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P Jaeger

Publications and source records attributed to P Jaeger.

At least 163 records · Page 9Linked to original sources
PubMed1986

[Pyridoxine can normalize oxaluria in idiopathic renal lithiasis].

Pyridoxine (vitamin B6), given to patients with primary hyperoxaluria of type I, generally leads to a decrease in urinary excretion of oxalate owing to stimulation of conversion of glyoxylate to glycine instead of oxalate. It is not known, however, whether pyridoxine would equally influence hyperoxalurias of other origins, e.g. idiopathic or enteric. Two groups of patients were therefore given pyridoxine orally for 2 months (300 mg/d). Group 1 consisted of 10 idiopathic stone formers with mild hyperoxaluria of unknown origin. Group 2 consisted of 4 patients with enteric hyperoxaluria after intestinal bypass surgery. As a mean, enteric hyperoxaluria was not influenced by vitamin B6, which suggests that this disorder is the consequence of intestinal hyperabsorption of oxalate rather than of glyoxylate. In contrast, idiopathic hyperoxaluria was influenced by vitamin B6: urinary excretion of oxalate decreased in 8 patients out of 10 and became normal in 7. However, two patients did not respond to pyridoxine; both had concomitant severe hyperuricosuria (greater than 1 g/24 h), an observation suggesting that in these cases hyperoxaluria was of dietary origin. Four of the patients whose urinary excretion of oxalate became normal while on pyridoxine were followed up for 8 to 36 months after treatment: in all of them oxaluria remained normal. One whose oxaluria had returned to the upper normal limit was retreated after 2 years and again displayed a fall in urinary oxalate. It is concluded that pyridoxine given to idiopathic hyperoxalurics may correct the disorder, as in primary hyperoxaluria of type I; this is not the case in enteric hyperoxaluria. The mechanisms governing this sensitivity to vitamin B6 remain to be clarified.

Adult↗
PubMed1986

[Paget's disease of bone treated per os with APD in 5 days].

Amino-hydroxy-propylidene bisphosphonic acid (APD) is a potent inhibitor of bone resorption. Its oral use in Paget's disease of bone has proved effective and safe when the drug is administered on a long-term basis. Since APD was found not to impair bone mineralization, it was assumed that a long remission would be obtained by administering a high dose of the compound over a very short period of time. Therefore, 12 patients with symptomatic Paget's disease received 1200 mg/d APD orally over 5 consecutive days. Follow-up is 2 months for all patients, 6 months for 6 patients and one year for one patient. Clinical improvement and biochemical remission were observed in all patients. Side effects were negligible (transient nausea in 2 patients and +1 degree C temperature increment noted for 2 days in 3 patients). Urinary hydroxyproline started decreasing within 2 days and became normal as a mean (+/- SEM) after 5 days (1.9 +/- 0.3 mumol/lGF, nl less than 2.3) and in all cases after 15 days. Thereafter it remained within the normal range (1.9 +/- 0.2 mumol/lGF) for 6 months. Plasma alkaline phosphatase activity fell progressively and significantly, and became normal after 1-3 months in all patients but one, a man with very active disease in whom the parameter remained slightly above normal and stable. At the end of the sixth month, mean plasma alkaline phosphatase activity was 100 +/- 13 U/l (nl less than 120 U/l). Plasma calcium and phosphate fell transiently between days 4 and 15.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1986

Anticystinuric effects of glutamine and of dietary sodium restriction.

