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Biomedical subjects

G Mioni

Publications and source records attributed to G Mioni.

At least 37 records · Page 2Linked to original sources
PubMed1992

Factors affecting fasting urinary calcium excretion in stone former patients on different dietary calcium intake.

The effects of variable calcium content on daily and fasting urinary calcium and other lithogenic solutes excretion, on the bone turnover index (fasting hydroxyproline urinary excretion) and on the calciotropic hormones were studied in 312 stone former patients with an outpatient protocol and 15 stone former patients in an inpatient study. Furthermore in 60 of these patients, 30 while on a low calcium diet (LCD) and 30 on a free calcium home diet (FCD), the effects of an oral calcium load (OCL) on bone turnover index, calciotropic hormones and calcium excretion were evaluated. The results demonstrate that an LCD is effective in reducing daily calcium excretion. Fasting calcium excretion is apparently not affected by changes in dietary calcium content. On the other hand, LCD induces a marked increase in bone resorption, without apparent signs of increased parathyroid activity. This may explain the failure to reduce fasting urinary calcium excretion by the LCD. The OCL greatly reduced bone resorption rate, without any change in calciotropic hormones, especially in patients on LCD. In conclusion, the LCD induces a reduction in the lithogenic factors in the urine of stone formers, but induces a marked increase in bone resorption. The lack of any change in fasting urinary calcium excretion in conditions of different dietary calcium intake may be due to an opposite change in the intestinal and osseous components that affect this parameter, and is therefore of little value.

Adolescent↗
PubMed1980

Serum trypsin-like immunoreactivity and secondary hyperparathyroidism in renal failure.

UNLABELLED: In 46 kidney patients aged from 30 to 71 years, after an overnight fast, serum levels of trypsin (TLI), gastrin (Gas), parathromone (PTH), calcium (Ca), magnesium (Mg), phosphate (iP), amylase, were evaluated. Ten patients had a normal renal function; in 18 patients glomerular filtration rate (GFR) ranged from 5 to 70 ml/m'; 18 patients with GFR below 2 ml/m' were treated with 4 hours hemodialysis. In dialysed patients TLI was evaluated before and after dialysis. In patients with FGR ranging from 120 to 5 ml/m' a significant inverse correlation (p < 0.001) appeared between TLI and GFR values. In the same group a significant direct correlation (p < 0.001) was found between PTH and TLI. The study showed also a significant direct correlation between amylase and TLI (p < 0.001); likewise TLI, amylase was inversely correlated to GFR (p < 0.01) and directly to PTH (p < 0.001). No correlation was found between TLI and Gas, Ca, Mg, iP. A significant inverse correlation was found between PTH and GFR (p < 0.01). Because serum level of PTH, amylase and TLI were related to GFR values, we calculated partial correlation between these parameters. The partial correlation coefficients of the relation between PTH and TLI, PTH amylase, holding GFR constant, were higly significant (p < 0.001). On the contrary, holding a constant PTH, the correlations between pancreatic enzymes and GFR were not confirmed. Pre-dialysis TLI levels were significantly higher than post-dialysis (p < 0.05). IN CONCLUSION: 1) TLI and amylase have the same behaviour in renal failure; 2) the levels of both enzymes are high in renal insufficiency; their values seem to be correlated to secondary byperparathyroidism.

Adult↗
PubMed1979

Thiazide diuretics in renal hypercalciuria.

Forty-six renal hypercalciuric normocalcaemic patients were treated with hydrochlorothiazide (50mg/day) and amiloride (5 mg/day), both to reduce new stone formation and to suppress parathyroid hyperfunction. A reduction of hypercalciuria and suppression of parathyroid hyperactivity were observed in 41 patients, while in the other five patients no evidence of parathyroid suppression was found and hypercalcaemia developed. Four of five patients underwent parathyroidectomy which was followed by a normalisation of biochemical signs of hyperparathyroidism. These results suggest that the appearance of hypercalcaemia in renal hypercalciuric patients during hydrochlorothiazide/amiloride treatment may be of diagnostic value in unmasking pharmacologically non-suppressible normocalcaemic hyperparathyroidism.

