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Biomedical subjects

P Jaeger

Publications and source records attributed to P Jaeger.

At least 181 records · Page 10Linked to original sources
PubMed1985

Evidence for a particularly severe secondary hyperparathyroidism in analgesic abuse nephropathy.

Ca metabolism was compared in two groups of patients with chronic interstitial nephritis: in 21 patients (analgesic abuse nephropathy (AAN) group), nephropathy was due to exposure for 5-50 years (mean 21.1) to phenacetin-containing analgesics, whereas in 21 other patients (controls) it was due to exposure for 1-80 years (mean 21.4; NS) to other causes. Patients were followed for 2.5 +/- 0.6 and 1.6 +/- 0.6 years, respectively (mean +/- SEM; NS). Blood Ca, P, protein, creatinine, alkaline phosphatase, parathyroid hormone (PTH), 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D) as well as arterial acid-base status and urinary excretion rate of Ca, P and creatinine were determined serially. Results were included only when P was maintained between 0.7 and 1.9 mmol/l. The range of creatinine levels studied was 95-1,600 mumol/l. No differences were found between the two groups with respect to creatinine clearance, blood P, protein, arterial pH and bicarbonate, and urinary excretion rates of Ca and P. Mean plasma Ca was significantly lower, and PTH was significantly higher in the AAN group than in the control group; mean plasma alkaline phosphatase activity was also significantly higher in the AAN group. In both groups Ca was negatively correlated with creatinine, but the slope of the regression line was steeper in the AAN group than in controls. The degree of hypocalcemia was related to the increase in plasma PTH and alkaline phosphatase, but not to the plasma level of 25(OH)D or 1,25(OH)2D.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Fate of parathyroid hormone during hemodialysis and ultrafiltration.

In order to shed light on the discrepant changes in plasma immunoreactive parathyroid hormone (iPTH) during hemodialysis (HD) and ultrafiltration (UF) in end-stage renal failure, the influence of filtration of PTH fragments on the iPTH level in plasma was examined in 2 sets of experiments: in vitro dialysis of 125I-bPTH 1-84, 125I-hPTH 1-34 and 125I-hPTH 53-84 added to plasma was successively performed through a cuprophane membrane. Gel filtration on a Biogel P-100 column and subsequent counting of the eluate were performed with the plasma before and after dialysis, and with the dialysate fluid after dialysate fluid after dialysis. An ultrafiltrate obtained from a patient with renal failure was also analyzed for iPTH with a 'C-' and with an 'N-terminal' antiserum (GP 500 MA and AS 211/32), and so was his plasma before and after UF, and after a subsequent dialysis session. Fluid obtained by lavage of the filter with acetic acid after dialysis was also analyzed. Chromatography with measurements of iPTH in the eluate was performed in each case, and the procedure was repeated applying a different transmembrane pressure. Immunoreactive material found in the concentrated ultrafiltrate, but not in plasma, was characterized by means of dilution curves in different RIA performed with the C-terminal antiserum preincubated with various synthetic PTH fragments. Results showed that intact PTH does not cross the cuprophane membrane during both in vitro dialysis and in vivo UF. The 1-34 fragments are poorly dialyzed in vitro; either they stick to the membrane or they are disintegrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Chromatography, Gel↗
PubMed1985

Quantitative assessment of in vivo backscatter enhancement from gelatin microspheres.

Experimental work using a quantitative C-scan technique to measure in situ enhancement of hepatic backscatter resulting from the administration of gelatin microspheres to dogs is reported. We have found that reproducible enhancement of hepatic backscatter on the order of 2 dB followed the peripheral administration of gelatin within minutes, the magnitude of the effect was not sensitive to the rate of infusion, but was likely to be dose dependent, changes in the overlying tissue attenuation had a pronounced effect on the measurement, and the effect was sustained for up to one half hour or longer.

Animals↗
PubMed1984

Drinking water for stone formers: is the calcium content relevant?