We studied four patients with cystinuria to assess the effects of glutamine and dietary sodium on the urinary excretion of dibasic amino acids. In Patient 1, at an ad libitum dietary sodium intake of about 300 mmol per day, oral administration of glutamine led to reproducible and marked anticystinuria and antiornithinuria, whereas the excretion of lysine and arginine was not significantly affected. In Patient 2, at an ad libitum dietary sodium intake of about 150 mmol per day, no effect of glutamine could be demonstrated in studies lasting up to three weeks. Since the principal difference between Patients 1 and 2 was their dietary intake of sodium, Patient 3 was studied during dietary sodium intakes of 150 and 300 mmol per day. His cystine excretion was found to be higher at 300 than at 150 mmol per day. Glutamine suppressed his cystine excretion at a sodium intake of 300 mmol per day but had no effect at 150 mmol per day. When the effect of a further reduction in sodium intake alone was studied in a fourth patient, a decrease of 150 to 50 mmol per day was found to reduce cystine excretion markedly within 17 days. The low-sodium diet alone also reduced the excretion of lysine, arginine, and ornithine. We conclude that glutamine may reduce the excretion of dibasic amino acids at a high sodium intake but not at an intake of about 150 mmol per day. However, since a sodium-dependent excretion of the dibasic amino acids occurs at an intake down to about 50 mmol of sodium per day, dietary restriction of sodium can provide a safe approach to the treatment of cystinuria.

Administration, Oral↗
PubMed1986

[Renal lithiasis: the internist's viewpoint 1986].

This study is presented as a debate on nephrolithiasis by a urologist and an internist. The reason is that in 1986 the urologist has become successful at desintegrating almost any stone without open surgery, whereas the internist's approach to the same problem is entirely based upon an understanding of pathophysiological mechanisms. After having reviewed the major risk factors for renal stone disease, i.e. small urine volume, hypercalciuria, hyperoxaluria, hyperuricosuria, very high or very low urine pH and hypocitraturia, the author shows that now it is not only possible to selectively correct each of these disorders, but that in doing so the internist does change the natural history of the disease. For instance, definite remissions have been obtained by advising patients to increase water intake, by administering thiazides to hypercalciurics, pyridoxine to some hyperoxalurics, allopurinol to hyperuricosurics, urease inhibitors to struvite stone formers and citrate to hypocitraturics. Therefore, the author concludes that the role of the urologist and that of the internist are complementary: although the former now desintegrates the stone without open surgery, the latter, who takes care of the same patient next, is now largely able to prevent relapse of nephrolithiasis after determining the cause of the disease.

Calcium↗
PubMed1986

[Indication of the urinary citrate levels in idiopathic renal calculosis].

The reported incidence of hypocitraturia among stone formers (SF) varies between 15 and 50%. It is not known whether this incidence depends on the subtype of SF. The recent simplification of the method of measurement of U-citrate (Boehringer-Mannheim kit) led us to address this issue in 118 male idiopathic (I) SF, with either idiopathic hypercalciuria of the renal (n = 6), absorptive (n = 19) or dietary (n = 41) type, or with normocalciuria (n = 52). Results were compared with those of 42 normal male volunteers. 9 patients had hypocitraturia (less than 215 mg/24 h), all of whom belonged to the group of normocalciuric ISF; only this group of patients had mean U-citrate X V significantly lower than controls (p = 0.025). The cause of hypocitraturia in these patients remains unknown: there were no significant correlations between U-citrate X V and U-pH or blood HCO3 or Cl. Moreover, the patients with hypocitraturia had neither urinary infection nor signs of distal tubular acidification dysfunction as assessed by fasting morning urinary pH. Extended to our whole population of ISF (250 patients) 75% of whom have idiopathic stone disease, it appears that measurement of U-citrate decreased the number of ISF without detectable disorder from 34 to 26, i.e. to 10% of the whole population of stone formers. Since hypocitraturia can easily be corrected by oral administration of citrate, routine measurement of U-citrate in normocalciuric ISF appears a promising method.

Calcium↗
PubMed1986

[Optimal dosage of chlorthalidone in the prevention of the recurrence of nephrolithiasis is 25 mg per day].

