Severe Renal Osteodystrophy Without Elevated Serum Immunoreactive Parathyroid Hormone Concentrations in Hypomagnesemia Due to Renal Magnesium Wasting

PEDIATRICS ◽  
1987 ◽  
Vol 79 (3) ◽  
pp. 403-409
Author(s):  
Israel Zelikovic ◽  
Shermine Dabbagh ◽  
Aaron L. Friedman ◽  
Mark L. Goelzer ◽  
Russell W. Chesney
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Elevated Serum ◽  
Fractional Excretion ◽  
Calcium Deficiency ◽  
Deficiency Rickets ◽  
Renal Magnesium Wasting ◽  
Magnesium Excretion ◽  
Moderate Renal Failure ◽  
Immunoreactive Parathyroid Hormone

An 8½-year-old girl presented with a long history of seizures, growth retardation, muscle weakness, gait disturbance, and hearing loss. Her evaluation revealed chronic moderate renal failure (serum creatinine 2.2 mg/dL), severe hypocalcemia (5 mg/dL), hyperphosphatemia (8.1 mg/dL), hypomagnesemia (1.5 mg/dL), increased urinary magnesium excretion (2 mg/kg/d), high fractional excretion of magnesium (21.7%), hypokalemia (3.2 mEq/L), and hyperkaliuria (26 mEq/L). Low circulating immunoreactive parathyroid hormone levels for the degree of the hypocalcemia (serum N-parathyroid hormone 212 pg/mL) and severe rickets without evidence of osteitis fibrosa cystica were found. The patient probably has primary renal leak hypomagnesemia (magnesuric hypomagnesemia) which caused impaired secretion of immunoreactive parathyroid hormone leading to severe hypocalcemia and calcium deficiency rickets. Treatment with magnesium and calcium supplements, calcitriol, and aluminum hydroxide resulted in marked clinical, biochemical, and radiologic improvement. Calcium deficiency rickets due to primary or secondary renal magnesium wasting in conjunction with moderate renal failure represents a largely unrecognized metabolic bone disease.

Pregnancy decreases immunoreactive parathyroid hormone level in rats with chronic renal failure

1999 ◽  
Vol 96 (4) ◽  
pp. 427-430 ◽  
Author(s):  
M. BLUM ◽  
Y. WEISMAN ◽  
S. TURGEMAN ◽  
S. CABILI ◽  
Y. WOLLMAN ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Virgin Female ◽  
Normal Pregnancy ◽  
High Serum ◽  
Female Rats ◽  
Pregnant Rats ◽  
Serum Ipth ◽  
Immunoreactive Parathyroid Hormone

Normal pregnancy is associated with an increase in serum parathyroid hormone and 1,25-dihydroxyvitamin D3 (calcitriol). The effect of pregnancy on these hormones in chronic renal failure (CRF) is unknown. The present work was undertaken to study the changes of serum immunoreactive parathyroid hormone (iPTH) and calcitriol in pregnant rats with CRF. The following experimental groups were studied: CRF1 (5/6 nephrectomized virgin female rats), CRF2 (5/6 nephrectomized pregnant rats at day 20–21 of pregnancy), CRF3 (5/6 nephrectomized rats 2 weeks after delivery) and their respective sham-operated control groups: N1, N2 and N3. The 5/6 nephrectomy (CRF1) resulted in renal failure with very high serum iPTH (100±18 pg/ml) and low calcitriol levels (10.6±4.3 pg/ml) compared with normal rats [N1: 14±2.5 pg/ml (P< 0.001) and 18.2±4.2 pg/ml (P< 0.01) respectively]. The pregnancy in CRF rats (CRF2) resulted in normalization of serum iPTH levels (18.2±5.41 pg/ml), which was associated with a parallel increase in serum calcitriol (29.4±8.0 pg/ml) similar to that in pregnancy of normal rats (N2). Two weeks after delivery the CRF rats (CRF3) once again had high serum iPTH (87±17 pg/ml) and low calcitriol levels (9.3±1.2 pg/ml), similar to those observed in non-pregnant uraemic rats (CRF1). It is concluded that pregnancy decreases serum iPTH in 5/6 nephrectomized CRF rats most probably by the increased level of calcitriol synthesized by the feto-placental unit.

