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Biomedical subjects

B M Iversen

Publications and source records attributed to B M Iversen.

At least 19 recordsLinked to original sources
PubMed1992

[Rapidly progressing glomerulonephritis].

20 patients with rapidly progressive glomerulonephritis were treated at the nephrological section, Medical Department A, Haukeland Hospital from 1973 to 1988. Nine patients had an idiopathic type of nephritis, while seven patients had this type of glomerulonephritis secondary to systemic lupus erythematosus, endocapillary glomerulonephritis, Henoch-Schönleins purpura or Wegener's granulomatosis. Four patients had antibodies to glomerular basement membrane. All renal biopsies showed extracapillary proliferation and tubular cell damage. All patients were given immunosuppressive treatment with corticosteroids and cytotoxic drugs. Nine patients who were admitted to the hospital from 1973 to 1978 were not treated with plasmapheresis, 11 patients from 1978-1988 were all treated with plasmapheresis. After one year of observation, six of the nine patients in the first group had died, while this applied to only two in the group treated with plasmapheresis. Early diagnosis and plasma exchange, in addition to immunosuppression, seems to be the best treatment for these patients.

Adrenal Cortex Hormones↗
PubMed1992

[Severe renal failure during treatment with angiotensin-converting enzyme inhibitors].

Three case histories are described which highlight some of the predisposing risk factors and therapeutic strategies in the event of acute severe renal failure during treatment with ACEI. With appropriate therapy, renal function is usually restored within a few days. Renal artery stenosis, dehydration and diuretics stimulate the renin angiotensin system and make preservation of normal renal function, increasingly dependent on angiotensin II. The prevalence of renal artery stenosis is substantially increased in patients with peripheral vascular disease or with coronary artery disease with concomitant hypertension. Patients should be told about the increased risk of adverse effects to the kidneys if they become dehydrated. In these cases it is essential to reduce the dose diuretics and ACEI, and it may be necessary to give parenteral fluid substitution.

Acute Kidney Injury↗
PubMed1992

Effect of mesangiolysis on autoregulation of renal blood flow and glomerular filtration rate in rats.

Interlobular arteries and afferent arterioles are involved in autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR). The question of whether the contractile mesangial cells are also involved in autoregulation was investigated in Wistar rats. Autoregulation of RBF was examined before and 1 h after infusion of antithymocyte (anti-Thy 1-1) antibodies, and both RBF and GFR autoregulation were examined 30 h after the infusion of antibodies. Mesangial cell destruction was present 30 h after the infusion of antibodies. The angiotensin II-induced contraction of isolated glomeruli (70% of control volume, P less than 0.001) was abolished after the glomeruli had been exposed to anti-Thy 1-1 in vitro. RBF, as well as the lower limit of RBF autoregulation, were not different from control 30 h after the infusion (82 +/- 5 vs. 79 +/- 4 mmHg, P greater than 0.10). Autoregulation of GFR was maintained in the control group but was restricted in the experimental group (autoregulatory index: 0.71 +/- 0.42 for left kidney, 0.02 +/- 0.35 for control; P less than 0.05). The afferent arteriolar diameter was unchanged 30 h after the infusion of antibodies (17.8 +/- 0.8 vs. 17.6 +/- 0.4 microns, P greater than 0.10). One hour after infusion of the antibodies, RBF autoregulation was normal. It is concluded that mesangial cells do not seem to be involved in RBF autoregulation, but may in part influence autoregulation of GFR during pressure reduction.

Angiotensin II↗
PubMed1992

Effect of cyclooxygenase inhibition on renal blood flow autoregulation in SHR.

