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Biomedical subjects

J Lloveras

Publications and source records attributed to J Lloveras.

At least 73 records · Page 4Linked to original sources
PubMed1987

Relative hyperphosphaturia in diabetic chronic renal failure: a protective factor of hyperparathyroidism.

Relative low serum levels of parathormone (PTH) and low incidence of secondary hyperparathyroidism have been reported in diabetic uremic patients. The pathogenesis of this reported resistance to uremic secondary hyperparathyroidism in diabetes remains controversial. We have measured the serum C-terminal parathormone (C-PTH) renal phosphorus threshold (TmPO4) and nephrogenous cyclic AMP (N-cCAMP), in 2-hour urine collection in 22 patients with diabetic nephropathy with moderate chronic renal failure and in 27 controls with similar creatinine clearance values (18.16 +/- 9.14 and and 19.1 +/- 8.47 ml/min). In spite of the lower levels of serum C-PTH (1.07 +/- 0.43 ng/ml) diabetic patients exhibited an increased phosphaturia (TmPO4: 1.97 +/- 0.9 mg/100 ml GFR) when compared with the control group (C-PTH: 2.01 +/- 1.17 mg/ml, and TmPO4: 2.5 +/- 0.7 ml GFR). When the C-PTH values were plotted against the logarithm of creatinine clearance values, both groups showed a significant linear relationship reflecting the progressive increase in PTH when GFR fell. This progressive parathyroid stimulus was also present in diabetic patients but in a lower intensity. We believe that increased phosphaturia in diabetics with moderate chronic renal failure may be a major factor in precluding the appearance of secondary hyperparathyroidism in these patients once they reach the dialysis and transplantation programs.

Diabetic Nephropathies↗
PubMed1987

Hypertension and nephrotoxicity in the rate of decline in kidney function in diabetic nephropathy.

Serum creatinine levels were determined prospectively every 2 to 3 months in 40 patients with diabetic nephropathy for a global observation period of 864 months. The monthly creatinine increasing rate was significantly lower in normotensive periods, mean arterial pressure (MAP) less than 115 mmHg, when compared with hypertensive periods, MAP greater than 125 mmHg. No significant difference was shown in periods with borderline hypertension (MAP between 115-124 mmHg). The mean creatinine increases were of 0.036 mg/dl/month, 0.3 mg/dl/month and 0.046 mg/dl/month respectively. Normotension was associated with a slowing down of the rate of decline in renal function in this group of moderate kidney failure with an initial mean serum creatinine of 2.26 mg/dl. The exposure of patients to nephrotoxics (aminoglycosides, and possibly anesthesia) significantly accelerated the decline in renal function: 0.39 mg/dl/month and 0.17 mg/dl/month respectively according to the concomitance or not of toxics and hypertension. The reported protective effect of diabetes against aminoglycosides nephrotoxicity in experimental conditions was not reflected in our clinical results. On the contrary, we suggest a possible enhanced sensibility of the diabetic patient with diabetic nephropathy to aminoglycosides leading to an acceleration of the progression of renal failure.

Adult↗
PubMed1985

Action of hemicholinium-3 on phospholipid metabolism in Krebs II ascites cells.

Incorporation of [Me-14C]choline or/and [2-14C]ethanolamine into phospholipids of Krebs II ascites cells in toto have been tested in the presence of hemicholinium-3. With [Me-14C]choline, labelling of cell pellet, intracellular choline, phosphocholine and total lipid extract is inhibited by hemicholinium-3 in a dose-dependent way between 6.25 X 10(-6) M and 10(-3) M. These effects are caused by a diminution of the choline or/and ethanolamine transport across the cell membrane and by a choline-kinase inhibition. In Krebs cells, choline is taken up by a low affinity Na+ sensitive uptake system (KT = 46 X 10(-6) M) which is competitively inhibited by hemicholinium-3 (KTi = 161 X 10(-6) M). Krebs cells exert a counter-transport (i.e. an exchange of choline across the membrane) against a concentration gradient of 10 mM choline whereas 10 mM hemicholinium-3 has no effect. Choline-kinase is also inhibited (I50 = 57 X 10(-6) M) in Krebs cells in toto and time-course data suggest that choline transport and phosphorylation might be tightly coupled. Specific radioactivities of phosphocholine and choline-glycerophospholipids decrease owing to the effect of the drug on the uptake and phosphorylation system. With 4 X 10(-5) M hemicholinium-3 and [Me-14C]choline as a marker, labelled choline-glycerophospholipids are decreased by 22%. With [2-14C]ethanolamine, labelled ethanolamine-phospholipids are decreased by 26% and choline-glycerophospholipids remain unlabelled. With the two markers, the additional effect produces a 35% decrease. It is concluded that hemicholinium-3 might be able to induce a depression of the intracellular choline and phosphocholine pool which could provoke a serious quantitative deficiency of major phospholipids in Krebs cells.

Animals↗
PubMed1985

Interaction of DNA with lysine-rich polypeptides and proteins. The influence of polypeptide composition and secondary structure.

