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PubMedDate not supplied

Acute phosphate intoxication in seven infants under parenteral nutrition.

After major surgery, seven infants aged 4 to 29 weeks, under parenteral nutrition, received monosodium phosphate (4.2 to 14.3 mEq/kg body weight) instead of prescribed calcium gluconate. The wrong solution was perfused during 16 hours. At the 15th hour, blood samples showed hyperphosphatemia in all (8.0 to 14.4 mg/100 mL) and hypocalcemia in four infants (6.1 to 8.0 mg/100 mL), but all were asymptomatic. Under a perfusion of glucose in water, calcemia and phosphatemia returned to normal within 24 hours. In a review of the pediatric literature, we found 11 subjects with symptomatic acute phosphate intoxication, who also presented with hypocalcemia and hyperphosphatemia. The differences were that they received high bolus doses of phosphate orally or rectally and showed symptomatic features. Normalization of the calcemia occurred only when hyperphosphatemia was corrected throughout intravenous hydration.

Calcium Gluconate↗

PubMed2005

Fibroblast growth factor-23 in patients with Graves' disease before and after antithyroid therapy: its important role in serum phosphate regulation.

OBJECTIVE: Hyperthyroidism is a well-described cause of hyperphosphatemia. We aimed to clarify the physiological role of fibroblast growth factor (FGF)-23 in serum phosphate homeostasis in patients with Graves' disease during the course of treatment for hyperthyroidism. CONTEXT: The study group comprised 56 patients (45 for a cross-sectional study and 11 for a longitudinal study) with Graves' disease. For the cross-sectional study, patients were assigned, on the basis of their serum phosphate level, to a hypophosphatemia group (n = 14), a normophosphatemia group (n = 16), or a hyperphosphatemia group (n = 15). Serum FGF-23, calcium, phosphate, PTH, and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] levels were compared between the three groups. For the longitudinal study, we assessed changes in these biochemical indices before and after antithyroid treatment. RESULTS: In the cross-sectional study, the serum FGF-23 level was significantly higher (P < 0.05) in the hyperphosphatemia group than in the other groups (61 +/- 36 ng/liter vs. 31 +/- 22 ng/liter and 30 +/- 9 ng/liter). In the longitudinal study, serum levels of FGF-23 decreased significantly (P < 0.05) from a high of 54 +/- 12 ng/liter before treatment to 29 +/- 14 ng/liter after treatment. In contrast, the serum 1,25(OH)(2)D level increased significantly (P < 0.005) from 55 +/- 22 pmol/liter before treatment to 185 +/- 76 pmol/liter 3 months after treatment. Serum FGF-23 levels were positively correlated with serum phosphate levels (P < 0.0001) and negatively correlated with serum 1,25(OH)(2)D levels (P < 0.0001). CONCLUSIONS: The significant positive correlation between serum levels of phosphate and FGF-23 indicates that FGF-23 may play an important role in serum phosphate homeostasis by its up-regulation in the hyperphosphatemic condition.

Adult↗

PubMed1980

Phosphorus excretion in tumoral calcinosis: response to parathyroid hormone and acetazolamide.

The cause of hyperphosphatemia in patients with tumoral calcinosis never been explained. We studied two related patients who had tumoral calcinosis and hyperphosphatemia and two normal controls to determine their renal tubular response to parathyroid hormone (PTH) and acetazolamide (ACZ). During baseline periods, the patients had abnormally low fractional excretion of phosphorus (FEP) despite their hyperphosphatemia. Values for patients were 0.114 and 0.128; for controls, values were 0.193 and 0.165. PTH caused an increase in FEP and urinary cAMP in both patients and controls. ACZ also increased FEP in both groups, and the effects of PTH and ACZ were additive, suggesting that patients with tumoral calcinosis have normal sensitivities to PTH and normal responses to ACZ. Levels of vitamin D metabolites in the patients were normal. We conclude that patients with tumoral calcinosis have a reduced ability to excrete phosphorus. This defect does not seem to be due to impaired PTH secretion, an abnormal phosphaturic response to this hormone, or a disturbance of vitamin D metabolism.