Thiazides are considered to be effective in preventing recurrence of various types of nephrolithiasis, but the optimum dosage has not been established. To address this issue, 5 idiopathic stone formers with hypercalciuria on low Ca diet received chlorthalidone (CT) in 3 different oral doses and were randomly assigned either to the sequence 25-50-100 mg/day or the reverse (2 months per dose, monthly blood and urine measurements). The anticalciuric effect of CT was significant only at 50 and 100 mg/day, at the expense of a dose-dependent decrease in U-citrate excretion. We also observed a dose-dependent decrease in blood levels of K, increases in those of HCO3 and urate, as well as in U-pH, a tendency for blood levels of Mg and U-oxalate excretion to fall, and no change in U-urate excretion. Therefore, to derive the optimal CT dose the Tiselius' risk index was applied, which is based on the values of urinary [Ca], [oxalate], [Mg], [citrate] and volume. CT produced a decrement in risk index which was similar at each of the doses tested. Thus, raising CT doses beyond 25 mg/day does not hold out the prospect of improved prophylaxis. This agrees with Ettinger's preliminary data (Urol. Res., 1984) showing a similar protective effect of CT at 25 and 50 mg/day despite the absence of a significant anticalciuric effect at 25 mg/day.

Calcium↗
PubMed1986

A single-day treatment of tumor-induced hypercalcemia by intravenous amino-hydroxypropylidene bisphosphonate.

Twenty patients with malignant hypercalcemia were treated with amino-hydroxypropylidene bisphosphonate (AHPrBP, previously APD), a potent inhibitor of osteoclast-mediated bone resorption. To assess the efficacy of a single-day treatment and determine the optimal dose of this compound, all patients received AHPrBP intravenously over 24 h, but they were divided into two subsequent groups of 10 patients: Group A received a single dose of 60 mg AHPrBP and group B received a single dose of 30 mg. In both groups all patients responded to AHPrBP with a decrease in plasma calcium concentration after a mean time lag of 1 day. Within 6 days, plasma calcium (corrected for serum proteins) fell from 3.24 +/- 0.14 to 2.24 +/- 0.06 mmol/liter in group A (p less than .001), but only from 3.22 +/- 0.15 to 2.49 +/- 0.10 mmol/liter in group B (p less than .005). Whereas in all patients from group A plasma calcium was within the normal range at days 9 and 14, in 4 patients of group B it was still above the normal range at day 9, and in 5 patients at day 14. There was a significant difference in plasma calcium between group A and group B from days 5 to 14 (p less than .005). In both groups, urinary calcium excretion fell dramatically and similarly, and plasma phosphate concentration decreased significantly (p less than .01) to values slightly below the normal range from days 4 to 6.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Oral versus intravenous AHPrBP (APD) in the treatment of hypercalcemia of malignancy.

Twenty patients with malignant hypercalcemia were treated with aminohydroxypropylidene bisphosphonate (AHPrBP, previously APD) a potent inhibitor of osteoclast-mediated bone resorption. To assess the efficacy of oral vs intravenous therapy, the patients were divided into two groups: group A received AHPrBP intravenously (30 mg/day), and group B received the drug orally (1200 mg/day) for 6 days. In both groups all the patients responded to AHPrBP with a rapid decrease in plasma calcium concentration after a mean time lag of 1 day. Within 9 days plasma calcium concentration fell from 3.42 +/- 0.13 (mean +/- SEM) to 2.26 +/- 0.13 mmol/l in group A and from 3.28 +/- 0.12 to 2.24 +/- 0.09 mmol/l in group B. There was no significant difference in plasma Ca level between both groups on days 4, 6, and 9, and plasma Ca was within the normal range in all patients on day 9. On both treatment regimens urinary calcium excretion fell dramatically and similarly. Plasma phosphate concentration decreased significantly on AHPrBP in both groups of patients, reaching values slightly below the normal range from day 4 to day 9. TmP/GFR decreased progressively on AHPrBP. However, this decrement was significant at day 6 only. Plasma parathyroid hormone concentration rose significantly in both groups from day 4 to day 9. We conclude that at the doses used in the present study treatment of tumor-induced hypercalcemia with AHPrBP is equally effective whether given orally or intravenously.

Administration, Oral↗
PubMed1986

Tubulopathy in nephrolithiasis: consequence rather than cause.

