Detection of cardiac calcinosis in hemodialysis patients by whole-body scintigraphy with 99m-technetium methylene diphosphonate.

A noninvasive method for the diagnosis of cardiac calcinosis, a life-threatening complication in hemodialysis patients with end-stage renal disease (ESRD), has not, as yet, been firmly established. We tested whether whole body scanning with 99m-technetium methylene diphosphonate (MDP) might visualize cardiac calcinosis. In 19 consecutive chronic hemodialysis ESRD patients (13 males and 6 females, aged 40-81, mean 63 +/- 8 years) with cardiovascular disease [mitral annular calcinosis and/or calcified aortic valve (n = 4), hemodialysis cardiomyopathy (n = 1), coronary artery disease (n = 9) and peripheral artery atherosclerotic disease (n = 6)], MDP uptake in the heart was compared to that in 7 non-ESRD controls with hyperparathyroidism due to adenoma. Cardiac and lung field MDP uptake was confirmed in only 3 (16%) and 5 (26%) of the 19 ESRD subjects, respectively, but was absent in controls. Positive cardiac uptake was related to cardiac calcified complications (mobile intracardiac calcinosis, myocardial calcinosis and mitral annular calcification) and the duration of hemodialysis (p = 0.015). While it was statistically insignificant, subjects showing MDP uptake were elder and had higher serum Ca or Ca x P product and lower intact parathyroid hormone levels. These results suggest that cardiac calcinosis in ESRD patients can be detected noninvasively by myocardial scintigraphy with 99m-technetium MDP.

Mobile intracardiac calcinosis: a new risk of thromboembolism in patients with haemodialysed end stage renal disease.

Cardiac calcinosis is a common complication of end stage renal disease. A newly observed risk of thromboembolism is reported in four patients with mobile cardiac calcinosis, treated with long term dialysis. Rapidly growing mobile calcification was confirmed by echocardiography. Each patient had an imbalance in serum calcium x inorganic phosphate (Ca x P product >/= 50); this imbalance could not be treated due to the sudden death of the patient or the need for surgical resection to prevent recurrent cerebral thromboembolism. Histological examination revealed intracardiac calcinosis in three cases, and each case showed haemodialysis hypoparathyroidism (intact PTH < 160 pg/ml). Thromboembolism in such cases is rare, however it indicates a need for cautious echocardiographic monitoring in end stage renal disease in patients with an uncontrolled Ca x P product.

[Effects of intravenously infused magnesium on renal calcium metabolism and plasma parathyroid hormone in patients with essential hypertension].

This study aimed to elucidate the effects of intravenously infused magnesium on renal calcium and sodium metabolism in patients with essential hypertension. Mean arterial pressure (MAP), heart rate (HR), urine volume (UV), endogenous creatinine clearance (Ccr), urinary excretion of calcium (UCaV) and sodium (UNaV), fractional excretion of calcium (FECa) and sodium (FENa), plasma ionized calcium (pCa2+) and parathyroid hormone(PTH) were measured before and after intravenous infusion of 10% magnesium sulfate (initial dose: Mg 13.5mg/m2.BSA/15 min.: maintenance dose: Mg 2.7mg/m2.BSA/105min) in 6 normotensive subjects (NT) and 13 mild-to-moderate essential hypertensives (EHT). After the magnesium infusion, significant increases of UV, UCaV, UNaV, FECa and FENa, and a significant decrease of PTH were observed in both NT and EHT while MAP and HR did not change in either group. PCa2+ significantly decreased and Ccr tended to increase only in EHT. Although no significant difference was found in the change in Ccr (delta Ccr) or PTH (delta PTH) between NT and EHT, the changes of UCaV (delta UCaV), UNaV (delta UNaV), FECa (delta FECa) and FENa (delta FENa) were greater in EHT than each in NT. A positive correlation was found between delta UCaV and delta FECa, as well as delta UCaV and delta Ccr, but the former was more remarkable in both groups. In addition, delta UCaV was positively correlated with delta FENa in EHT, but not in NT. No significant relationship was observed between delta UCaV and delta PTH in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypocalcemic cardiomyopathy in a patient with idiopathic hypoparathyroidism.

An idiopathic hypoparathyroidism-induced cardiomyopathy patient had severe long-lasting hypocalcemia. The dramatic improvement of cardiac function with correction of only the serum calcium concentration could be quantitatively demonstrated on both echocardiogram and ventriculogram. The concentration of the extracellular calcium ion was considered to have a direct effect on the strength of the myocardial contraction through excitation-contraction coupling. Furthermore, elevated serum creatine phosphokinase and lactate dehydrogenase levels which were thought to be delivered from skeletal muscle returned to the normal range concomitant with the correction of hypocalcemia. The serum calcium concentration and these enzyme level showed significant inverse correlations.

[Study on uric acid metabolism in patients with primary aldosteronism].