Acetazolamide↗

PubMed1993

Elevation of serum phosphate affects parathyroid hormone levels in only 50% of hemodialysis patients, which is unrelated to changes in serum calcium.

Hyperphosphatemia is said to cause hyperparathyroidism either by depressing the plasma levels of ionized calcium and/or by affecting serum 1,25(OH)2 vitamin D3 levels. Direct evidence that hyperphosphatemia contributes to hyperparathyroidism in hemodialysis patients is unclear because previous published data are with older parathyroid hormone (PTH) assays. Phosphate was added to the dialysate of 15 patients for 12 wk whose predialysis serum phosphates were between 1.5 and 1.9 mM (4.7 to 5.9 mg/dL) in order to further increase their serum phosphate by 0.75 mM (2.4 mg/dL) without adjustments in other medications. No patient was on vitamin D therapy. In half of the patients, PTH levels remained unchanged (nonresponders; 214 +/- 64 versus 219 +/- 60 ng/L), whereas in the other patients, PTH rose from 204 +/- 53 to 338 +/- 60 ng/L (P < 0.05; responders). The degree of induced hyperphosphatemia was virtually identical in both groups, 1.7 mM increasing to 2.4 mM. Ionized calcium was unchanged in both groups after phosphate. Plasma 1,25(OH)2 vitamin D3 levels were low to start with and remained low throughout. Nonresponders had been on dialysis twice as long as responders and had consumed over seven times more aluminum salts. Nonresponders had higher postdeferoxamine increments in plasma aluminum (3,588 +/- 1,466 versus 603 +/- 390; P < 0.05), although neither these amounts nor plasma levels were in the toxic range.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗

PubMedDate not supplied

Phosphorus homeostasis in dairy cows with abomasal displacement or abomasal volvulus.

Abnormal phosphorus homeostasis occurs in dairy cows with an abomasal displacement or volvulus. The goal of this study was to identify potential mechanisms for hypophosphatemia and hyperphosphatemia in cows with a left displaced abomasum (LDA), right displaced abomasum (RDA), or abomasal volvulus (AV). Accordingly, the results of preoperative clinicopathologic analyses for 1,368 dairy cows with an LDA (n = 1,189), RDA, or AV (n = 179) (data set 1) and for 44 cows with an AV (data set 2) were retrieved. Laboratory values were compared by Student's t-tests, and correlation and regression analyses were performed. Thirty-four percent of the animals from data set 1 (463/1,368) were hypophosphatemic (serum phosphorus concentration ([Pi]) < 1.4 mmol/L), and 9% (122/1,368) were hyperphosphatemic ([Pi] >2.3 mmol/L). Serum [Pi] was significantly lower (P < .05) in cows with an LDA (1.60 +/- 0.53 mmol/L; mean +/- SD) than in cows with an RDA or AV (1.85 +/- 0.68 mmol/L). For cows with an LDA, [Pi] was correlated with serum urea nitrogen concentration ([SUN]) (r = 0.34) and serum concentration of magnesium ([Mg]) (r = 0.20). For cows with an RDA or AV, linear correlations existed between [Pi] and [SUN] (r = 0.45), [Mg] (r = 0.43), and serum chloride concentration ([Cl]) (r = -0.27). Stepwise logistic regression analysis indicated that low [SUN] and the diagnosis of an LDA had the strongest associations with hypophosphatemia. In cows with hyperphosphatemia, [Pi] was most strongly associated with azotemia. In cows with an AV, the strongest correlations with [Pi] were found for [SUN] and serum creatinine. We conclude that hypophosphatemia in cows with an LDA is primarily due to decreased feed intake. In contrast, hyperphosphatemia in cattle with an RDA or AV appears to result from dehydration and decreased renal blood flow.

