Biomedical subjects

A Pomeranz

Publications and source records attributed to A Pomeranz.

At least 19 recordsLinked to original sources

PubMed1992

Once daily cefixime compared with twice daily trimethoprim/sulfamethoxazole for treatment of urinary tract infection in infants and children.

We conducted a randomized prospective multicenter study to compare the safety and efficacy of once daily oral cefixime (8 mg/kg) to twice daily oral trimethoprim/sulfamethoxazole (TMP/SMX) (8/40 mg/kg/day) for the treatment of acute urinary tract infection in children ages 6 months to 13 years. Seventy-six patients (38 in each group) were studied. Thirty-seven percent were younger than 3 years of age. Escherichia coli was the most common isolate in both groups (85%). Eighty-five percent of all Gram-negative organisms were susceptible to TMP/SMX and all were susceptible to cefixime. Seventy-two percent of all patients were febrile at the time of diagnosis. Both groups were treated for 7 to 10 days. Peripheral white blood cell counts, erythrocyte sedimentation rate, body temperature and urinalysis returned to normal at the same rate in both groups. No failures were observed and relapse occurred in 3 cases within the 4 weeks after treatment (2 in the cefixime group and one in the TMP/SMX group). Side effects were observed in 14% of the cefixime group and 16% of the TMP/SMX group and were all mild enough not to necessitate discontinuation of therapy. We conclude that the efficacy and safety of cefixime administered once daily compared favorably with TMP/SMX administered twice daily for acute uncomplicated urinary tract infection.

Administration, Oral↗

PubMed1992

Adriamycin nephropathy: a model to study effects of pregnancy on renal disease in rats.

The influence of pregnancy on the evolution of primary renal disease is still a matter of controversy. Hypertension and derangement of renal function may occur. The pathophysiology of these complications is poorly understood. In the present study, we assessed the influence of pregnancy on the evolution of adriamycin (Adr) nephropathy. Four groups of animals were studied: 1) control virgin rats (C), 2) normal pregnant rats (NP), 3) virgin rats with nephropathy (Adr), and 4) pregnant rats with nephropathy (Adr-P). Inulin clearance measured at the end of pregnancy in awake rats was similar in NP (1.68 +/- 0.20 ml/min) and C (1.39 +/- 0.03 ml/min). In Adr-P rats, it tended to decrease (1.22 +/- 0.7 vs. 1.93 +/- 0.44 ml/min in Adr rats). Mean arterial pressure was increased in Adr-P rats (137 +/- 2.5 vs. 95 +/- 3.2 mmHg in NP; P < 0.001). Urinary protein excretion was 216 +/- 61 mg/day in Adr-P compared with 28.7 +/- 18 mg/day in Adr (P < 0.001). A significant increase in the glomerular thromboxane B2-to-prostaglandin E2 ratio was found in Adr-P rats (1.15 +/- 0.26 vs. 0.52 +/- 0.12 in Adr rats; P < 0.03). In NP rats, no change was observed. Kidneys and placentas were normal on light and electron microscopy. Thus pregnant rats with adriamycin nephropathy developed a clinical picture with several features of preeclampsia. Changes in glomerular prostanoid synthesis might play a role in the development of this complication.

Anesthesia↗

PubMed1992

Neonatal hyperparathyroidism. Conservative treatment with intravenous and oral rehydration solutions.

A neonate with primary hyperparathyroidism was successfully managed by conservative medical treatment. This treatment consisted of intravenous saline load, followed by oral rehydration solutions containing between 60-90 mmol/l of sodium. The combined administration of sodium and diuretics maintained normal levels of serum calcium. Similar cases were previously treated by parathyroidectomy with or without autotransplantation. In selected patients, medical treatment should be considered as the initial approach in mild neonatal hyperparathyroidism. It poses no specific risks and offers an alternative to surgical intervention.

Fluid Therapy↗

PubMed1991

Effect of the prostacyclin analogue iloprost in sodium-depleted rats pretreated with captopril.

