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Renal Refractoriness to Phosphaturic Action of Parathyroid Hormonein A

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Renal Refractoriness to Phosphaturic Action of Parathyroid Hormonein A CASE REPORT Renal Refractoriness to Phosphaturic Action of Parathyroid Hormonein a Patient with Hypomagnesemia Masahiro Mihara, Keita Kamikubo, Keiko Hiramatsu, Satomi Itaya, Tom Ogawa and Shigeki Sakata* A 50-year-old tetanic womanwith hypomagnesemiais described. She had partial resection of the stomach and thejejunum at the age of20 years. Lack of parathyroid hormone (PTH) function was indicated by hypocalcemia, hyperphosphatemia and high tubular reabsorption of phosphate. However, both plasma concentration of PTHand nephrogenous CAMPwere normal. Administra- tion of magnesiumsulfate completely normalized serum phosphate and tubular transport of phosphate with only a modest increase in nephrogenousCAMP.The present findings suggest that phosphaturic action of PTHis impaired in magnesiumdeficiency and that steps distal to CAMP production may be responsible for the renal refractoriness to the hormonal action. (Internal Medicine 34: 666-669, 1995) Key words: magnesium deficiency, hyperphosphatemia, hypocalcemia, nephrogenous CAMP Introduction Case Report Hypocalcemia and much less frequently hyperphosphatemia A 50-year-old womanwas admitted to our hospital because develop in severely hypomagnesemic patients (1). There are of tetany. She had had an appendectomy at the age of 15 years several possible mechanismsproposed for these abnormalities and partial resection of the stomach and thejejunum due to ileus in calcium and phosphate metabolismdue to magnesiumdefi- at the age of 20 years. She had been having paresthesia in ciency. The secretion of parathyroid hormone (PTH) is sup- bilateral legs for a month prior to admission. Three days before pressed in chronic hypomagnesemia(2- 1 2). The refractoriness admission the paresthesia also developed in bilateral forearms. of target organs, kidney and bone, to PTHactions has also been On the day of admission she manifested symptomsof tetany. reported in some hypomagnesemic subjects (5, 7, 9, 12-19). In Trousseau's sign and Chvostek's sign were positive. the kidney, PTHreduces phosphate reabsorption at the proxi- Someblood chemical and endocrinological findings are mal tubules via a CAMP-dependentprocess (20-22). Little is presented in Table 1. Serumcalcium concentration corrected knownabout impaired steps of phosphaturic PTHaction in with serum albumin level, serum inorganic phosphate, and hypomagnesemichyperphosphatemia, a rare complication of serum magnesium were low. Serum potassium (3.0 mEq/1) magnesium deficiency. In this report we describe a tetanic was also low. Arterial blood gas analysis revealed metabolic patient with hypomagnesemiaand hypocalcemia whoshowed alkalosis (pH 7.52, HCO3~30.1 mM, base excess 7.6 mM). hyperphosphatemia and high tubular reabsorption of phosphate Creatinine clearance was 1 14 I/day, Plasma intact PTHlevel despite normal plasma concentrations of PTHand nephro- (Allegro Intact PTH Kit, Japan Mediphysics, Tokyo, Japan) genous CAMP.Administration of magnesiumcompletely nor- and mid-portion PTH level (210 pg/ml) (PTH Kit Yamasa, malized serum phosphate and tubular transport of phosphate Yamasa, Choshi, Japan: normal, 160 to 520 pg/ml) were nor- with only a modest increase in nephrogenous CAMP.The mal. NephrogenousCAMPwaswithin the normal range. Per- present findings suggest that the phosphaturic action of PTHis centage of tubular reabsorption of phosphate and Tmpo4/GFR impaired in magnesium deficiency and that steps distal to were high. Urinary magnesium excretion (0.9 mEq/day) was CAMPresponse maybe responsible for the renal refractoriness low. FEca was 2.0%. Plasma 1,25(OH)2 D3 concentration to PTHaction. (1,25(OH)2 D3 Kit SRL, Yamasa) was low. Plasma 25(OH)D3 From the Department of Internal Medicine, Takayama Red Cross Hospital, Takayama and *the Third Department of Internal Medicine, Gifu University School of Medicine, Gifu Received for publication October 3 1, 1994; Accepted for publication March 20, 1995 Reprint requests should be addressed to Dr. Keita Kamikubo, the Department of Internal Medicine, Takayama Red Cross Hospital, 3- 1 1 Tenman-cho, Takayama 506 666 Internal Medicine Vol. 34, No. 7 (July 1995) PTHResistance in Magnesium Deficiency Table 1. Laboratory Findings Vari abl e D a y 1 D a y 6 D a y 1 2 D a y 3 0 N o r m a l rang e C a l c i u m ( m E q / 1 ) 2.9 3. 3 3. 7 4. 5 4 . 0- 5 . 0 M a g n e s i u m ( m E q / 1 ) 0. 6 0. 9 1. 0 1. 6 1. 6 - 2 . 1 P h o sp h a te (m g /d l) 5.4 4. 4 3. 1 3. 8 2 . 7 ^ . 4 In t a c t P T H ( p g /m l ) 17 6 9 3 8 1 5 - 5 0 1 , 25 ( O H) 2 D 3 ( p g/ m l ) 9 .6 17 2 3 2 2 -6 5 n - C A M P ( n m o l / d l ) 0. 71 0 . 80 0. 4-2. 8 % T R P 9 5 9 1 8 7 - 9 3 T m P O 4 / G F R ( m g / d l ) 8.7 3. 1 2 .5 - 4 . 