The effect of acute and chronic indomethacin treatment on renal blood flow (RBF) autoregulation was studied in 10- and 40-wk-old spontaneously hypertensive rats (SHR). RBF autoregulation was substantially reduced in 40-wk-old SHR both during acute and chronic indomethacin treatment, whereas no effect was seen in the young SHR. The pressure range of autoregulation was 169 +/- 9 to 130 +/- 5 mmHg in the untreated 40-wk-old SHR, and 154 +/- 14 to 146 +/- 6 mmHg in indomethacin-treated 40-wk-old SHR (P less than 0.001). Indomethacin treatment had no effect on control RBF, mean arterial pressure, or renal vascular resistance in the 40-wk-old SHR. After removal of the renal nerves, RBF autoregulation during indomethacin treatment was restored in 40-wk-old SHR. The pressure range of RBF autoregulation was 158 +/- 7 to 142 +/- 7 mmHg in sham-operated animals, significantly different from the denervated 40-wk-old SHR, where RBF was autoregulated from 150 +/- 5 to 118 +/- 6 mmHg (P less than 0.01) during indomethacin treatment. The afferent arteriolar diameter (DAA) was studied by the microsphere method in 10-wk-old SHR and in untreated and indomethacin-treated 40-wk-old SHR. DAA was significantly greater in 40-wk-old compared with 10-wk-old SHR (22.1 +/- 0.4 vs. 17.9 +/- 0.5 microns) (P less than 0.01), whereas indomethacin treatment in 40-wk-old SHR did not influence the DAA significantly (21.5 +/- 0.3 microns, P greater than 0.10).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Acute effect of passive Heymann nephritis on renal blood flow and glomerular filtration rate in the rat: role of the anaphylatoxin C5a and the alpha-adrenergic nervous system.

In earlier studies, we have shown that induction of passive Heymann nephritis (PHN) by intrarenal infusion of anti-Fx1A antibodies provokes an immediate fall in renal blood flow (RBF) and glomerular filtration rate (GFR). This was probably mediated via the complement system, as infusion of the F(ab')2 fraction of anti-Fx1A did not reduce RBF and GFR. In the present study, the effects of alpha-adrenergic blockade upon the acute hemodynamic changes during induction of PHN and of C5a infusion were studied. Group 1 was infused with anti-Fx1A antibodies during blockade of the sympathetic nervous system with the alpha-blocker phentolamine; control animals were treated similarly, but infused with normal rat IgG. Group 2 was infused with the anaphylatoxin C5a, normally produced during complement activation, and compared with control animals infused with saline. In group 1, RBF did not differ from control animals after the infusion of anti-Fx1A antibodies (6.6 +/- 0.5 compared to 7.3 +/- 1.0 ml/min/g in the controls). GFR in the left, antibody-infused kidney fell compared to controls, and was 0.25 +/- 0.08 ml/min/g at the end of the experiment compared to 0.60 +/- 0.13 ml/min/g (p less than 0.05 with Student's t test, p = 0.07 with two-way analysis of variance (ANOVA). GFR in the right kidney remained unchanged compared to controls. In group 2, C5a induced a significant fall in RBF (from 7.9 +/- 0.9 to 3.1 +/- 0.4 ml/min/g kidney weight), significantly different from control animals where it fell from 8.1 +/- 0.5 to 6.8 +/- 0.7 ml/min/g (p less than 0.0001 with two-way ANOVA, p less than 0.001 with t test).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Increased total body fat during PD treatment.

UNLABELLED: Sufficient nutritional intake is important to adjust the increased catabolic rate in uremic patients during dialysis treatment. Increased glucose absorption during PD treatment may, however, interfere with the amount of muscle- and fat-mass in the body. We have therefore studied the amount of total body fat composition in 8 male PD patients (treatment period 79 months, range 3-23 before and 165.5 months, range 8-35.5 after the study). Food intake was recorded for 7 days twice in four patients with an interval of 6-8 months. Total body fat (%) was measured by means of a computerized model of near infrared interactance (IRI) ("FUTREX") on the dominant upper arm. The energy and protein intake were 1731 +/- 292 kcal. and 86.9 +/- 17.2 g (n = 4) during the first recording period of food intake. In the second period the energy and protein intake were 1676 +/- 105 kcal and 72.7 +/- 10.2 g (n = 4) (NS). The total body fat increased from 19.8 +/- 2.9 to 22.5 +/- 3.0 (p < 0.05), in spite of unchanged total body weight. CONCLUSION: PD patients seem to accumulate fat during PD treatment with glucose as osmotic agent. This may influence the cardiovascular risks. The results indicate nutritional adjustments and possibly also increased physical activity.