Previous studies have shown that administration of captopril to sodium-depleted rats decreases the glomerular filtration rate (GFR) and blunts the increase in glomerular prostacyclin synthesis normally occurring in response to sodium depletion. To clarify the relationship between these two responses, iloprost, a stable analogue of prostacyclin, was administered to Na-depleted, captopril-treated (LNC) rats. At a dosage not affecting systemic blood pressure (12.5 ng/kg/min), iloprost increased GFR in LNC rats by 25% (from 0.26 +/- 0.03 to 0.35 +/- 0.03 ml/min/100 g body wt, P less than 0.01), without significant effects on renal plasma flow. No effect was observed in control rats. The results suggest that altered prostacyclin synthesis could contribute to the decrease of GFR in this model.

Animals↗

PubMed1991

Dietary-induced hyperlipidemia and renal function in the uremic rat.

Rats made uremic by 2-stage 5/6 nephrectomy and sham-operated control animals were fed either a normal laboratory chow, a high-sucrose (60%) or a high-fat (10% cholesterol; 20% olive oil) diet, all containing 21% protein and identical amounts of electrolytes, vitamins and trace elements. Serum creatinine levels remained unchanged in the control animals but rose in the 5/6 nephrectomised uremic animals by a factor of 2.7 from a mean of 0.44 +/- 0.05 mg/dl to 1.20 +/- 0.11 mg/dl at 8 weeks, without differences between the dietary groups. During 8 weeks of dietary regimen the high-sucrose and high-fat diets induced significant hypertriglyceridemia, generally similar in control and uremic rats. The uremic animals on a high-sucrose and high-fat diet had the most pronounced rise in serum triglycerides, 331.5 +/- 89.0 and 298.0 +/- 45.0 mg/dl, respectively (control: 159.9 +/- 14.0 mg/dl). After 4 and 8 weeks, only the animals on the high-fat diet had significant hypercholesterolemia, most pronounced in the uremic animals (356 +/- 56.3 mg/dl; control: 71.6 +/- 12.9 mg/dl). The animals in the latter group also had significant proteinuria and renal histologic abnormalities consisting of xanthoma-like glomerular lesions, infiltrates and fibrosis not seen in the other groups of animals. These data indicate that dietary-induced hyperlipidemia of short duration causes or aggravates renal damage in the rat with mild-moderate uremia, induced by ablation.

Animals↗

PubMed1990

NaCl modulates captopril effects on glomerular prostaglandin synthesis and glomerular filtration.

Captopril stimulates glomerular prostaglandin (PG) synthesis and increases glomerular filtration rate (GFR) in Na-repleted rats, whereas, in Na-depleted rats, it fails to stimulate PG synthesis and decreases GFR. In the present work the influence of chronic and acute NaCl loading on PG synthesis and renal function was studied in Na-depleted rats receiving captopril (LNC rats). Glomerular PGE2 and 6-keto-PGF1 alpha were not increased in LNC rats and were significantly lower than in Na-depleted rats (LN). Na repletion, while continuing captopril, increased PG synthesis above control levels. Addition of captopril in vitro to the incubation medium stimulated PGE2 synthesis in glomeruli of control rats, whereas it depressed it in LN rats. Acute loading with NaCl in LNC rats increased inulin and PAH clearances to values significantly greater than in control rats and similar to those of normal rats receiving captopril. Comparable volume loading with isotonic mannitol or 3% albumin increased inulin and PAH clearances only to control values. The specific effect of NaCl in acute loading was prevented by cyclooxygenase inhibition and was not mediated by increased systemic blood pressure. The results provide evidence that the effects of captopril on glomerular PG synthesis and renal function depend on the state of Na balance.

Animals↗

PubMed1990

Potassium load prevents the decrease of GFR induced by captopril in sodium-depleted rats.