Abomasum↗

PubMed2002

Oral doxercalciferol therapy for secondary hyperparathyroidism in a peritoneal dialysis patient.

Control of hyperphosphatemia and the administration of vitamin D are the primary treatment modalities for the prevention and management of secondary hyperparathyroidism. Vitamin D therapy for secondary hyperparathyroidism has been limited by the development of hypercalcemia and/or hyperphosphatemia due to increased intestinal absorption of these minerals. Recently, selective vitamin D analogs specifically designed to suppress parathyroid hormone (PTH) without causing hypercalcemia or hyperphosphatemia have shown promise for the treatment of secondary hyperparathyroidism in uremia. This case report describes the successful use of doxercalciferol to treat severe secondary hyperparathyroidism in an adult male patient undergoing chronic peritoneal dialysis, with a follow-up period of 9 months. During this period, the patient's hyperparathyroidism was rapidly and easily controlled. Treatment was complicated by a single incident of over suppression of PTH, with concomitant hypercalcemia. This quickly resolved upon temporary discontinuation of doxercalciferol therapy, after which therapy was resumed without further incident.

Administration, Oral↗

PubMed1980

Calcium and phosphate metabolism in tumoral calcinosis.

We have recently seen a patient with tumoral calcinosis, a syndrome comprising hyperphosphatemia, normocalcemia, normal glomerular filtration rate (GFR), and extensive periarticular calcific masses. Parathyroid hormone (PTH) deficiency or target organ resistance was ruled out by demonstration of normal serum PTH and urinary 3'5'cyclic AMP excretion and normal response to exogenous PTH and to endogenous stimulation by ethylenediaminetetraacetate. An intrinsic proximal tubular defect allowing enhanced renal PO4 reabsorption was probably present because there was no phosphaturic response to acetazolamine and renal PO4 threshold remained abnormally elevated even after PTH infusion. We then studied the mechanism by which serum calcium level is maintained in the normal range despite hyperphosphatemia and absence of secondary hyperparathyroidism. Normal 1,25-(OH)2 vitamin D was found, suggesting normal gastrointestinal calcium absorption. This, combined with markedly reduced urinary calcium excretion, perhaps a direct effect of hyperphosphatemia, may maintain calcium balance and prevent secondary hyperparathyroidism. A rise in urinary cyclic AMP excretion after furosemide-induced calciuria supports this hypothesis.

Adult↗

PubMedDate not supplied

Calcium, phosphate, and PTH levels in the hemodialysis population: a multicenter study.

BACKGROUND: Hyperphosphatemia is one of the main factors in the pathogenesis of secondary hyperparathyroidism. In addition, in dialysis patients elevated levels of phosphate and calcium times phosphate (Ca x P) ion product are associated with extraskeletal calcifications, as well as an increased risk of death. Cardiovascular calcifications may possibly be related to the high cardiovascular mortality seen in dialysis patients. In the USA the prevalence of hyperphosphatemia among dialysis patients is very high, over 60% of patients having serum P levels > 5.5 mg/dl, but no data are available for the Italian population, which follows different diet and dialysis schedules. METHODS: We looked at a random sample of 638 patients enrolled in 29 outpatient dialysis units in Southern Italy (Campania and Sicily). Data were centrally analyzed after extraction from a computerized database. In each patient the average of two or more values obtained in the six-month observation period (from Jan. 99 to June 99) was calculated. Mean age was 61.2 years (95% CI 59.9-62.5) years, dialytic age 72.2 months (95% CI 67.4-77.0). RESULTS: Mean +/- SD (95% CI) levels of phosphate were 5.74 +/- 1.57 (5.62-5.86) mg/dl; total calcium 9.06 +/- 0.98 (8.98-9.14) mg/dl; Ca x P 51.4 +/- 14.4 (50.3-52.5) mg2/dl2; alkaline phosphatase was 167 +/- 119 (157-177) IU/L; intact parathyroid hormone (PTH) levels, available in a subset of 239 patients, were 318 +/- 413 (265-370) pg/ml. Among these patients 51.6% had serum P > 5.5 mg/dl, 36% > 6 mg/dl; Ca x P levels were > 55 mg2/dl2 in 35.5% of the population, 24% > 60 mg2/dl2; iPTH levels were < 100 pg/ml in 43%; 25.4% had hyperparathyroidism (defined as iPTH > 400 pg/ml), and only 19.5% of patients had PTH in the desired interval of 100 to 250 pg/ml. CONCLUSIONS: Compared to data reported from the USA, mean levels of phosphate, Ca x P, and PTH seem better controlled in this Italian hemodialysis population. However, in a significant number of patients these parameters were still outside the normal range. Both over-suppression of PTH levels and hyperparathyroidism are present, although surprisingly the former was more frequent. Treatment of hyperphosphatemia should be more aggressive in hemodialysis patients; PTH levels are difficult to maintain in the desired range of 100-250 pg/ml.