Immunoreactive Parathyroid Hormone in Early and Advanced Renal Failure

Nephron ◽  
1982 ◽  
Vol 31 (2) ◽  
pp. 116-122 ◽  
Author(s):  
H. von Lilienfeld-Toal ◽  
I. Gerlach ◽  
H.U. Klehr ◽  
S. Issa ◽  
E. Keck
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Advanced Renal Failure ◽  
Immunoreactive Parathyroid Hormone

Determinants of Intact Parathyroid Hormone and Free 1,25-Dihydroxyvitamin D Levels in Mild and Moderate Renal Failure

Nephron ◽  
1992 ◽  
Vol 61 (4) ◽  
pp. 422-427 ◽  
Author(s):  
Andrew St. John ◽  
Mark B. Thomas ◽  
Charmian P. Davies ◽  
Brian Mullan ◽  
Ian Dick ◽  
...  
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Intact Parathyroid Hormone ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Moderate Renal Failure

REGULATORY HYPERPARATHYROIDISM IN A PIG BREED WITH VITAMIN D DEPENDENCY RICKETS

1979 ◽  
Vol 92 (2) ◽  
pp. 295-308 ◽  
Author(s):  
R. Wilke ◽  
J. Harmeyer ◽  
C. von Grabe ◽  
R. Hehrmann ◽  
R. D. Hesch
Keyword(s):  
Vitamin D ◽  
Parathyroid Hormone ◽  
Binding Assay ◽  
Clinical Symptoms ◽  
Plasma Concentrations ◽  
Fold Increase ◽  
Protein Binding Assay ◽  
Deficiency Rickets ◽  
Clinical Healing ◽  
Immunoreactive Parathyroid Hormone

ABSTRACT A radioimmunoassay for porcine parathyroid hormone has been developed and applied to measure immunoreactive parathyroid hormone (PTH) in plasma of pigs with hereditary vitamin D dependency rickets (VDDR) (pseudovitamin D deficiency rickets). Levels of 25-hydroxycholecalciferol (25-(OH)-D3) in plasma were measured by a protein binding assay. Both plasma concentrations of PTH and 25-(OH)-D3 showed an approximately 4-fold increase compared to normal pigs. PTH levels increased with duration of the disease. Daily dosing of the animals with 1–4 μg of 1,25-dihydroxycholecalciferol (1,25-(OH)2-D3) reduced PTH concentrations and resulted in clinical healing. Iv administration of 10 μg of 25-(OH)-D3/day did not alter PTH concentrations nor the clinical symptoms. The results suggest that these animals suffer from regulatory hyperparathyroidism. The metabolic defect could be due to a failure of the kidney to convert 25-(OH)-D3 to 1,25-(OH)2-D3.

Endogenous ANP augments fractional excretion of Pi, Ca, and Na in rats with reduced renal mass

1988 ◽  
Vol 255 (6) ◽  
pp. F1091-F1097 ◽  
Author(s):  
F. V. Ortola ◽  
B. J. Ballermann ◽  
B. M. Brenner
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Sodium Phosphate ◽  
Renal Mass ◽  
Sodium Intake ◽  
Fractional Excretion ◽  
Sodium Restriction ◽  
Calcium And Magnesium ◽  
Excretion Rates ◽  
Magnesium Excretion

