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3.
Nephron ; 20(4): 196-202, 1978.
Article in English | MEDLINE | ID: mdl-634417

ABSTRACT

Parathyroid hormone (PTH), creatinine, calcium and phosphate blood levels were repeatedly measured in 5 patients with acute renal failure. 1 patient developed hypercalcemia during the recovery phase of the illness. PTH was elevated in all cases before starting hemodialysis treatment and returned to normal when renal function recovered. Calcium and PTH were inversely correlated in 3 patients including the patient with transient hypercalcemia. These data show that parathyroid function in acute renal failure is closely related to changes in renal function and the hypercalcemia, when occurring, is not necessarily due to parathyroid hyperactivity.


Subject(s)
Acute Kidney Injury/complications , Hypercalcemia/etiology , Parathyroid Hormone/blood , Adult , Calcium/blood , Creatinine/blood , Female , Humans , Male , Middle Aged , Phosphates/blood
4.
Horm Metab Res ; 9(3): 239-42, 1977 May.
Article in English | MEDLINE | ID: mdl-885478

ABSTRACT

Immunoreactive PTH was measured by amino terminal and carboxyl terminal specific assays in the femoral artery, the right renal vein and the suprahepatic vein of ten hyperparathyroid patients. A marked arterio venous difference for amino terminal immunoreactivity was observed in the kidney and the liver. In contrast, the arterio venous difference for carboxyl terminal immunoreactivity was small in the kidney and not significantly in the liver. It is concluded that intact PTH and possibly amino terminal fragments of the hormone are metabolized by the kidney and the liver. Considering the fact that a carboxyl terminal specific antiserum is also capable of recognizing intact hormone, the finding of a small positive arterio venous difference for carboxyl terminal immunoreactivity does not permit us to exclude the possibility that the kidney and/or the liver are capable of generating carboxyl terminal fragments.


Subject(s)
Kidney/metabolism , Liver/metabolism , Parathyroid Hormone/metabolism , Adenoma/metabolism , Aged , Female , Humans , Hyperparathyroidism/metabolism , Kidney/blood supply , Liver/blood supply , Male , Middle Aged , Organ Specificity , Parathyroid Hormone/blood , Parathyroid Neoplasms/metabolism
7.
Eur J Clin Invest ; 6(2): 127-30, 1976 Mar 31.
Article in English | MEDLINE | ID: mdl-177292

ABSTRACT

Urinary cyclic adenosine 3'5' monophosphate (AMP) excretion has been determined by radioimmunoassay in children with rickets and in control children. Cyclic AMP was greatly increased in children with rickets. The excretion of cyclic AMP correlated significantly with parathyroid hormone levels (PTH) and alkaline phosphatase, but not with age, calcaemia and serum inorganic phosphate. Calcium infusion led to a decrease in the excretion of cyclic AMP. The data are consistent with following hypothesis. During vitamin D deficiency, high PTH levels can increase the renal excretion of cyclic AMP. The effects of PTH on bone resorption fail to maintain the levels of serum calcium due to the lack of vitamin D. The mechanism by which the secondary hyperparathyroidism develops during vitamin D deficiency remains to be investigated.


Subject(s)
Cyclic AMP/urine , Vitamin D Deficiency/urine , Alkaline Phosphatase/blood , Calcium/blood , Calcium/pharmacology , Child, Preschool , Female , Humans , Infant , Male , Parathyroid Hormone/blood , Phosphorus/blood
8.
Nephron ; 17(2): 144-54, 1976.
Article in English | MEDLINE | ID: mdl-940620

ABSTRACT

In 42 untreated patients at various stages of chronic renal failure, plasma level of parathyroid hormone was directly proportional to the degree of renal failure and inversely proportional to the serum calcium level. Plasma parathyroid hormone levels were frequently elevated in 21 patients undergoing regular dialysis treatment, in spite of normal levels of serum total calcium and magnesium. Serum-ionized calcium levels measured in dialyzed patients were usually reduced and inversely correlated with the creatinine levels. Parathyroid hormone levels were correlated with the creatinine levels, but the inverse relationship with ionized calcium was not significant.


Subject(s)
Kidney Failure, Chronic/blood , Parathyroid Hormone/blood , Renal Dialysis , Thyroid Hormones/blood , Adult , Aged , Calcium/blood , Creatinine/blood , Female , Humans , Kidney Failure, Chronic/therapy , Magnesium/blood , Male , Middle Aged , Phosphates/blood , Radioimmunoassay
11.
Biomedicine ; 22(1): 35-40, 1975 Jan.
Article in English | MEDLINE | ID: mdl-810189

ABSTRACT

A proximal renal tubular acidosis (RTA) is the mechanism underlying the systemic acidosis found in vitamin D deficiency rickets. Acidotic subjects have high levels of PTH. In non-acidotic subjects proximal bicarbonate wasting can be induced by exogenous PTH injection. Carbonic anhydrase activity is not involved in this process. Calcium infusion is able to suppress both the spontaneous and the PTH-induced bicarbonate leak. The development of RTA in vitamin D deficiency is related to a particular equilibrium between two antagonizing factors at tubular level, parathyroid hormone and calcium.


Subject(s)
Acidosis, Renal Tubular/etiology , Rickets/complications , Acetazolamide , Acid-Base Equilibrium , Adolescent , Bicarbonates/blood , Bicarbonates/metabolism , Calcium/administration & dosage , Calcium/blood , Carbonic Anhydrases/physiology , Child, Preschool , Female , Humans , Infant , Kidney Tubules, Proximal/physiopathology , Male , Parathyroid Hormone/blood , Perfusion , Phosphorus/blood , Vitamin D Deficiency/complications
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