Calcium↗

PubMed2002

The analysis of the risks for the development of tumour lysis syndrome in children.

BACKGROUND: Acute renal failure (ARF) during the course of cytostatic therapy is a serious complication. ARF can be isolated or became as component of tumour lysis syndrome (TLS). TLS comprises a number of metabolic abnormalities (hyperuricemia, hyperphosphatemia, hyperkalemia, azotemia and hypocalcemia) which are associated with lymphoproliferative malignancies following spontaneous or chemotherapy-induced cytolysis. There exist probably no clear prediction for the development of TLS that could enable early detection of manifestation of this severe condition. SUBJECTIVE: Conventional management with aggressive hydration, alkalization of the urine, administration of allopurinol, and the slow introduction of chemotherapy is often unable to prevent metabolic instability and ARF. Recent studies define a subgroup of patients at higher risk of renal failure during induction chemotherapy. ARF was encountered during initial therapy of patients with a lactate dehydrogenase (LDH) index greater than 3.3. METHODS AND MATERIAL: A retrospective analysis of 10 children (3 girls, 7 boys, average age 9.7 years) with LDII index greater than 3.3 has been done. All children were treated for lymphoproliferative malignancy with conventional preventive measures. RESULTS: Three children needed haemodialysis--2 boys had fully expressed TLS with ARF shortly after starting chemotherapy, in 1 boy the dialysis was indicated because of extreme hyperuricemia and high creatinine level presented before chemotherapy. We consider that LDH index is not specific criterium for prediction of TLS. In conclusion, our cases demonstrate the pathophysiologic spectrum of ARF in TLS between hyperuricemia and hyperphosphatemia. CONCLUSION: The LDH index, urine output, and hyperphosphatemia could be used to identify those paediatric patients who would benefit from the prospective use some of extracorporeal elimination methods. Further investigation of this techniques in a larger number of patients is warranted. (Tab. 5, Ref. 12.)

Acute Kidney Injury↗

PubMed1992

[Renal and electrolyte disturbances in chronic myelogenous leukemia].

Renal and electrolyte disturbances in 91 patients with chronic myelogenous leukemia (CML) were analyzed over a period of these twenty years. At diagnosis, renal and electrolytes were studied in 72 patients including 65 in chronic cases, 5 in accelerated phase and 2 in blastic crisis. There were 8 cases of hypocalcemia among 62 patients and 5 cases of hyperphosphatemia among 48 patients. The cases of hyperphosphatemia and renal dysfunction had short median survival. There were no significant differences of renal and electrolyte disturbances between before and after chemotherapy. Various electrolyte disturbances, that is, hyponatremia, hypo-, hyperkalemia, hypocalcemia, hypo-, hyperphosphatemia, were found in the blastic crisis of CML. In the last admission, renal dysfunction and various electrolyte disturbances were present in almost half of the cases. Pathological studies were performed in 18 autopsy cases. Acute tubular insufficiency or necrosis, hypercalcemic nephropathy, and renal infiltration of leukemic cells were recognized in patients who had renal dysfunction.