Atrial natriuretic peptide (ANP) infusion increases fractional excretion of many solutes including sodium, chloride, bicarbonate, phosphate, calcium, and magnesium. Because fractional excretion of these solutes increases with advancing renal disease, and because plasma ANP levels are known to be elevated in chronic renal failure, we sought to determine whether ANP mediates increased solute excretion rates per nephron in rats following extensive renal ablation, a model of chronic renal failure. Because sodium restriction decreases plasma ANP levels in the setting of reduced renal mass, we also determined the effect of sodium restriction on sodium, phosphate, calcium, and magnesium excretion rates in rats with 5/6 nephrectomy (NX). We also assessed whether high endogenous ANP levels influence fractional sodium, phosphate, calcium, and magnesium excretion in rats with 5/6 NX, by inhibiting ANP action via infusion of a high-affinity ANP antiserum. Whole-kidney glomerular filtration rate in 5/6 NX rats averaged approximately one-third that of shams, and plasma ANP levels were significantly elevated in these rats above those of shams, but to a lesser extent in rats on low- vs. high-salt intakes. Fractional sodium, phosphate, and calcium, but not magnesium excretion rates were significantly greater in 5/6 NX rats on the higher sodium intake compared with those in 5/6 NX rats on the lower sodium intake. Moreover, in 5/6 NX rats on the higher sodium intake, ANP antiserum significantly reduced fractional sodium, phosphate, and calcium excretion, but was without effect on magnesium excretion. These data implicate endogenous ANP in promoting the adaptive increase in sodium, phosphate, calcium, but not magnesium excretion per nephron in chronic renal disease.

scholarly journals Effect of uric acid on plasma levels of 1,25(OH)2D in renal failure.

1993 ◽  
Vol 4 (4) ◽  
pp. 1035-1038
Author(s):  
R Vanholder ◽  
S Patel ◽  
C H Hsu
Keyword(s):  
Vitamin D ◽  
Renal Failure ◽  
Uric Acid ◽  
Parathyroid Hormone ◽  
Plasma Concentrations ◽  
Vitamin D Supplementation ◽  
Hydroxylase Activity ◽  
Short Term ◽  
Term Administration ◽  
Moderate Renal Failure

Previous studies from these laboratories have demonstrated that uremic biologic fluids contain substances that suppress 1,25(OH)2D metabolism. Among these substances, it was found that uric acid suppresses 1 alpha-hydroxylase activity and synthesis of 1,25(OH)2D in rats. In this study, the effect of uric acid on plasma concentrations of 1,25(OH)2D in patients with renal failure was examined. Nine patients with stable chronic renal failure (serum creatinine, 1.9 to 6.4 mg/dL) were studied. None of the patients received vitamin D supplementation. Plasma concentrations of Ca, P, parathyroid hormone, creatinine, uric acid, 1,25(OH)2D, and 25(OH)D were measured before and 1 wk after the patients received allopurinol, 300 mg daily. Plasma creatinine, Ca, P, parathyroid hormone, and 25(OH)D did not change before or after allopurinol treatment. However, plasma uric acid decreased significantly from 7.3 +/- 0.4 to 4.0 +/- 0.4 mg/dL (P < 0.01) and plasma concentration of 1,25(OH)2D rose from 30.8 +/- 2.7 to 38.2 +/- 4.8 pg/mL (P < 0.01) after the ingestion of allopurinol. Allopurinol itself did not appear to directly enhance 1 alpha-hydroxylase activity in rats. It was concluded that a short-term administration of allopurinol suppresses plasmic uric acid and increases plasma 1,25(OH)2D in patients with chronic mild to moderate renal failure.

Renal Phosphate Adaptation in Uraemic Dogs with a Remnant Kidney

1981 ◽  
Vol 60 (3) ◽  
pp. 273-282 ◽  
Author(s):  
S.-F. Wen ◽  
R. W. Stoll
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Chronic Renal Failure ◽  
Volume Expansion ◽  
Extracellular Volume ◽  
Fractional Excretion ◽  
Phosphate Transport ◽  
Extracellular Volume Expansion ◽  
Fractional Excretion Of Phosphate ◽  
Remnant Kidney