2 calcium: serum calcium concentration corrected with serum albumin level, n- cAMP: nephrogenous CAMP. 1 i MgSO4 | Calcium gluconate | == 8r -.4- -i80 \ o- A. iS" "^ 5-5 6- /à""~~J^\/ -. "3X -60^ ^e 4å /'' ^*\ ^^-^-^=^"21 "40i f| <^>^^>-^^» à"^^ | E Is2- .-'' ^_« å å å à"--å _]s -20S || t-^*-*^ | £ <^^ o1 ' à" ' ' ' ' ' '-"o h 2 4 6 8 10 12 14 16 Day Figure 1. Clinical course after admission. Serumconcentrations of magnesium(å ), inorganic phosphate ( à") and calcium corrected with serum albumin ( O) are indicated. Plasma intact PTHlevels (A) are also shown. The patient was given calcium gluconate (1,700 mg/day) and magnesium sulfate (500 to 1,500 mg/day) as indicated. level ( 1 0. 1 ng/ml) was normal (Special Reference Laboratories, cal Industry, Tokyo, Japan) (23) was performed on the 12th day Tokyo, Japan: normal, 9 to 35 ng/ml) and 24,25(OH)2 D3 level when baseline nephrogenous CAMP,%TRPand Tmpo^GFR (0.45 ng/ml) was also normal (Special Reference Laboratories: were normal (Table 1 ). The test indicated a normal response for normal, 0.40 to 2.0 ng/ml). Plasma calcitonin concentration both urinary CAMPand urinary phosphate (Fig. 2). The serum (18 pg/ml) was normal (Calcitonin Kit Mitubishiyuka, calcium level was restored to normal on the 16th day. Serum Mitubishiyuka, Tokyo, Japan: normal, 17 to 58 pg/ml). magnesium, calcium, inorganic phosphate, plasma intact PTH The patient was given calcium gluconate intravenously and 1 ,25(OH)2D3 were normal one month after admission with (1,700 mg/day) as well as magnesium sulfate orally later (500 magnesium supplementation (Table 1 ). to 1,500 mg/day) (Fig. 1). Plasma intact PTH level (30 pg/ml) wasagain normal on the third day. Hyperphosphatemiacontin- Discussion ued for five days after admission. Onthe sixth day, the plasma intact PTH level was slightly high and the plasma 1 ,25(OH)2 D3 Onadmission, serumcalcium waslow, and serumphosphate concentration was still low (Table 1). Intravenous calcium and tubular reabsorption of phosphate were abnormally high administration was terminated on the nineth day. Standardized despite the normal plasma PTHlevel and nephrogenous CAMP. Ellsworth-Howard test using human PTH1-34 (Asahi Chemi- With supplementation of magnesiumand calcium, serum phos- Internal Medicine Vol. 34, No. 7 (July 1995) 667 Mihara et al PTH increased slightly. Cyclic AMPis thought to mediate the tubular phosphaturic action of PTH(20-22). Although other 50r -,5 possibilities, such as the possibility that normal nephrogenous CAMPwas brought about by increased leakage of low tubular intracellular CAMPlevel, are not completely eliminated, the 40- / -4 present findings suggest that steps distal to the CAMPresponse in renal PTHaction may have been impaired in this patient. 1 f/ l Tubular resistance to phosphaturic PTHaction at points distal |¥30- / -3£| to CAMPproduction is also knownin dietary phosphate depri- vation (28). There have been discrepancies in renal responsiveness to E / 1 ^= PTHin magnesiumdeficiency. Renal hyporesponsiveness to the phosphaturic action of PTHhas been reported in some 10å / -1 patients with magnesium deficiency (5, 13, 16). Nodata on urinary CAMPis available in these patients. Other patients with hypomagnesemia,however, shownormal renal responses to PTH(3, 4, 6). Hyperphosphatemia is a rare complication in ol_J 1 1 1 1 1-lo magnesium deficiency (16, 29), whereas hypocalcemia has -3 -2 -1 0 1 2 been reported frequently. In the present case, serum phosphate Time(hour) and tubular reabsorption of phosphate returned to normal before serumcalcium was restored. These findings maysuggest Figure 2. Renal response to PTH. The results of Ellsworth- that the renal phosphaturic action is more resistant to magne- Howardtest are shown. sium deficiency than the hypercalcemic action of PTH. In addition to severity and duration of magnesiumdeficiency, accompanying abnormalities in other electrolytes and genetic predisposition may account for the patient-to-patient variation phate and renal phosphate transport returned to normal and in renal responsiveness to PTH. serumcalcium wasrestored later. After calcium administration Plasma level of 1,25(OH)2 D3 was low despite normal had been terminated, serum calcium and phosphate were main- plasma concentrations of 25(OH) D3. This suggests that la- tained at the normal levels with magnesiumsupplementation. hydroxylation of 25 (OH) D3 was impaired. Hyperphosphatemia These results suggest that hypomagnesemiawas the pricnipal seems to be responsible for the reduced la-hydroxylation at causative factor responsible for the hypocalcemia and least in part (30). Hypomagnesemic patients without hyperphosphatemia in this patient. Since the urinary magne- hyperphosphatemia, however, frequently show a low 1 ,25 (OH)2 sium excretion was low, low magnesiumabsorption probably D3 level (3 1). Since intracellular magnesium is required for 1a- due to the partial resection of the jejunum seems to be respon- hydroxylation (32), magnesium deficiency itself may impair sible for the magnesium deficiency. the enzymereaction.
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