in human serum, in which commercially available reagents are used almost exclusively. This assay can be done by any laboratory with experience in radloimmunoassay. Thirty-two of thirty-three patients with surgically proven primary hyperparathyroidism had detectable concentrations of parathyroid hormone in their serum, and concentrations of the hormone exceeded the normal range in 24 of them. Significant positive correlations were found between pre-operative serum calcium, pre-operative serum parathyroid hormone, and the weight of parathyroid tissue removed at operation. These three parameters were also significantly correlated with severity of the skeletal changes as assessed by semiquantitative histological methods. Additional Keyphrases: indexes to hyperparathyroidism #{149} diagnostic aid #{149} calculous disease #{149} parathyroid adenoma e normal values

Parathyroid HormoneAssayinPrimary Hyperparathyroidism: Experiences witha Radioimmunoassay Basedon Commercially Available Reagents

The nature of the original renal disease was determined in 403 consecutive cases of end-stage renal failure, in 317 of which the clinical diagnosis was corroborated by histological examination of the kidney. Five diseases accounted for 20 or more cases--glomerulonephritis (31% of the total), analgesic nephropathy (29%), primary vesicoureteral reflux (8%), essential hypertension (6%), and polycystic kidneys (5%). In only four cases did renal failure result from chronic pyelonephritis without a demonstrable primary cause. Greater use of micturating cystography and cystoscopy and routine urine testing for salicylate are advocated for earlier diagnosis of the major causes of "pyelonephritis". The incidence of end-stage renal failure in people aged 15-55 in New South Wales was estimated to be at least 34 new cases per million of total population each year.

https://www.bmj.com/content/bmj/1/5955/440.full.pdf

Diseases causing end-stage renal failure in New South Wales.

Renal transplantation reduced circulating parathyroid hormone in recipients of renal allografts. Nevertheless, biochemical and histological evidence of mild hyperparathyroidism persisted up to eight years after renal transplantation despite good graft function.

https://www.bmj.com/content/bmj/3/5985/680.full.pdf

Hyperparathyroidism after renal transplantation.

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Parathyroid Hormone Assay in Primary Hyperparathyroidism: Experiences with a Radioimmunoassay Based on Commercially Available Reagents

Parathyroid HormoneAssayinPrimary Hyperparathyroidism: Experiences witha Radioimmunoassay Basedon Commercially Available Reagents

Diseases causing end-stage renal failure in New South Wales.

Hyperparathyroidism after renal transplantation.