PubMed Health⌕ Search

Biomedical subjects

F Llach

Publications and source records attributed to F Llach.

101 records · Page 6Linked to original sources
PubMed1977

Acute actions of 1,25-dihydroxy-vitamin D3 in normal man: effect on calcium and parathyroid status.

The present study was undertaken to evaluate the acute effect of 1,25-dihydroxy-vitamin D3 (1,25 (OH)2D3) on serum Ca, P and immunoreactive parathyroid (iPTH) and urinary Ca, P. and cyclic AMP. In 8 normal subjects, samples were collected over intervals of 30 to 60 min during a control day and on a treatment day following oral ingestion of 1,25(OH)2D3, 2.7 microgram. For the entire group there were no significant changes in serum Ca. P, iPTH or urinary P. Urinary Ca increased significantly 7 h after administration of 1,25(OH)2D3, and urinary cAMP decreased at 12 h. In 4 patients (group A). showing an increase in serum Ca by 0;2 to 0.4 mg/dl, serum iPTH decreased in 3, and the decrease in urinary cAMP appeared sooner. Among 4 patients showing no change in serum Ca after 1,25(HO)2D3 (group B), 3 showed an increase in iPTH. These data document the early onset of action of 1,25(OH)2D3 following its administration to normal man; increments in urinary Ca provide the most sensitive index of its action. The data provide no support for the view that 1,25(OH)2D3 exerts any direct inhibitory effect on the secretion of parathyroid hormone.

Adult↗
PubMed1977

On the incidence of renal vein thrombosis in the nephrotic syndrome.

Forty-eight patients with nephrotic syndrome were evaluated prospectively; the studies included inferior venacavagrams and ventilation perfusion lung scans. Eleven patients were found to have renal vein thrombosis (RVT). Eight of 21 patients with membranous glomerulonephritis (MGN) or membranoproliferative glomerulonephritis (MPGN) has RVT (38%). Clinical, laboratory, and pathological findings were not different among those patients with MGN and MPGN whether RVT was present or not. Patients with diabetic nephropathy or lupus nephritis did not have RVT. There was a high incidence of other thromboembolic phenomena as well as asymptomatic perfusion defects demonstrated by the lung scan, especially in patients with MGN or MPGN. These data suggest the disease process underlying the nephrotic syndrome may play a paramount role in the genesis of RVT or thromboembolic phenomena.

Adult↗
PubMed1976

Renal transplantation in a Community Hospital.

Eighty renal transplantations were performed at an urban community hospital over a ten-year period. Forty-two transplants were from living related donors and 38 from cadaver donors. The one-year rejection rate for cadaveric transplants was 35% and for transplants between parents and children, 31%, whereas only one of 21 (5%) transplants between siblings was rejected during the first year. These results compare favorably with those reported by others and appear to justify performance of kidney transplantation in the community hospital setting where large numbers of transplant surgeons and nephrologists are involved, and where the number of transplants never has exceeded 15 per year.

Adolescent↗
PubMed1976

Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes.

1. An attempt was made to evaluate the pathophysiology of symptoms of hyponatremia as related to changes in brain water and electrolytes. Studies were carried out in 66 hyponatremic patients and 5 groups of experimental animals. 2. In hyponatremic patients, symptoms (depression of sensorium, seizures) correlated well with plasma Na+ (r = 0.64, p less than .001), but there was substantial overlap. In patients with acute hyponatremia, all were symptomatic and 50% died. Among patients with hyponatremia of at least 3 days duration, sympatomatic patients had plasma Na+ (115 +/- 1 mEq/L) which was significantly less (p less than .001) than that of asymptomatic patients (plasma Na+ = 122 +/- 1 mEq/L). Among symptomatic patients, mortality was 12% and 8% had seizures, while none of the asymptomatic patients died or had seizures. 3. Among 14 patients with acute (less than 12 hrs) hyponatremia, the mean plasma Na+ was 112 +/- 2 mEq/L. All such patients had some depression of sensorium and four had grand male seizures. Seven of these patients were treated with hypertonic (862 mM) NaCl, while four were treated only with fluid restriction. Of the seven patients treated with hypertonic NaCl, five survived, while three of four patients treated with fluid restriction died. There was no evidence of circulatory congestion or cerebral damage in the patients treated with hypertonic NaCl. 4. Among rabbits with acute (2-3 hours) hyponatremia (plasma Na+ = 119 +/- 1 mEq/L), all had grand mal seizures and 86% died. All such animals had cerebral edema (brain H2O content 17% above control value) but brain content of Na+, K+ and Cl- was normal. 5. Rabbits with 3 1/2 days of hyponatremia (plasma Na+ = 122 +/- 2 mEq/L) appeared to be asymptomatic, even though brain water content was 7% above normal (p less than .01). 6. Rabbits with 16 days of more severe hyponatremia (plasma Na+ = 99 +/- 3 mEq/L) were weak, anorexic, lethargic and unable to walk. Brain water content was 7% above normal, although brain osmolality (218 +/- 12 mOsm/kg H2O) was similar to plasma (215 +/- 8 mOsm/kg). Brain content of Na+, K+, Cl- and osmoles was 17 to 37% less than normal values, so that the brain established osmotic equilibrium with plasma primarily by means of a loss of electrolytes. 7. These studies suggest that in patients with hyponatremia, symptoms and morbidity are only grossly correlated with either magnitude or duration of hyponatremia. Symptoms appear to correlate best with the interplay between a net increase in brain water versus a loss oof brain electrolytes. However, even asymptomatic animals have subclinical brain edema when plasma Na+ is below 125 mEq/L, and such edema may cause permanent brain damage. Thus, many patients with similar levels of plasma Na+, particularly when they are symptomatic, should probably be treated with hypertonic NaCl infusions.

