Hyperparathyroidism Acidosis

In lithium treated subjects, there is no evidence of reduced bone mass at any of the measured sites in relation to that of control subjects. The mechanism responsible for the maintenance of bone mass despite biochemical evidence of hyperparathyroidism is not clear [45]. We suspect that it is due to renal calcium retention. Indeed, in dogs lithium administration for only 3 days causes a striking decrease in urinary calcium excretion which is independent of the presence of parathyroid hormone and occurs despite the concurrent development of metabolic acidosis [Batlle D, Arruda J, and Kurtzman NA 1981 unpublished observations]. 

PTH increases the renal clearance of bicarbonate and phosphate. In hyperparathyroidism, a mild hyperchloremic metabolic acidosis may be observed whereas in nonparathyroid hypercalcemia, a mild hypochloremic metabolic alkalosis may be observed. Although hypophosphatemia is often seen in hyperparathyroidism, the measurement of serum phosphate is of limited value because hypophosphatemia is also found in hypercalcemic cancer patients. 

In the kidneys, PTH (1) induces 25-hydroxyvitamin D-la-hydroxylase, increasing the production of l,25(OH)2D, which stimulates intestinal absorption of both calcium and phosphate, (2) increases calcium reabsorption in the distal convoluted tubule of the nephron, (3) decreases reabsorption of phosphate by the proximal tubule, and (4) inhibits Na -H antiporter activity, which favors a mild hyperchloremic metabolic acidosis in hyperparathyroid states. 

The common N-terminal explains the ability of PTHrP to interact with the PTH/PTHrP receptor, mimicking the biological actions of PTH in classic target tissues, including bone and kidney. Like PTH, PTHrP causes hypercalcemia and hypophosphatemia t and increases urinary cyclic AMP. However, when compared with patients with primary hyperparathyroidism, patients with PTHrP-induced hypercalcemia have lower concentrations of l,25(OH)2D and more typically have metabolic alkalosis (instead of hyperchloremic metabolic acidosis), reduced distal tubular calcium reabsorption, and reduced and uncoupled bone formation. 

Common complications of Stages 3 to 5 CKD include anemia, hyperphosphatemia, secondary hyperparathyroidism, fluid and electrolyte abnormalities, metabolic acidosis, and malnutrition. 

Other chronic disorders cause osteomalacia. " " Phosphate depletion from low dietary intake, phosphate-binding antacids, and oncogenic osteomalacia (potentially phosphaturic effect) can cause osteomalacia. Hypophosphatasia is an inborn error of metabolism in which deficient activity of alkaline phosphatase causes impaired mineralization of bone matrix. Acidosis from renal dysfunction, distal renal tubular acidosis, hypergammaglobulinemic states (e.g., multiple myeloma), and drugs (e.g., chemotherapy) compromises bone mineralization. Renal tubular disorders secondary to Fanconi s syndrome, hereditary diseases (e.g., Wilson s disease, a defect in copper metabolism), acquired disease (e.g., myeloma), and toxins (e.g., lead) cause osteomalacia to varying degrees. Chronic wastage of phosphorus and/or calcium limits mineralization, which may be further compromised by acidosis and secondary hyperparathyroidism. 

Indications Heart/kidney dual vacuity. Polyuria, spermatorrhea, nocturnal emission, turbid urine due to cystitis, loss of memory due to nervous exhaustion, chronic nephritis, diabetes mellitus, diabetes insipidus, tubular acidosis, primary aldosteronism, hyperparathyroidism, neurosis, prolapsed uterus, and autonomic dystonia... 

Patients with primary hyperparathyroidism tend to suffer from some degree of metabolic acidosis even when they are not uremic (T7). Four-man et al. have shown that failiure of acidifying power may be a feature of primary hyperparathyroidism (F5) but if it is a specific effect of the hormone, it is surprising that this function does not always improve after operation. It is possible that it may be the result of structural damage... 

Calcium phoxpliare may be a consequence of primary hyperparathyroidism or renal tubular acidosis. 

Tables 63-6.5 list some of the causes that affect plasma calcium, magnesium, and phosphate. Increased plasma calcium concentration may occur when the xeno-biotic specifically targets calcium metabolism, behaves similarly to vitamin D, and causes hyperparathyroidism or renal disease. Lead and cadmium enter bone and inhibit bone growth, increase calcium release from bone, and inhibit renal tubular reabsorption of calcium salts lead inhibits the renal bioactivation of 25-hydroxy-cholecaliciferol (Sauk and Somerman 1991). In longer-term studies, increased plasma calcium may be associated with tumor burden. Because roughly half of circulating calcium is bound to plasma albumin, hypercalcemia can also arise from dehydration. Hypoparathyroidism, pancreatitis, and renal disease can reduce plasma calcium. Acidosis increases plasma-ionized calcium concentrations, whereas alkalosis causes a decrease due to the effects of pH in the ECF or on protein binding.

If, for some reason, the diffusible Ca is lowered, the kidney conserves the serum level of calcium, partly because of a lowered filtration rate, but mostly by an increased reabsorption. At a total serum Ca concentration of less than 1.8 mmol/liter the net urinary excretion is almost zero. This regulatory function of the kidney can be disturbed by a low glomerular filtration rate, phosphate retention, acidosis, secondary hyperparathyroidism, and disturbances in the vitamin D metabolism [4],... 

In an attempt to compensate for the acidosis, bone salts are mobilized. Unless the patient is treated with alkalies, bone salt mobilization results in osteomalacia. Calcium is excreted in the urine, and the combination of high calcium levels, high pH, and low citrate concentration in the tubular fluid facilitates precipitation of calcium salts, thus leading to nephrocalcinosis. Secondary hyperparathyroidism develops as a consequence of the negative calcium balance. The inability to concentrate urine and the accompanying polyuria result in part from the hypokalemia and in part from the hypercalciuria. 

Hy percalciaemia -Williams syndrome -Distal tubular acidosis -Hyperparathyroidism (3)... 

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