Captopril decreases the glomerular filtration rate (GFR) in Na-depleted rats and inhibits the stimulation of glomerular prostanoid synthesis induced by Na depletion. Because K loading stimulates glomerular prostanoid production in normal rats, we studied the effects of K loading in Na-depleted captopril-treated (LNC) rats. Potassium, but not Cl, loading stimulated the glomerular synthesis of 6-ketoprostaglandin F1 alpha (PGF1 alpha) and thromboxane B2 (TxB2). Urinary kallikrein-like activity (UKALLV) and plasma aldosterone increased in K-loaded animals. LNC rats had lower clearances of inulin (CIN) and p-aminohippurate (CPAH) than controls (0.22 +/- 0.02 vs. 0.94 +/- 0.07 and 0.56 +/- 0.12 vs. 2.23 +/- 0.23 ml.min-1.100 g body wt-1, both P less than 0.01). KCl-loaded LNC rats had CIN and CPAH greater than LNC (0.64 +/- 0.16 and 1.90 +/- 0.28 ml.min-1.100 g body wt-1, P less than 0.01). Similar results were observed in LNC rats loaded with a K solution not containing Cl, but not in LNC rats loaded with a mixture of CaCl2, MgCl2, and HCl. In KCl-loaded LNC rats, cyclooxygenase inhibition decreased CIN from 0.49 +/- 0.09 to 0.30 +/- 0.08 ml.min-1.100 g body wt-1 (P less than 0.01). Aprotinin did not affect renal function despite significant decrease of UKALLV. We conclude that K loading prevents the decrease of GFR induced by captopril in Na-depleted rats and that this might be mediated by stimulation of glomerular prostanoid synthesis.

Aldosterone↗

PubMed1990

Captopril, but not diltiazem, favorably affects the course of early chronic renal disease in rats.

The concepts that increased intracellular Ca2+ content and increased glomerular capillary pressure play an important role in the progression of chronic renal diseases has led to the suggestion that treatment with calcium-blocking agents (diltiazem; CBB) or converting enzyme inhibitors (captopril; CEI) may be indicated to prevent renal failure. We studied the effects of CCB and CEI on the early course of adriamycin (ADR) nephropathy, where glomerular pressure has been shown to be unchanged, blood pressure was only mildly elevated and renal failure incipient. Animals were studied 2, 7, 12, 16 and 20 weeks after the second injection of ADR, 2 mg/kg. In treated rats, blood pressure remained normal. At the end of the study, proteinuria and serum creatine were lower in ADR-CEI than in ADR rats (149 +/- 42 vs. 616 +/- 90 mg/day, p less than 0.01 and 0.36 +/- 0.04 vs. 0.58 +/- 0.02 mg%, p less than 0.01, respectively). ADR-CCB had values similar to those of untreated ADR rats. Mesangial expansion and focal glomerulosclerosis were present only in ADR and ADR-CCB rats, whereas in ADR-CEI rats the glomeruli were virtually normal. Glomerular 45Ca uptake was increased in ADR, decreased in ADR-CCB rats, and normal in ADR-CEI. Glomerular 6-keto PGF1 alpha and TxB2 were significantly increased in ADR rats, and both treatments decreased TxB2. The results suggest that endogenous angiotensin II is important for the early progression of glomerular injury toward renal insufficiency, while tissue Ca2+ accumulation may play an important role in more advanced phases.

Animals↗

PubMed1990

Atrial natriuretic peptide-induced increase of glomerular filtration rate, but not of natriuresis, is mediated by prostaglandins in the rat.

This study addressed the question of whether some renal effects of atrial natriuretic peptide (ANP) are mediated by prostaglandins (PGs). Inhibition of PG synthesis (aspirin, 10 mg/kg) abolished the increase in inulin clearance (CIN) induced by ANP in rats. In contrast, diuresis and natriuresis remained significantly elevated after aspirin administration. ANP, either infused in vivo immediately before sacrifice or added to the incubation tubes, stimulated the synthesis of PGE2 and 6-keto-PGE1 alpha by isolated rat glomeruli but not by medullary or papillary slices. We conclude that the effect of ANP on the glomerular filtration rate is PG dependent, whereas that on diuresis and natriuresis is direct.