1. Clearance and micropuncture studies were performed in 27 dogs made uraemic by segmental infarction to examine the factors responsible for phosphate adaptation in chronic renal failure. 2. The animals were studied before and after extracellular volume expansion to 10% of body weight in the presence and absence of parathyroid glands. The results were compared with 19 normal dogs studied under similar experimental conditions. 3. In the dogs with a remnant kidney and intact parathyroids adaptation of phosphate transport was evident, with a high fractional excretion of phosphate. Thyroparathyroidectomy 3 days before study in the dogs with a remnant kidney and moderate renal failure reduced fractional excretion of phosphate to near normal values, indicating a major role of parathyroid hormone in phosphate adaptation. Extracellular volume expansion in these thyroparathyroidectomized uraemic dogs led to an exaggerated phosphaturic response with fractional excretion of phosphate returning towards the value in the uraemic dogs with intact parathyroid glands. Thus acute extracellular volume expansion could also contribute to the increase in fractional phosphate excretion, but extracellular volume probably plays a relatively minor role in the adaptation of phosphate excretion. 4. With more advanced renal failure fractional excretion of phosphate remained high, even after thyroparathyroidectomy, indicating that parathyroid hormone-independent factors become important for phosphate adaptation in the advanced stage of renal failure. The nature of parathyroid hormone-independent changes in fractional phosphate reabsorption in chronic renal failure remains unknown. 5. Proximal tubular fluid/plasma ultrafiltrate phosphate ratios were high in all groups of dogs with a remnant kidney regardless of thyroparathyroidectomy or the degree of renal failure. The non-specific nature of the proximal tubule pattern of phosphate transport indicates that phosphate adaptation is primarily determined by alterations in phosphate transport at a site distal to the proximal convoluted tubule. Alternatively, deep nephrons may play a greater role in determination of the overall phosphate adaptation in the chronically diseased kidney.

Phosphorus restriction reverses hyperparathyroidism in uremia independent of changes in calcium and calcitriol

1990 ◽  
Vol 259 (3) ◽  
pp. F432-F437 ◽  
Author(s):  
S. Lopez-Hilker ◽  
A. S. Dusso ◽  
N. S. Rapp ◽  
K. J. Martin ◽  
E. Slatopolsky
Keyword(s):  
Renal Failure ◽  
Renal Insufficiency ◽  
Secondary Hyperparathyroidism ◽  
Filtration Rate ◽  
Concomitant Increase ◽  
Hydroxylase Activity ◽  
Circulating Levels ◽  
Moderate Renal Failure ◽  
Insight Into ◽  
Immunoreactive Parathyroid Hormone

Phosphorus is a well-known modulator of renal 1 alpha-hydroxylase activity. In early and moderate renal failure it is proposed that dietary Pi reduction ameliorates secondary hyperparathyroidism through increased circulating levels of calcitriol (i.e, 1 alpha, 25-dihydroxycholecalciferol). To gain further insight into the mechanisms by which a low-Pi diet ameliorates secondary hyperparathyroidism in advanced renal insufficiency, studies were performed in five dogs before and 6 mo after the induction of uremia by 5/6 nephrectomy. Glomerular filtration rate decreased from 69.0 +/- 2.3 to 10.5 +/- 0.5 ml/min, immunoreactive parathyroid hormone (irPTH) increased from 66.0 +/- 8.8 to 321.0 +/- 46 pg/ml, and calcitriol decreased from 39.0 +/- 10.4 to 27.0 +/- 6.2 pg/ml. Thereafter, dietary Pi was decreased gradually every 2 wk from 0.95% to 0.6, 0.45, and 0.3%, respectively. Dietary Ca was reduced from 1.6 to 0.6% to prevent development of hypercalcemia. Ionized Ca (ICa) decreased from 5.4 +/- 0.04 to 5.2 +/- 0.05 mg/dl (P less than 0.02), and plasma Pi decreased from 6.3 +/- 0.7 to 4.7 +/- 0.2 mg/dl (P less than 0.05). Calcitriol remained low (23.3 +/- 4.7 pg/ml). However, irPTH gradually decreased from 321.0 +/- 46.0 to 94.7 +/- 22.9 pg/ml (P less than 0.005). These studies indicate that a decrease in dietary Pi from 0.95 to 0.3% suppressed irPTH by approximately 70%. Reduction of irPTH was observed in the absence of a concomitant increase in levels of ICa or calcitriol. These studies suggest that reduction in dietary Pi in advanced renal insufficiency improves secondary hyperparathyroidism by a mechanism that is independent of the levels of calcitriol or plasma ICa.

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