Adipose Tissue↗
PubMed1992

Glomerular hemodynamics in progressive renal disease.

A descriptive survey of renal hemodynamics in the major experimental models of progressive renal disorders (primary loss of renal tissue, primary glomerular injury and primary hypertension) is given. Although the pathogenesis in the different models differs in several respects, increases in glomerular capillary pressure and renal growth factors are important for the development of progressive renal disorders. In primary glomerular disorders, interstitial immune reactions seem to be critical. In glomerular nephritis with increased capillary wall thickness, the increase in glomerular capillary pressure may be of less importance than in other models. A third important factor for progression of renal disorders is a gradual breakdown of autoregulation of renal blood flow and glomerular filtration rate exposing the glomerulus to the variations in systemic blood pressure.

Animals↗
PubMed1991

Acute effect of passive Heymann nephritis on renal blood flow and glomerular filtration rate in rat: the effect of infusion of F(ab')2 fraction of anti-FX1(A) antibody.

We have earlier shown that there is an immediate fall in renal blood flow (RBF) and glomerular filtration rate (GFR) during induction of passive Heymann nephritis (PHN) by infusion of rabbit antibodies towards rat renal brush-border antigens (anti-Fx1A). To investigate the role of complement activation in this stage of the disease, we infused the F(ab')2 fraction of anti-Fx1A (aFFab) in one group of rats and the F(ab')2 fraction of normal rabbit IgG in another group (controls). aFFab produced no hemodynamic changes when compared to controls. Sixty minutes after infusion of aFFab, RBF was 5.7 +/- 0.4 ml/min/g kidney weight (control 7.3 +/- 1.0, NS), after anti-Fx1A RBF was 3.2 +/- 0.7, p less than 0.05 compared to control. GFR after infusion of aFFab was 1.0 +/- 0.1 ml/min/g (control 0.8 +/- 0.1, NS), after infusion of anti-Fx1A 0.2 +/- 0.1 (p less than 0.02 compared to control). The blood pressure was unaffected by aFFab infusion, while there was a temporary fall in blood pressure to a minimal value of 76 +/- 4 mm Hg 10-20 min after infusion of anti-Fx1A (p less than 0.01 compared to control). Immunofluorescence studies showed granular immune deposits in the subepithelial region of the glomerular basement membrane as shown after infusion of anti-Fx1A antibodies. In addition, fluorescence was seen in the brush-border of proximal tubuli. The results indicate that the immediate fall in RBF and GFR during induction of PHN in mediated via activation of the complement system.

Animals↗
PubMed1991

CAPD in patients above 70 years of age.

This report shows our experience with 13 patients aged 70-83 years who started CAPD treatment 1981-1989. There were 7 females and 6 males. The total treatment time was 298 months (range 4-104). Nine of the patients were able to perform all CAPD procedures while 4 patients needed some help. The patients who were able to take care of all procedures had the lowest period of terminal care, i.e. the period preceding death when the patients had to be taken care of by the hospital staff. The terminal care period was 5.1% of the total treatment period. In the patients who needed help from the beginning of the treatment, the terminal care was 17.2% of the total treatment period. The frequency of peritonitis was 1 per 10.2 treatment month. The main cause for hospitalization was peritonitis and terminal care at the end of the lives of the patients. No patients died due to peritonitis. However, two patients were transferred to hemodialysis due to recurrent peritonitis and ultrafiltration loss, one was transplanted and one was transferred to IPD due to weakness. The causes of death were myocardial infarction, cerebral stroke and cardiac insufficiency. No deaths were due to peritonitis. CAPD in patients above 70 years of age is acceptable both on the basis of the somatic situation and of quality of life.

Activities of Daily Living↗
PubMed1990

[Treatment of heart failure with angiotensin converting enzyme inhibitors].