Acute Disease↗
PubMed1976

Acute renal failure in patients with acute pancreatitis.

We describe five patients with acute pancreatitis in whom acute renal failure developed in the absence of hypotension. Pancreatitis was diagnosed clinically, with mean serum and urinary amylase levels of 766 +/- 197 (SE) and 2,378 +/- 572 units/100 ml, respectively. Acute renal failure developed within 24 hours after admission in all patients. It was manifested by oliguria, elevated levels of serum creatinine (mean, 6.9 +/- 1.1 mg/100 ml) and BUN (105 +/-28 mg/100 ml); a urinary sodium level of 72.0 +/- 6.6 mEq/liter; and isosmotic urine (355 +/- 31 mOsm/liter). The mean uric acid level was 18.6 +/- 1.6 mg/100 ml. Blood pressure was recorded frequently, and the lowest mean diastolic pressure was 96 +/- 6 mm Hg. The duration of the oliguric phase of acute renal failure was 8.2 +/- 1.7 days, and all patients recovered from both the acute pancreatitis and acute renal failure. In summary, acute pancreatitis, per se, can precipitate acute renal failure. It occurs early in the course of the pancreatitis, and extreme hyperuricemia is frequent finding that does not adversely affect the recovery of renal function.

Acute Disease↗
PubMed1975

Dietary management of patients in chronic renal failure.

A new oral amino acid preparation was given to two groups of patients: group 1, five patients on hemodialysis; and group 2, five patients with chronic renal failure (CRF). In group 1 significant pre- and postdiet changes were: BUN 93-37 mg% (p smaller than 0.01); creatinine 13.0-9.7 mg% (p smaller than 0.001); phosphorus 6.6-4.2 mg% (p smaller than 0.05); uric acid 8.7-6.0 mg% (p smaller than 0.01); CO2 16.3-21.3 mEq/I (p smaller than 0.01); hematocrit 18.0-20.8% (p smaller than 0.05). In group 2: BUN 93-66 mg% (p smaller than 0.05); phosphorus 5.6-3.8 mg% (p smaller than 0.05); hematocrit 27.3-30.7% (p smaller than 0.05). Nitrogen balance was positive in all patients. It is concluded that this oral amino acid mixture is well-tolerated and can be utilized in CRF to attain protein anabolism.

Acid-Base Equilibrium↗
PubMed1975

Skeletal resistance to endogenous parathyroid hormone in pateints with early renal failure. A possible cause for secondary hyperparathyroidism.

Studies were carried out to evaluate whether skeletal resistance to acute increments in endogenous parathyroid hormone exists in patients with mild to moderate renal insufficiency. Hypocalcemia was induced with the infusion of ethyl-enediamine-tetra-acetate (EDTA) in 10 normal subjects and 13 patients with mild renal failure. After the induction of hypocalcemia, the concentration of serum calcium increased gradually and reached preinfusion levels by 22 h in the normal subjects; in contrast, the levels of serum calcium in patients with mild renal insufficiency were significantly lower than the preinfusion values even at the end of 26 h following the EDTA infusion. This delayed recovery occurred despite significantly higher levels of serum immunoreactive parathyroid hormone (IPTH) in the patients than in the normal subjects. The increase in the levels of IPTH reflect elevations in the concentrations of biologically active hormone since urinary cyclic AMP increased significantly. Urinary calcium excretion following the EDTA infusion was not different in both groups and, therefore, could not account for the delayed recovery of serum calcium values in the patients with renal insufficiency. These results indicate that secondary hyperparathyroidism exists early in patients with renal failure and such patients have exaggerated parathyroid hormone secretion in response to acute hypocalcemia. The data are consistent with the concept that skeletal resistance to increments in endogenous parathyroid hormone is present in such patients. This abnormality is, at least partly, responsible for the hypocalcemia and secondary hyperparathyroidism of renal insufficiency.

Bone and Bones↗
PubMed1975

Renal vein thrombosis and nephrotic syndrome. A prospective study of 36 adult patients.

During 2 years we studied 36 of 41 consecutive patients with nephrotic syndrome. Twelve (Group 1) had renal vein thrombosis; the renal pathology was membranous glomerulonephritis in 10 and membranoproliferative glomerulonephritis in 2. Eighteen without renal vein thrombosis (Group 2) had either membranous (10 patients) or membranoproliferative (8 patients) glomerulonephritis. Clinical presentation, laboratory data, renal function, renal histology, and immunopathology were similar in both groups; thromboembolic phenomena were frequent. Ten of 12 patients with renal vein thrombosis were given oral anticoagulants and followed for 4 to 24 months. None died or had thromboembolic episodes. The results show that one third of the patients with nephrotic syndrome associated with either membranous or membranoproliferative glomerulonephritis had renal vein thrombosis, and there were no clinical, laboratory, histological, or immunopathological finding(s) diagnostic of renal vein thrombosis. Our data indicate that renal vein thrombosis is a frequent complication in nephrotic syndrome and membranous or membranoproliferative glomerulonephritis.

Adolescent↗
PubMed1975

Homeostasis and action of parathyroid hormone in normal man and patients with mild renal failure.

Patients with mild renal failure have elevated blood levels of PTH, and acute hypocalcaemia in these patients produced a greater increment in blood PTH than in normal subjects. There was also a delay in the recovery from hypocalcaemia in patients with mild renal failure as compared to normal subjects. The data are consistent with the presence of skeletal resistance to the calcaemic action endogenous PTH in patients with mild renal failure. This abnormality is probably responsible for the hypocalcaemia of patients with renal failure and to the state of secondary hyperparathyroidism in such patients.

Edetic Acid↗