Stone formers are often told to select a drinking water with low Ca content. To see whether this measure has a rational biochemical background, 4 Ca hyperabsorbers were asked to drink, first tap water ad libitum, then 2 liters/day of tap water, then 2 liters/day of a low Ca water (A) and finally 2 liters/day of a high Ca water (B). On A, subjects were normocalciuric but hyperoxaluric; whereas on B, they were markedly hypercalciuric but normooxaluric. Therefore, Ca . Ox concentration products were similar on B and A. However, on A as well as on B, Ca . Ox products were much lower than on tap water ad libitum due to the high fluid intake which had thus been imposed. It is concluded that, in the prevention of the recurrence of nephrolithiasis, 'have a high fluid intake' is probably a more relevant advice than 'select a water with a particularly low Ca content'.

Calcium↗
PubMed1983

[Idiopathic calcium nephrolithiasis: therapeutic aspects].

The 75% of the renal stone formers have a so-called idiopathic calcium urolithiasis. The majority of these patients, however, do have a detectable biochemical disorder such as hypercalciuria, hyperuricosuria or hyperoxaluria. A high fluid intake unequivocally represents the first step in the therapeutic approach to these patients. Nevertheless, the detection of any type of biochemical disturbance is of great importance since the addition of a specific therapy will then become possible. Patients with absorptive idiopathic hypercalciuria will be advised to decrease their intake of dairy products as a function of the degree of calcium hyperabsorption, and simultaneously the major dietary sources of oxalate such as chocolate, spinach, rhubarb and asparagus will be eliminated; neutral orthophosphates (3-4 times 500 mg/d) or a thiazide, resp. an analogue as chlorthalidone (50 mg/d) are reasonable alternatives. Renal idiopathic hypercalciuria should be treated, according to the authors, with chlorthalidone (50 mg/d), with or without allopurinol (300 mg/d) depending on the presence of concomitant hyperuricosuria. Patients with dietary idiopathic hypercalciuria should be advised to better equilibrate the various components of their dietary intake. Finally, patients with isolated idiopathic hyperuricosuria whose disease would remain active despite a high fluid intake should receive allopurinol (300 mg/d). The treatment of isolated idiopathic hyperoxaluria is not yet well established. Two main arguments favor this so to say "tailored" approach to the idiopathic stone former: first, some metabolic disturbances are causally related to a particularly active and severe urolithiasis, whereas others are less so; second, the lack of efficacy of some types of treatment appears more and more to be due to insufficient screening of the patients before starting a given treatment.

Calcium↗
PubMed1983

Bilateral fractures of femoral neck in patients with moderate renal failure receiving fluoride for spinal osteoporosis.

Two patients with moderate renal failure sustained spontaneous bilateral hip fractures during treatment with fluoride, calcium, and vitamin D for osteoporosis. They had been taking sodium fluoride (40-60 mg/day) for 11 and 21 months, respectively. Histological examination of a specimen of the bone showed severe fluorosis in the first case, and quantitative analysis of bone showed osteomalacia and skeletal fluorosis in the other case. These abnormalities were considered to be the consequence of excessive retention of fluoride due to renal insufficiency. As bilateral femoral neck fractures are very rare these data suggest a causal link between fractures and fluoride in patients with renal failure. Thus fluoride should be given at a lower dosage, if at all, to patients with even mild renal failure.

Aged↗
PubMed1983

Luminal buffer transport in rat cortical tubule: relationship to potassium metabolism.