Adolescent↗

PubMed2004

[Atherosclerosis and vascular calcification in hemodialysis patients].

Cardiovascular disease is the largest cause of mortality in hemodialysis patients. Cardiovascular mortality is fivefold to twentyfold higher in hemodialysis patients than in the general population. Atherosclerosis and vascular calcification are the characteristic complications in hemodialysis patients. Hemodialysis patients have traditional risk factors such as abnormal lipid metabolism and uremia-related risk factors such as oxidative stress and hyperphosphatemia. Oxidative stress takes place by increased production of oxidants by leukocytes and antioxidant loss of vitamin C and E. Oxidatively modified LDL exist in the circulation by excess of oxidative stress in hemodialysis patients. Oxidative stress is a major contributor to accelerated development atherosclerosis. Oxidative stress and hyperphosphatemia also influence vascular calcification. The pattern of vascular calcification in hemodialysis patient is characterized by mineral deposition in the tunica media. It is reported that the obvious calcification in aorta and artery of the MGP knockout mouse is recognized. It is indicated that MGP has the inhibitory effect of the calcification of vessel wall. Vitamin E protects atherosclerosis and vascular calcification in hemodialysis patients. It is also important to control hyperphosphatemia for vascular calcification.

Animals↗

PubMed2006

The CARE study and cardiovascular calcification.

Cardiovascular disease (CVD) remains the major mortality risk in dialysis patients, accounting for almost 50 percent of deaths. Risk is related to the increased prevalence of traditional risk factors for CVD and to the contribution of abnormalities in mineral metabolism as well as cardiovascular calcification. Hyperphosphatemia invariably is present among patients with end-stage renal disease and is becoming an increasingly important clinical entity. In addition to its role in the pathogenesis of secondary hyperparathyroidism, elevated serum phosphorus increases the mortality risk among these patients. The pathophysiologic mechanisms by which persistent hyperphosphatemia enhances mortality risk in dialysis patients are not yet completely understood. Given that inadequate control of serum phosphorus contributes to elevated calcium-phosphorus (Ca x P) product, hyperphosphatemia may play a key role in cardiovascular calcification. The National Kidney Foundation's Kidney Disease Outcomes Quality Initiative (K/DOQI) "Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease" recommends more stringent levels for controlling serum phosphorus and Ca x P product to improve patients' quality of life and longevity. Several studies, including the CARE study, have shown that calcium acetate is more cost-effective than sevelamer as a phosphate binder. Although concern has been raised about its purported link to cardiovascular calcification, the author demonstrates in this review that calcium acetate can be used effectively with doses of elemental calcium that meet the K/DOQI guidelines.

Acetates↗

PubMed1988

[Acute kidney failure caused by hyperphosphoremia in tumor lysis].

We report the cases of two children presenting with tumor lysis syndrome responsible for major hyperphosphatemia, hypocalcemia and acute renal failure and treated by hemodialysis. Twenty similar cases have been reported in the literature. Hyperphosphatemia responsible for hypocalcemia and renal failure occurs within 24 to 48 hours after the onset of chemotherapy, is maximal on the 2nd or 3rd day and is, on the average, of 7 days duration. Short-term functional renal prognosis is good but long-term studies are lacking. The usual preventive measures are not always sufficient to prevent these accidents. A dialysis is appropriate when phosphatemia rises rapidly and exceeds 5 mmol/l, when the creatinine plasma level exceeds 200 mumol/l and kaliemia 6 mmol/l and when hyperphosphatemia is associated with severe clinical signs.

Acute Kidney Injury↗

PubMed1994

[Hyperparathyroidism secondary to renal insufficiency. Physiopathology, clinicoradiological aspects and treatment].