Adult↗
PubMed1977

Blood pressure control in end-stage renal disease in man: indirect evidence of a complex pathogenic mechanism besides renin or blood volume.

1. In twenty-three uraemic patients on regular dialysis, plasma renin activity and blood volume were measured before and after a single dialysis. Three groups were identified; the first had a low or normal plasma renin activity and a high or normal blood volume, the second had a high plasma renin activity and a low blood volume and the third had both variables above normal. 2. In spite of these differences, diastolic blood pressure before and after dialysis was the same in the three groups and multiple regression analyses failed to demonstrate any dependence of blood pressure on plasma renin activity, blood volume or body weight taken separately or together. 3. We conclude that other factors besides plasma renin activity and blood volume are important in maintaining arterial hypertension in terminal renal failure.

Adult↗
PubMed1975

Calcium and phosphorus metabolism in chronic uremia.

In chronic uremia, the clinical disorders o calcium and phosphorus metabolism are influenced by the following factors: (1) intestinal absorption of calcium and phosphate, resulting in a negative calcium and phosphate balance at normal dietary intakes; (2) renal handling of calcium and phosphate: the fractional transport of calcium (the isoosmotic reabsorption taking place in the proximal tubule) is not affected by GFR modifications, whereas the Tm-limited reabsorption is severely impaired; the external phosphate balance is kept, even in the presence of a reduced nephron population, by means of a proportional reduction in TmPO4 values; (3) physiochemical state and turnover of body calcium and phosphate: in uremic patients, the distribution spaces, turnover rate of calcium, and accretion rate of bones are increased in comparison with the controls; the calcium infusion test in patients with renal osteomalacia is followed by a regular increase in plasma [PO4], whereas a significant decrease is observed in patients with renal osteitis fibrosa, due to the extreme 'avidity' of bones for calcium phosphate; the role of hyperphosphatemia is critical in keeping the plasma [Ca] lower than the expected values for a given metabolic set; moreover, an increased cell uptake of phosphate could counteract to some extent the reduced renal clearance of phosphate; (4) structural and biochemical modifications of bone tissue: uremic osteodystrophy consists mainly of two components: (a) osteomalacia, with osteoid excess, disappearance of the calcification front, and diffuse pathologic mineralization, and (b) osteitis fibrosa, with severe resorption of normally mineralized bone, slight osteoid excess, and almost normal calcification front; (5) hormonal factors: chronic stimulation of parathyroid glands may result in suppressible or even autonomous hyperparathyroidism. As to vitamin D, it has been suggested that the uremic kidney is not able to synthesize the 1,25-di-OH-cholecalciferol, the active metabolite of vitamin D: this results in an impaired intestinal absorption of calcium. On the contrary, the role of calcitonin in chronic uremia is still uncertain, since low values of plasma [Ca] are usually observed.

Calcium↗
PubMed1975

Alterations in renal tubular sodium and water transport in polycystic kidney disease.

Thirty patients with chronic renal diease -10 with polycystic kidney disease (PKD) and normal GFR; 10 with PKD and GFR is less than 30 ml+min; 10 with chronic glomerulonephritis (CGN) and GFR is less than 30 ml+min -and 10 normal subjects were investigated. The ability to concentrate urine maximally (T-CH2O) after water deprivation and the renal handling of water and electrolytes following hypertonic volume expansion were studied. A defect in T-CH2O was common in PKD patients even with normal GFR. In PKD patients with normal GFR, volume expansion was not followed by a natriuretic effect of the same magnitude as in controls. This ""inadequate natriuresis after volume expansion"" may be explained partly by chronic hyponatremia and partly by a functional defect, i.e. the incomplete arterial vasodilation in the kidney. At comparable degrees of renal insufficiency, T-CH2O was lower in PKD than in CGN patients. It seems likely that in PKD patients the increased endogenous osmotic load has exaggerated the tubular defect in urine concentration already present at normal GFR. Furthermore, volume expansion was followed by a significant increase in fractional sodium excretion only in PKD patients with renal insufficiency.

Adult↗