Animals↗

PubMed1990

Cat-scratch bacillus and Streptococcus pneumoniae causing submandibular suppurative adenitis and acute glomerulonephritis.

Acute cervical adenitis is a frequent problem in pediatrics. It is occasionally followed by acute postinfectious glomerulonephritis, which has a well-defined set of clinical and histological manifestations. We present two rare cases of acute postinfectious glomerulonephritis, one associated with Streptococcus pneumoniae and the second with cat-scratch disease. Cultures of material from the lymph nodes yielded S. pneumoniae type 15 in case 1. A pleomorphic gram-negative micro-organism, identified by silver stain as cat-scratch bacillus, was found in case 2.

Cat-Scratch Disease↗

PubMed1989

Endogenous digoxin-like factor raises blood pressure and protects against digitalis toxicity.

Digoxin-like immunoreactive factor (DLIF) is an endogenous natriuretic material which causes diuresis and natriuresis after salt or fluid loading and which may play a pathogenetic role in various hypertensive states. In order to study the cardiovascular effects of DLIF, we administered partially purified material (500 ng/kg) iv to normal rats. DLIF administration caused a significant rise in blood pressure, induced a brisk diuresis, and slowed the heart rate. In addition, DLIF protected against digitalis toxicity. While iv digoxin, 1 mg/kg, uniformly produced lethal arrhythmias, administration of DLIF 15 min prior to digoxin infusion consistently protected against arrhythmias. These findings support the theory that DLIF may play a role in hypertension. In addition, DLIF may compete with digoxin for cardiac receptors.

Animals↗

PubMed1989

Presence of an anti-viral factor in peritoneal dialysis effluent.

Viral peritonitis is an exceptionally rare occurrence in peritoneal dialysis. In fact, up to now, only one case report has been documented in the literature. In a prospective study, peritoneal dialysis effluent (PDE) was specifically cultured for the following viruses: the herpes group of viruses, including herpes simplex types I (HSV) and II, cytomegalovirus (CMV) and varicella-zoster (V-Z), and the enteroviruses group including coxsackie B-5 (Cox B), echo, enterovirus and polio. Cultures were performed under both basal conditions and in the presence of peritonitis. No viral growth was demonstrated. The possible existence of an anti-viral factor in the PDE was therefore raised. In order to investigate this hypothesis, the PDE of 16 patients undergoing intermittent peritoneal dialysis and of 24 patients on continuous ambulatory peritoneal dialysis were examined for anti-viral activity. The method used was analogous to that employed for testing the anti-viral effect of interferon (IFN). The inhibition of the cytopathic effect (CPE) of various viruses was examined in the following tissue cultures: Vero cells (a line of monkey kidney cells) incubated with HSV, vesicular stomatitis virus (VSV) and Cox B; human kidney cells incubated with parainfluenza 3 (Para-3); human foreskin fibroblasts incubated with CMV, HSV and VSV and L-929 (a line of mouse cells) incubated with VSV. As control, unused Dianeal (Travenol, Ashdod, Israel) 1.5 and 4.25 g/dl, normal saline and 5 g/dl dextrose solutions were tested under the same conditions using VSV on Vero. The PDE was also examined for the presence of specific anti-viral antibodies by microneutralization and ELISA tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Effects of sodium depletion on renal prostanoid synthesis in rats: influence of the converting enzyme inhibitor captopril.