Using X-ray diffraction we have studied fibres obtained from complexes of DNA with lysine-rich polypeptides and with proteins that have different conformations, to ascertain whether the conformations of the polypeptides and the DNA are maintained upon interaction. Substances investigated include N-acetyl-Lys-Ala-Tyr-Ala-Lys-ethylamide, random poly(Leu50, Lys50), sequential poly(Leu-Lys), poly(Val-Lys), poly(Ala-Lys), poly(Lys-Ala-Ala-Lys), poly(Lys-Ala-Ala), poly(Lys-Leu-Ala), poly(Lys-Ala-Gly), protein phi 0 from sea cucumber spermatozoa, histone H1 and two fragments of this protein obtained by chemical cleavage. In general, the B form of DNA with ten base-pairs per helical turn is maintained upon interaction at high levels of humidity. The A form is never observed; it appears to be forbidden in a protein environment. No evidence for transition into any novel DNA conformation has been observed, although the B form is altered in some cases, in particular upon dehydration. Such alteration occurs always in the sense of tightening the double helix, so that the number of base-pairs per helical turn diminishes. The polypeptides may interact with DNA in both the alpha and beta conformations. We have found different types of complexes in which either a monolayer or a double layer of beta-pleated sheets is intercalated between layers of DNA molecules. Alternatively, the polypeptide chain may be wrapped around the DNA, following one of the grooves. The polypeptide conformation may be either maintained or changed upon interaction. The charge density of the polypeptide is an important parameter of the interaction. When it matches the charge density of the DNA, the polypeptide conformation is maintained in most cases; otherwise it is modified. The globular part of histone H1 gives a unique X-ray pattern upon interaction, indicative of a loss of order of DNA in the complex. On the other hand, the C-terminal part of histone H1 gives a very well-ordered complex, similar to a nucleoprotamine, in spite of its lower charge density.

Amino Acid Sequence↗
PubMed1985

Low incidence of hyperparathyroidism in diabetic renal failure.

The first study compared two groups on dialysis: 25 patients with diabetes mellitus and 25 matched non-diabetic patients, in relation to the presence of signs of hyperparathyroidism, to assess the reported low incidence of hyperparathyroidism in these patients. The diabetic group showed significantly lower values of PTH, Alk phosphatase, percentage of patients requiring vitamin D treatment, and less evidence of hyperparathyroidism on X-ray and in bone histomorphometry. In the second study 16 patients with chronic renal failure due to diabetic nephropathy were compared to 27 patients with the same degree of renal failure of other origin, the diabetic nephropathy group showed no increase in PTH, with falling creatinine clearance. Despite this low PTH, the phosphaturia was higher in the diabetic nephropathy group (Tm PO4/C Cr: 1.94 +/- 0.43 vs 2.5 +/- 0.68). In conclusion, patients with diabetes mellitus are less prone to develop hyperparathyroidism in progressive renal failure. This could be due to a relative increase in phosphaturia during declining function.

Diabetic Nephropathies↗
PubMed1983

An in vitro study of hemicholinium-3 on phospholipid metabolism of Krebs II ascites cells.

With [Me-14C]choline as marker and after separation of choline and phosphocholine by ion-exchange column chromatography or thin layer chromatography on alumina, it is shown that 40 microM hemicholinium-3 (HC-3) inhibits the cytosolic choline-kinase of rat liver and Krebs cells. This inhibition is competitive (Km different, Vm similar) in the first case and mixed in the second (Km and Vm different). Despite this general inhibition of the phosphocholine formation, the synthesis of phosphatidylcholine (PC) by post-nuclear supernatants of rat liver and Krebs cells is different when tested with HC-3. It is unaffected in rat liver; however, HC-3 induces a PC deficiency in Krebs cells which is time-course dependent between 15 and 120 min and proportional to the drug concentrations in the interval 5-40 microM. Incorporation of AT-[gamma 32P] or [2-14C]ethanolamine into phospholipids shows that the sequential methylation pathway is not detectable in Krebs cells. These results are discussed in relation to those established concerning HC-3 action on phospholipid metabolism in other tissues.

Adenosine Triphosphate↗
PubMed1982

Mycobacterial infections in renal transplant recipients. Seven cases and a review of the literature.

During an 11-year period, 1,069 patients received renal allografts at the University of Minnesota Hospital, Minneapolis, and infections developed in seven (0.65%) due to mycobacteria (Mycobacterium tuberculosis and M kansasii). The primary infection was in joint or subcutaneous tissue in six patients and pulmonary (miliary) in one. Infections in joint or skin shared common features regardless of the species of Mycobacterium and usually mimicked acute pyogenic bacterial infection; all responded to antimycobacterial drugs. The clinical manifestations in our patient in miliary tuberculosis were compared with those of 19 other patients described in the literature. Although their systemic manifestations were more severe, the symptoms were often ill-defined and the diagnosis overlooked. Five of these 20 patients (25%) died of uncontrolled infection.

Adult↗