Free-flow micropuncture studies were performed on superficial rat tubules and titratable acid (TA), sodium and potassium concentrations, and tubular pH were measured in control, acutely K-loaded, and chronically K-depleted animals. The proximal tubule is a key site of TA formation. Under control conditions, significant amounts of TA were lost along the loop of Henle. TA delivery (in pmol X min-1) to the late proximal tubule (LP) was 23.66 +/- 2.38 (mean +/- SE), that to the early distal tubule (ED) was 17.24 +/- 1.73, and little further loss occurred along more distally located nephron sites. In acute hyperkalemia, urinary TA excretion (in mumol X min-1) was lower than under control conditions (0.56 +/- 0.04 vs. 1.01 +/- 0.07); TA delivery to the LP (18.50 +/- 1.93) was slightly reduced compared with the controls (a change not reaching statistical significance). TA delivery to the ED was also reduced (11.54 +/- 1.04); significant amounts of TA were lost along the loop of Henle and a significant further loss occurred along the distal tubule since TA delivery to the late distal tubule (LD) was only 7.41 +/- 0.83. As luminal pH along both proximal and distal tubules in K-loaded rats was indistinguishable from that of control rats, a major factor responsible for decreased distal TA formation in K-loaded animals was diminished buffer delivery. In chronic potassium depletion urinary TA excretion was also lowered (0.30 +/- 0.06); only a moderate part of this effect was due to increased pH along the nephron. Increased buffer reabsorption along the proximal tubule (TA delivery to LP was 14.32 +/- 2.01) contributed mainly to the reduced rate of titratable acid excretion.

Acid-Base Equilibrium↗
PubMed1983

Ammonium transport in rat cortical tubule: relationship to potassium metabolism.

Free-flow micropuncture studies were carried out in rats to study the relationship between ammonium and potassium transport along superficial nephrons. Proximal and distal tubular fluid was analyzed for [3H]inulin, potassium, and ammonium. Ammonium was measured by a titrimetric formaldehyde method using a glass electrode to measure pH and an antimony electrode to deliver OH ions. In addition to experiments carried out under control conditions, the rats were also acutely potassium loaded, chronically potassium depleted, or given glutamine intravenously to stimulate ammonium excretion. Ammonium production along the proximal tubule was sharply enhanced in potassium depletion and, most likely, also following glutamine infusion, but it remained unchanged during hyperkalemia. Significant amounts of ammonium were lost along the loop of Henle in all experimental conditions. During stimulation of ammonium excretion by either potassium depletion or glutamine infusion the urine became alkaline. No loss or gain of ammonium beyond the late distal tubule was observed in any of the experimental conditions. With respect to potassium transport the glutamine-induced rise in urinary ammonium excretion was associated with stimulation of potassium reabsorption beyond the late distal tubule.

Acid-Base Equilibrium↗
PubMed1983

Influence of acute potassium loading on renal phosphate transport in the rat kidney.

UNLABELLED: This study examined 1) whether potassium-induced depression of phosphate excretion is a parathyroid hormone-dependent phenomenon, and 2) whether such stimulation of tubular phosphate reabsorption capacity involves increased phosphate reabsorption in the distal tubule. Potassium was infused into intact rats (25 mumol X min-1 X kg-1) during stepwise addition of phosphate to the infusion and led to a significant drop in phosphate excretion; this effect was abolished in thyroparathyroidectomized (TPTX) animals. In intact rats the maximal tubular Pi reabsorption per milliliter of glomerular filtrate (max TRPi/ml GF) was significantly higher in the potassium group (2.54 +/- 0.06 mumol/ml GF) compared with the control group (2.31 +/- 0.06 mumol/ml GF) (means +/- SE). In TPTX rats no difference in max TRPi/ml GF was observed: 3.44 +/- 0.07 and 3.49 +/- 0.07 mumol/ml GF during potassium and sodium infusion, respectively. Free-flow micropuncture was carried out on superficial distal tubules of intact rats and fluid samples were analyzed for [3H]inulin and phosphorus (electron microprobe). Phosphorus delivery into the distal tubule was similar in control and potassium-loaded rats. Whereas net phosphorus reabsorption along the distal tubule was absent in the control group, intravenous potassium administration stimulated distal phosphorus reabsorption. CONCLUSION: potassium stimulates renal phosphate reabsorption capacity, an effect that is abolished after TPTX. The potassium effect on phosphate occurs along the distal tubule.

Animals↗