1. The synthesis of prostaglandin (PG) E2, PGF2 alpha, 6-keto-PGF1 alpha and thromboxane (TX) B2 by isolated glomeruli, cortical tubules, inner medullary slices and outer medullary slices was measured in salt-depleted (LNa) rats and in salt-depleted rats receiving captopril (LNa-CEI). Animals were studied before and after 4, 9 and 15 days of Na+ depletion. 2. Na+ balance was reached in LNa rats after 4 days. Blood pressure and creatinine clearance remained stable. Serum Na+ decreased from 140 +/- 1 to 126 +/- 1 mmol/l (mean +/- SEM, P less than 0.01). In contrast, LNa-CEI rats were unable to conserve Na+ adequately: fractional excretion of Na+ and natriuresis were constantly greater than in LNa animals. As a consequence, LNa-CEI rats developed severe hyponatraemia, lost weight and their creatinine clearance decreased. 3. The glomerular synthesis of PGE2, PGF2 alpha and 6-keto-PGF1 alpha, but not of TXB2, was significantly increased in LNa rats. In LNa-CEI rats, the synthesis of PGE2 and 6-keto-PGF1 alpha was similar to control values, but PGF2 alpha and TXB2 synthesis was elevated at day 9. In cortical tubules, PGE2 and PGF2 alpha were unaffected by Na+ depletion, but 6-keto-PGF1 alpha and TXB2 were increased and a similar trend was observed in LNa-CEI rats. In outer medulla of LNa rats, a decrease in all the eicosanoids measured was observed at day 4. In LNa-CEI animals, the synthesis of PGE2 and PGF2 alpha, but not of 6-keto-PGF1 alpha and TXB2, was significantly depressed. In inner medulla, Na+ depletion only tended to decrease PGF2 alpha and 6-keto-PGF1 alpha, but in the presence of captopril, the synthesis of all prostanoids was significantly decreased.

6-Ketoprostaglandin F1 alpha↗

PubMed1989

Thrombin inhibits the synthesis of prostanoids by isolated glomeruli and peritoneal macrophages in rats.

Activation of macrophages and release of mediators that activate the coagulation system characterize proliferative glomerulonephritis. To evaluate the possible role of prostanoids in this process, isolated rat glomeruli (G) and peritoneal macrophages (M) or a combination of the two (G + M) were incubated in the presence of thrombin (2 U/ml). In G, thrombin inhibited only the synthesis of thromboxane B2. In M and G + M incubations, the synthesis of prostaglandin I2 and thromboxane A2 was inhibited by thrombin. This effect was abolished by the addition of arachidonic acid. As prostanoids may play a modulatory role in the interaction between macrophages and glomerular cells, inhibition of their synthesis by thrombin might enhance macrophage activity.

6-Ketoprostaglandin F1 alpha↗

PubMed1989

Quantitative method of measuring anti-viral activity of peritoneal dialysis effluent.

We have previously documented the presence of anti-viral activity in the peritoneal effluent of uremic patients treated by peritoneal dialysis. Anti-viral activity was determined by recording the inhibition of the cytopathic effect (CPE) of various viruses on Vero cells in a semi-quantitative manner based on observer's subjective judgment of the degree of inhibition of CPE. This degree of inhibition is a measure of the anti-viral activity. Although peritoneal dialysis effluent (PDE) was consistently seen to inhibit CPE we sought a quantitative method to accurately assess such anti-viral activity. To this end, the CPE of Parainfluenza virus (Para-3) on human kidney (Hu-K) cells was evaluated. The CPE of this virus is manifested by distinct plaques which can be easily counted after staining the tissue culture plate. Eighty-three (83) samples of PDE (0.5 ml) were added to Hu-K cells after which Para-3 was added. As control para-3 on Hu-K was used. The number of plaques obtained by virus control was taken as 100% CPE. The anti-viral activity of PDE was then recorded as the percentage of the CPE shown by virus control and averaged 20.9 +/- 28.6% (p less than 0.001 vs virus control). In addition PDE was diluted down to 1/64 concentration and the inhibitory effect again determined. Percent CPE of undiluted, 1/2, 1/64 PDE samples were 18.11 +/- 24.2, 33.57 +/- 18.16 and 77.93 +/- 17.4% respectively (p less than 0.01 between undiluted and 1/64 PDE). These data reaffirm that PDE possesses an inherent anti-viral activity which can now be quantitatively assessed using Para-3 on Hu-K cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1988

Role of glomerular prostanoid in control of glomerular filtration rate in rats.