This study was conducted to elucidate renal uric acid metabolism in patients with primary aldosteronism (PA;16 cases) as compared with normotensive subjects (NT;25 cases) and essential hypertensives (EHT;51 cases). All subjects were hospitalized and received a regular diet(Na;120 mEq,K;75 mEq,daily) for more than two weeks, after which renal clearance tests were performed, and serum uric acid(SUA), fractional excretions of uric acid(FEUA), sodium(FENa), and inorganic phosphorus(FEP) were evaluated. Plasma aldosterone concentration(PAC) was measured in 16 patients with PA before treatment and in 8 patients after adrenalectomy. SUA was lower in PA than in either NT or EHT, and this lowering was more obvious in male subjects. In NT, PA and EHT, FEUA, an index of renal excretion of uric acid, correlated negatively with SUA and positively with FENa and FEP, which reflected sodium reabsorption at the renal total tubules and proximal tubules, respectively. Although FENa was nearly the same in all the three groups, FEUA and FEP were significantly higher in PA than in EHT or NT. However, no significant correlation was found between PAC and SUA or FEUA in PA. In PA a significant increase of SUA, and decreases of FEUA and FEP were observed after the removal of adenoma compared to before the surgery. These results suggest that uric acid transport might be closely related to sodium transport in the renal tubules, particularly at the proximal site, and also lead to the conclusion that the lower SUA in PA resulted from the suppression of reabsorption and/or an enhancement of secretion of uric acid in the proximal tubules, being related to the so-called escape phenomenon.

[The role of the renal dopaminergic and the prostaglandin systems in renal uric acid metabolism in patients with essential hypertension].

The present study aimed to elucidate the role of renal dopaminergic and prostaglandin (PG) systems in renal uric acid metabolism in essential hypertension. Mean arterial pressure (MAP), heart rate (HR), endogenous creatinine clearance (Ccr), serum uric acid (SUA), urinary excretions of uric acid (UUAV) and sodium (UNaV), fractional excretions of uric acid (FEUA) and sodium (FENa), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured before and after intravenous injection of a dopamine receptor antagonist, metoclopramide (MCP: 8 mg/m2.BSA), or before and after a single oral administration of prostaglandin synthesis inhibitor, indomethacin (IM: 75 mg), in 34 mild-to-moderate essential hypertensives (EHT). MCP injection or acute oral administration of IM caused significant decreases of UNaV and FENa in each group, whereas MAP, HR and SUA did not change in either group. Significant decreases in Ccr, UUAV and FEUA and increases in PRA and PAC were demonstrated by MCP injection, while no significant changes in these parameters were revealed by IM administration. There was a significant positive correlation between delta UUAV and delta Ccr or delta FEUA in both groups. In addition, a close positive correlation between delta UUAV and delta UNaV as well as between delta FEUA and delta FENa was found in the MCP group, but not in the IM group. On the other hand, no significant correlation was observed between delta UUAV and delta PRA or delta PAC in either MCP or IM administration. The decreases of UUAV and FEUA were significantly greater in MCP than in IM administration, despite similar changes in Ccr, UNaV and FENa between the two procedures. These data suggest that the endogenous renal dopaminergic system may contribute to renal uric acid metabolism, which is rather closely related to sodium handling in essential hypertension than the prostaglandin system. Furthermore, the attenuated renal dopaminergic activity may contribute to the elevation of serum uric acid level in patients with essential hypertension.

[The role of hyperinsulinemia on the renal mechanism of hyperuricemia in overweight patients with essential hypertension].

The aim of the present study was to investigate the role of insulin on the renal mechanism of hyperuricemia in overweight patients with essential hypertension. Thirty-four essential hypertensives(EHT), receiving a regular diet containing 120mEq of sodium, 75mEq of potassium and 2000 kilocalories daily, were divided into two groups of non-obese(NHT) and obese(OHT) EHT. NHT as categorized as a body mass index (BMI) less than, and OHT as a BMI equal to or more than, 25 kg/m2 in male patients and 24 kg/m2 in female patients. In the early morning after overnight fast, renal uric acid and sodium clearance were examined while the patients remained in a supine position. During the two-hour clearance period, mean arterial pressure(MAP), heart rate(HR), endogenous creatinine clearance(Ccr), immunoreactive insulin(IRI), serum uric acid(SUA), fractional excretion of uric acid(FEUA) and sodium(FENa) were measured. Although there were no significant differences in age, MAP, HR, Ccr, nor SUA between the two groups, a higher ratio of female to male patients was found in OHT than in NHT. On the other hand, higher SUA and IRI and lower FEUA and FENa were observed in OHT than in sex-and Ccr-matched NHT. SUA was negatively correlated with FEUA in all patients (r = -0.392, p less than 0.05) and in NHT (r = -0.553, p less than 0.05), unlike in OHT. A significant negative correlation between BMI and FEUA was revealed in all EHT (r = -0.441, p less than 0.01) and in OHT (r = -0.597, p less than 0.01) but not in NHT. FEUA was positively correlated with FENa in all EHT (r = 0.554, p less than 0.001) as well as in NHT (r = 0.548, p less than 0.05) and OHT (r = 0.507, p less than 0.05). Moreover, there was a significant negative correlation between IRI and FENa in all EHT (r = -0.361, P less than 0.05) and in OHT (r = -0.470, p less than 0.05). However, no significant relation was demonstrated between IRI and SUA or FEUA in NHT or OHT. From these results, it is concluded that an attenuated renal excretion of uric acid related to natriuretic ability may play an important role in hyperuricemia in EHT. However, the role of hyperinsulinemia, which contributes to the blunting of natriuresis, might be relatively small in the renal mechanism of hyperuricemia in EHT, particularly in OHT.