Stimulation of PTH secretion and synthesis in chronic renal failure involves direct and indirect factors. The indirect ones are those contributing to a decrease of plasma ionized calcium concentration which stimulates the release of PTH (1) primarily the negative calcium balance due to the iatrogenic reduction of dietary calcium intake associated with an inadequate synthesis of calcitriol, this latter being explained by a reduction in the nephronic mass, the phosphate retention, the acidosis and the retention of uremic toxins (2) more accessorily, the physicochemical dysequilibrium induced by the late occurring hyperphosphatemia. The factors acting directly on the parathyroid gland stimulating synthesis of prepro PTH at its transcription level: not only hypocalcitriolemia but also hypocalcemia and hyperphosphatemia. The clinicoradiological manifestations appear late, mostly only after the patient has been put on dialysis. The most precocious sign is the subperiosteal resorption assessed on the hand X-rays. Therefore diagnosis of hyperparathyroidism relies mainly on the measurement of plasma concentration of intact PTH. In dialysis patients the optimal range corresponding to the best bone histology is between 1 an 3 times the upper limit of normal. No such data exist for predialysis patients. Medical treatment of hyperparathyroidism should primarily be preventive, probably in predialysis lipin patient as soon as plasma intact PTH is greater than the normal upper limit. This treatment is based primarily on the prevention of phosphate retention, of negative calcium balance and acidosis by the use of oral alkaline salts of calcium given with the meals in association with appropriate dietary protein and phosphate restriction. Native vitamin D depletion should also be prevented but use of 1 alpha OH vitamin D3 metabolites in controversial: it is reasonable to administer them only when plasma intent PTH is above 3-7 the normal upper limit and when plasma phosphate is below 1.2 in predialysis patients below 1.5 mmol/l in dialysis patients and plasma calcium remains below 2.3 mmol/l in spite of CaCO3 administration. This situation is encountered in less than 50% of the dialysis patients and rarely in predialysis patients. In dialysis patients the calcium concentration in the dialysate should be chosen in relation to the dose of oral calcium and the use of 1 alpha OH vitamin D3. The superiority of the intermittent (oral or intravenous) over the daily oral administration is not yet clinically proven. The surgical parathyroidectomy is indicated when hypercalcemia and/or hyperphosphatemia occur under medical treatment, whereas the intact PTH levels remain very high (> 500 pg/ml).(ABSTRACT TRUNCATED AT 400 WORDS)

Humans↗

PubMed1998

[Differential diagnosis of hypercalcemia--a retrospective study of 46 dogs].

UNLABELLED: The case records of 46 dogs with hypercalcemia were studied retrospectively. The most common cause of hypercalcemia was malignancy, of which the majority were diagnosed as having lymphosarcoma (LSA, n = 23). Interestingly only 15 had palpable lymphadenopathy. Other neoplasia were apocrine adenocarcinoma of the anal sac (n = 4), mammary adenocarcinoma (n = 2), anaplastic carcinoma (n = 1), and malignant histiocytosis (n = 1). Non-neoplastic reasons for hypercalcemia were hypoadrenocorticism (n = 5), acute renal failure (n = 2), chronic renal failure (n = 2), hypervitaminosis D (n = 1), and primary hyperparathyroidism (n = 1). In 4 cases no definitive diagnosis could be obtained. Moderate to marked hyperphosphatemia and azotemia was found in all dogs with primary renal failure and in 4 of 5 dogs with hypoadrenocorticism. In contrast only 4 of 31 dogs with neoplasia showed (mild) hyperphosphatemia and 20 showed mild to moderate azotemia. Elevated PTH levels were found in dogs with primary chronic renal failure and with primary hyperparathyroidism, but also in one dog with neoplasia. Low PTH concentrations were measured in the dog with hypervitaminosis D and in 8 cases with neoplasia. Additional three cases with neoplasia had values in the reference range. CONCLUSIONS: 1. The most common cause of hypercalcemia is LSA. Absence of palpable lymphadenopathy does not exclude LSA and further diagnostic steps may be necessary 2. The combination of moderate to marked hyperphosphatemia suggests primary renal failure or hypoadrenocorticism. 3. An elevated PTH level is consistent with primary hyperparathyroidism, but does not exclude other causes of hypercalcemia.