Stimulation of the renin angiotensin system, catecholamines and antidiuretic hormone causes prominent vasoconstriction in severe heart failure. Angiotensin converting enzyme inhibitors reverse these effects, and thus ameliorate cardiac function and reduce mortality in severe heart failure. Angiotensin II is an important regulator of renal function in diseases with renal hypoperfusion, and treatment with angiotensin converting enzyme inhibitors may cause a serious decrease in glomerular filtration and hyperkalemia. Asymptomatic heart failure, acute heart failure and acute myocardial infarction are areas where angiotensin converting enzyme inhibitors may prove beneficial in the future.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Renal blood flow and glomerular filtration rate during the heterologous phase in passive Heymann nephritis in rats.

When passive Heymann nephritis (PHN) is induced by infusion of antibodies (anti-Fx1A), an acute fall in renal blood flow (RBF) and glomerular filtration rate (GFR) has been reported. Activation of the complement cascade by the local antigen-antibody reaction might be involved in this reaction. We therefore studied RBF and GFR during acute infusion of anti-Fx1A and after 3 days when heterologous antibodies are no longer present in the circulation. Two groups of rats were infused with 2 mg anti-Fx1A antibodies into the left renal artery; RBF was measured by the microsphere method and GFR by 125I-Na-iothalamate clearance. In the first group, the measurements were made 40 min after the infusion, and in the second group after 3 days. A third group was studied 3 days after infusion of 1 mg anti-Fx1A. Animals infused with normal IgG were used as controls. Forty minutes after infusion of 2 mg anti-Fx1A, GFR in the left kidney was reduced from 1.16 +/- 0.07 to 0.41 +/- 0.16 ml/min/g in the controls (p less than 0.05). Three days after the infusion, GFR was 1.04 +/- 0.07, not significantly different from control. RBF was reduced to 3.97 +/- 1.11 ml/min/g after 40 min, compared to 7.53 +/- 0.73 in controls (p less than 0.05), and was normalized after 3 days. The effect of 1 and 2 mg anti-Fx1A antibodies was not significantly different after 3 days. Anti-Fx1A antibodies were detected in serum in the acute stage, but not after 3 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Glomerular CR1 express in situ cofactor activity for degradation of C3b.

Adherence of sheep erythrocytes (E) sensitized with IgM antibodies (A) and C3b (EAC3b) to C3b/C4b receptors (CR1) in cryostat sections of human renal glomeruli was studied using the closed chamber technique. The adsorption was stable for at least 3 h at 37 degrees C. In the presence of purified factor I, the indicator cells, however, detached from the sections after 30 min at 37 degrees C. Factor H was not required. The release was not due to loss of CR1 activity in the tissue. The detached indicator cells were negative in the immune adherence test and were agglutinated by antibody to C3d, but not by antibody to C3c. Western blot of the detached indicator cells revealed the presence of C3d and C3c was found in the chamber fluid. Accordingly, detachment of the indicator cells was due to degradation of C3b to C3d with the release of C3c into the chamber fluid. Protease inhibitors did not prevent the detachment of the indicator cells. EAC3b incubated with sections of renal glomeruli preincubated with anti-CR1 antibody were not degraded. The results therefore indicate that CR1 in situ in renal glomeruli can provide the necessary cofactor activity for factor I-mediated degradation of C3b to C3d and C3c.

Complement C3b↗
PubMed1989

[Membranoproliferative glomerulonephritis].

During the period 1981-1986, membranoproliferative glomerulonephritis was demonstrated in ten patients admitted to the Medical Department, Haukeland Hospital. At the time of the diagnosis all patients had proteinuria and hematuria, and six of them had renal failure. Seven patients exhibited nephrotic syndrome and three patients developed progressive renal failure during the observation period. Three patients died during the follow-up period. Four patients were treated with Cyclosporine A and corticosteroids. With this therapy the proteinuria disappeared in two of the patients with nephrotic syndrome. Immunosuppressive treatment may be tried if the disease shows signs of progression. We believe that some of these patients may benefit from cyclosporine A.

Cyclosporins↗
PubMed1989

The acute effect of passive Heymann nephritis on renal blood flow and glomerular filtration rate in rats.