It is generally accepted that the main action of glomerular prostanoids (GPs) on glomerular filtration rate (GFR) is to modulate the activity of different vasoconstrictors, specially in states of renal hypoperfusion. However it was also suggested that GPs may directly affect GFR. The present study was focused on this last hypothesis, in different experimental models, in rats. In adriamycin induced acute renal failure, the transient decrease of GFR is associated with higher levels of thromboxane B2. Later on, when GFR returns to normal, vasodilator prostaglandins synthesis was also increased. In captopril induced renal failure in Na depleted rats (where GPs synthesis remained normal), stimulation of PGE2 and PGI2 production by K and NaCl was associated with a significant improvement of GFR. Furthermore, the increase in GFR induced by NaCl was prevented by inhibition of prostaglandin synthesis. Infusion of atrial natriuretic peptide in euvolemic rats induce a marked elevation both of GFR and PGE2 synthesis. It was abolished by previous administration of prostaglandin synthesis inhibitor. In conclusion, glomerular prostanoids may influence GFR, either directly, or as mediator or modulator of other vasoactive hormones.

Acute Kidney Injury↗

PubMed1988

Atrial natriuretic peptide administration to normal and salt depleted rats--effects on digoxin-like immunoreactive factor, aldosterone, ACTH, and renal function.

In view of the known interrelationships between renin, aldosterone, and atrial natriuretic peptide (ANP), we sought to examine whether there also exists an interaction between ANP and digoxin-like immunoreactive factor (DLIF). We therefore studied the effects of ANP administration on normal and salt-depleted rats, and measured the effects on blood pressure, urine output, glomerular filtration rate, sodium excretion, aldosterone, ACTH, and DLIF levels. ANP administration resulted in a significant elevation of sodium excretion and glomerular filtration rate and a fall in blood pressure. DLIF concentrations in plasma rose significantly, as did urinary DLIF excretion. ANP administration resulted in a fall in aldosterone as well as ACTH. These observations suggest that ANP has a direct inhibitory effect on ACTH secretion. Our findings support the concept of an interrelationship between ANP and DLIF.

Adrenocorticotropic Hormone↗

PubMed1988

Transcutaneous monitoring of blood gas tensions in patients on intermittent peritoneal dialysis.

A relative contraindication to intermittent peritoneal dialysis (IPD) is chronic lung disease. To evaluate whether the instillation of 2 L of fluid into the peritoneal cavity affects respiratory function, five IPD patients were studied in the supine position during the first 4 h of a routine IPD session. Blood gas tensions were monitored transcutaneously throughout the study period. At the onset of dialysis, mean transcutaneous blood oxygen tension (PtcO2) was 70.6 +/- 9.1 mm Hg. It decreased to 55 +/- 9.9 mm Hg (22% change from basal values) during the instillation of dialysate. Upon drainage, PtcO2 returned to baseline. This sequence of events repeated itself on subsequent exchanges, although with decreasing decrements of PtcO2 with each consecutive exchange (decrease to 58.6 +/- 7.05, 61 +/- 6.5, 63.8 +/- 5.2 mm Hg corresponding to 16%, 12.7%, and 9.6%, respectively, during the second to fourth exchanges). Transcutaneous blood carbon dioxide tension, PtcCO2, showed a very mild increase during the study (33 +/- 7.1 to 38 +/- 6.0 mm Hg). In two patients, the same study protocol was performed during the last 4 h of an IPD session. In these two patients, there was only a 5% variation of PtcO2 from baseline values. These results suggest that an adaptive response to the hypoxemia induced by dialysate instillation rapidly occurs in IPD patients.

Adult↗