Adrenal Insufficiency↗

PubMed2002

Cardiovascular calcification in patients with end-stage renal disease: a century-old phenomenon.

The mortality risk from cardiovascular disease is increased in patients with end-stage renal disease (ESRD). This is due to both traditional and dialysis-specific factors. Recently, a number of the dialysis-specific risk factors have been implicated in the pathogenesis of cardiovascular calcification. These include: hyperphosphatemia, high calcium-phosphate (Ca x P) product, elevated parathyroid hormone levels, duration of dialysis, and treatment with calcium-containing phosphate binders and vitamin D analogs. The recent availability of electron beam computed tomography (EBCT) has triggered increased awareness of the occurrence of cardiovascular calcification in ESRD patients. Given the development of transient hypercalcemia with calcium-containing binders, a link between calcium load from use of calcium-containing phosphate binders and development coronary calcification has been proposed. However, a causal relationship between use of these agents and cardiovascular calcification has not been established. Moreover, this phenomenon had been recognized over a century ago, long before these phosphate binders became available. Although its pathogenesis is likely to be multifactorial, available data strongly implicate elevated serum phosphorus as the primary culprit. Furthermore, the risk of calcification may be aggravated by vitamin D therapy, particularly in patients with severe secondary hyperparathyroidism. Therefore, achieving vigorous control of serum phosphorus, Ca x P product and parathyroid hormone level might decrease cardiovascular calcification and improve survival of patients on maintenance hemodialysis. Since calcium acetate is the most cost-effective phosphate binder available, we recommend that it should remain the first line treatment of hyperphosphatemia in patients with ESRD.

Calcinosis↗

PubMed2002

Severe hypophosphatemia: a rare cause of intravascular hemolysis.

A 3-year-old child presented with severe hyperphosphatemia (phosphate 45 mg/dL) secondary to chronic enema use. Following aggressive correction of the hyperphosphatemia, hypophosphatemia ensued (phosphate 1.7 mg/dL). Concurrently, the patient developed severe intravascular hemolysis and RBC morphologic defects. The hemolysis and morphologic defects corrected with return to normal serum phosphate levels. Severe hypophosphatemia is a rare cause of intravascular hemolysis.

Anemia, Hemolytic↗

PubMed1975

Effect of hydrochlorothiazide on phosphorus during treatment with diphosphonate.

The effects of probenecid and hydrochlorothiazide on renal handling of phosphorus during hyperphosphatemia induced by diphosphonate (ethane-1-hydroxy-1, 1-diphosphonate, EHDP) was studied. Measurements of calcium, phosphorus, and creatinine clearance were performed in 2 sessions on each of 3 consecutive days in 10 normal fasting volunteers during the morning hours from 8 A.M. to 12 noon. During 2 to 3 wk thereafter, each subject was treated with EHDP, 30 mg/kg/day. The second group of studies were performed in the same manner as the first except the EHDP administration was continued throughout. EHDP caused elevation of serum phosphorus in all cases. Probenecid did not affect urine phosphorus. Hydrochlorothiazide caused a transient phosphaturia of similar magnitude in the EHDP treated and untreated states. Creatinine clearance was not affected by any of the treatments and urine calcium was decreased by EHDP. It was concluded that hydrochlorothiazide inhibits tubular reabsorption of phosphorus but that it does not affect the mechanism whereby EHDP causes increased tubular reabsorption of phosphorus. Chronic administration of hydrochlorothiazide along with EHDP may inhibit hyperphosphatemia and may change the bone effects of EHDP.

Adult↗