To address whether a renal tubular dysfunction is encountered in a particular patient subgroup with urolithiasis, the following parameters of tubular function were measured in urine taken in the morning from 214 stone formers after fasting: pH, excretion of lysozyme and gamma-glutamyl transferase (gamma-GT); fractional excretion (FE) of glucose, insulin, Mg, K, and HCO3 after an alkali loading; and the renal threshold for phosphate (TmP/GFR). The following diagnoses were made in the patient group: primary hyperparathyroidism (N = 8), medullary sponge kidneys (N = 21), hyperuricemia (N = 10), cystinuria (N = 2), struvite stone disease (N = 6), idiopathic hypercalciuria of the absorptive (N = 25), dietary (N = 69) or renal (N = 7) type, and normocalciuric idiopathic urolithiasis (N = 66). In 31% of the patients TmP/GFR was below 0.80 mmole/liter and in 13% of the patients, FE HCO3 after alkali loading was above normal. Urinary excretion of lysozyme and that of gamma-GT both were elevated in 17% of the patients. FE glucose, FE insulin, FE Mg, and FE K were elevated in 8, 9, 3, and 7% of the patients, respectively. This study demonstrates that a significant number of stone formers present with signs of renal tubular dysfunction, primarily involving the proximal tubule since apparent leaks of phosphate and of bicarbonate were most frequently encountered. The defects were not specific for a given etiologic group of patients; on the other hand, occurrence was related to the presence of large stones in the pyelocaliceal system at the time data were gathered. Taken together these data suggest that the tubulopathy in nephrolithiasis is the consequence rather than the cause of the stone.

Adolescent↗
PubMed1986

Idiopathic acute interstitial nephritis and uveitis in the adult. Report of 1 case and review of the literature.

In a 59-year-old female, concurrence of acute interstitial nephritis and uveitis was observed. While the clinical signs resolved after a few weeks, signs of renal tubular dysfunction persisted for 9 months, and creatinine clearance was still impaired (22 ml/min) more than 2 years after beginning of the symptoms. This is the 5th case of idiopathic interstitial nephritis with concomitant uveitis reported in adult patients. In contrast to the benign evolution observed in children, the renal function may remain impaired in adults.

Creatinine↗
PubMed1986

Evidence that calcitonin stimulates 1,25-dihydroxyvitamin D production and intestinal absorption of calcium in vivo.

Although it is well established that parathyroid hormone and phosphate are important regulators of 1,25-dihydroxyvitamin D [1,25(OH)2D] production, it remains unclear whether calcitonin affects vitamin D metabolism in vivo. Experiments were performed in the rat to determine the effect of chronic calcitonin infusion (0.2 U X h-1) on plasma levels of vitamin D metabolites and on calcium metabolism. Thyroparathyroidectomized animals fed a calcium-replete or calcium-free diet were studied for as long as 2 wk before they were killed. In control rats, a calcium-free diet alone for 12 d resulted in an increase in 1,25(OH)2D levels from 24 +/- 5 to 139 +/- 37 pg . ml-1, P = 0.025. The infusion of calcitonin also stimulated 1,25(OH)2D levels compared with controls on a regular diet (80 +/- 17 vs. 38 +/- 6 pg . ml-1, P less than 0.05) and on a calcium-free diet (460 +/- 50 vs. 139 +/- 37 pg . ml-1, P less than 0.001). In addition, calcitonin increased plasma calcium levels in animals on a regular diet by 50%; this effect was most likely due to increased intestinal absorption of calcium, because removal of calcium from the diet markedly blunted this effect. In contrast, calcitonin administration did not significantly affect 25(OH)D plasma levels. Collectively, these data suggest that calcitonin and calcium are independent regulators of 1,25(OH)2D production and that calcitonin stimulates intestinal absorption of calcium, by increasing circulating levels of 1,25(OH)2D.

Animals↗
PubMed1986

[Diagnostic parameters and their value in testicular tumors].