The acute renal hemodynamic changes during induction of passive Heymann nephritis (PHN) may be of importance for the understanding of the pathogenesis of this model. We studied the renal blood flow (RBF) and glomerular filtration rate (GFR) during and after infusion of anti-FxlA into the left renal artery of rats for 10 min. 3 control groups were given 0.9% NaCl, 1 and 2 mg of normal rabbit IgG, respectively. The experimental groups were given 1 and 2 mg IgG fraction of anti-FxlA. Compared to controls, both RBF and GFR were substantially reduced during the first 20-30 min after infusion and remained unaltered for the rest of the observation period. After 20-30 min, RBF in the 1-mg group was 4.8 +/- 0.77 ml/min/g kidney weight versus control, 6.4 +/- 1.23 (NS), and in the 2-mg group, 3.5 +/- 0.65 ml/min/g versus control, 6.4 +/- 1.07 (p less than 0.05). Similarly, in the 1-mg group, GFR was 0.40 +/- 0.08 ml/min/g versus control, 0.76 +/- 0.11 (p less than 0.05), and in the 2-mg group, 0.14 +/- 0.05 versus control, 0.77 +/- 0.12 (p less than 0.0001). The reductions were greater in the 2-mg than in the 1-mg infused experimental groups, but this difference did not reach statistical significance. Immunofluorescence showed typical granular fluorescence of rabbit IgG along the glomerular basement membrane, and electron microscopy showed subepithelial immune deposits. This indicates that in the initial phase of PHN, corresponding with the formation of immune complexes, a pronounced fall in RBF and GFR occurs.

Animals↗
PubMed1988

Changes in lysosome populations in the rat kidney cortex induced by experimental proteinuria.

1. Experimental proteinuria (262.9 mg protein/24 hr urine) was induced in rats by repeated intraperitoneal injections of BSA. 2. Hypertrophy of the kidney cortex was significant 8 days after the start of the BSA injections, and the activities of lysosomal enzymes in kidney cortex and urine were significantly higher in proteinuric compared to nonproteinuric rats. 3. Lysosome populations in the kidney cortex were examined by rate sedimentation of the homogenate and by rate zonal and isopycnic centrifugation of the lysosome-rich ML fraction. 4. The activity of lysosomal enzymes in the kidney cortex increased slightly, essentially in the large, fragile lysosomes mainly recovered from the proximal tubule. 5. Proteinuria induced a shift/reduction in the density of small lysosomes from 1.235 and 1.20 g/ml to 1.225 and 1.185 g/ml, respectively. 6. Proteinuria induced a new population of small lysosomes (density 1.185 g/ml) enriched in cathepsin D.

Animals↗
PubMed1988

Effect of fasting on lysosomes in kidney cortex of glomerulonephritic rats.

The effect of food restriction (FR) on the kidney cortex lysosomes prepared by rate and isopycnic zonal centrifugation was studied in rats with passive Heymann glomerulonephritis (PHN). FR reduced the renal mass by 41%, but the capacity for handling of labelled endocytosed proteins by the lysosomes was not different from fed PHN rats. While PHN with heavy proteinuria increased the recovery of lysosomal enzymes in the large lysosomes located in the proximal tubule, no changes were observed in FR-PHN rats in spite of significant proteinuria. The density of the small lysosomes was significantly shifted/reduced (from 1,200 and 1,235 g/ml to 1,185 and 1,225 g/ml, respectively) in both fed and FR-PHN rats, suggesting that the handling of extra loads of protein may enhance the absorptive function of small lysosomes found in the lower part of the nephron. FR reduced the mechanical fragility of lysosomes in the kidney cortex of PHN-rats. The highly increased urinary excretion of lysosomal enzymes in fed PHN rats was not observed in FR-PHN rats. As a conclusion, FR reduces both the fragility of lysosomes and the proportion of digestive enzymes in fragile lysosomes. These lysosomal enzymes may be of pathogenic importance in PHN causing cell damage when liberated from disrupted lysosomes.

Animals↗