Diagnosis of the retroperitoneum to deliniate metastases of nonseminomatous germinal cell testicular cancer, when combined with Computer tomography, Sonography and Lymphography has a high specificity. With regard to treatment, the differentiation between stage I and stage II is very important. In the so called high risk groups (MTU-Tumour, T3-Primary tumour) a stage I can actually be a stage II. Computer Tomography of the thorax should be made to deliniate a stage III tumour.

Adult↗
PubMed1985

[Tubular dysfunction in renal lithiasis: cause or consequence?].

To investigate whether overall tubular dysfunction is encountered in a particular subgroup of patients with urolithiasis, the following parameters of renal tubular function have been measured in fasting morning urine in 124 male stone formers: excretion of lysozyme and gamma-glutamyl transpeptidase (gamma-GT), fractional excretion (FE) or glucose, insulin, bicarbonate after an alkali load, and theoretical phosphate threshold (TmP/GFR). The following have been diagnosed: primary hyperparathyroidism (n = 3), medullary sponge kidneys (n = 5), hyperuricemia (n = 8), cystinuria (n = 1), struvite nephrolithiasis (n = 2), idiopathic hypercalciuria of the absorptive (n = 16), dietary (n = 46) or renal (n = 5) type, and normocalciuric idiopathic urolithiasis (n = 38). Urinary excretion of lysozyme and of gamma-GT were elevated in 14% and 21% of patients respectively; FE glucose and FE insulin were elevated in 6% and 8% of patients respectively. In 62% of the patients TmP/GFR was below 0.95 mmol/l and in 52% of the patients FE HCO3 after alkali load was above normal. The findings show that a large number of stone formers have signs of renal tubular dysfunction; apparent renal leaks of phosphate and of bicarbonate are the most frequently encountered defects; while they are not specific for a given etiologic group of patients, they have been found in each group. The latter observation suggests that nephrolithiasis itself can damage renal tubular function.

Adult↗
PubMed1985

Influence of the calcium content of the diet on the incidence of mild hyperoxaluria in idiopathic renal stone formers.

Urinary oxalate excretion was measured in 101 male idiopathic calcium (Ca) stone formers studied on 3 dietary conditions (free-choice, Ca-enriched, and low-Ca diet). The population consisted of 38 normocalciuric and 63 hypercalciuric patients. Mean oxalate excretion was similar in normocalciuric and in hypercalciuric patients, on free-choice as well as on Ca-enriched diet. In both conditions the incidence of hyperoxaluria (greater than or equal to 435 mumol/24 h) within each group of stone formers was also similar, ranging from 11 to 22%. On low-Ca diet, however, mean oxalate excretion increased significantly (p less than 0.01) in hypercalciurics but not in normocalciurics; on this diet, the incidence of hyperoxaluria was particularly high in the hypercalciurics (33%), compared with the normocalciurics (13%). On low-Ca diet, oxalate excretion was positively correlated with the estimated degree of intestinal absorption of calcium (p = 0.01). These results show that among idiopathic stone formers, mild hyperoxaluria is not a rare finding and that this disorder can be encountered in each group of patients; its incidence, however, is influenced by the calcium content of the diet. On a low-Ca diet, patients with intestinal Ca hyperabsorption are particularly prone to develop hyperoxaluria, an observation which leads to question the relevance of such a dietary advice unless oxalate intake is simultaneously reduced.

Adult↗
PubMed1985

Distal renal tubular acidosis and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism. Report of 1 case without nephrocalcinosis.

In a 33-year-old woman concurrence of a complete distal renal tubular acidosis (RTA) and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism was observed. Until recently, the rare association of RTA and hyperthyroidism had been thought to be governed by nephrocalcinosis, via hypercalcemia and hypercalciuria. However, in this case, nephrocalcinosis was not present, but there were histological signs of renal interstitial mononuclear cell infiltration, and the RTA persisted despite the resolution of the hyperthyroidism. This observation supports the idea that immunological mechanisms may relate RTA and hyperthyroidism when the latter has an autoimmune origin.

Acidosis, Renal Tubular↗