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Biomedical subjects

S O Bohman

Publications and source records attributed to S O Bohman.

At least 37 records · Page 2Linked to original sources
PubMed1989

Markers for pancreas-graft rejection in humans.

Rejection episodes were studied in 15 patients, in whom no kidney graft could serve as a marker for rejection, subjected to pancreas transplantation with pancreatoenterostomy and temporary exteriorization of the pancreatic juice (10 pancreas alone, 3 pancreas after kidney, and 2 combined pancreas and kidney in which the kidney was not functioning.) Twelve patients (80%) had a total of 18 rejection episodes. In the first 11 patients, 13 rejection episodes were diagnosed by a decline in amylase activity in the pancreatic juice, whereas in the next 4 patients, 5 rejection episodes were diagnosed by positive cytology in the pancreatic juice. Neopterin in pancreatic juice and immunoreactive anionic trypsin in serum showed promise as rejection markers, whereas serum neopterin, serum amylase, and serum immunoreactive cationic trypsin did not. Unspecific signs of rejections were an increase in white blood cell count, clinical symptoms such as fever, abdominal pain, and arthralgia. All acute rejection episodes were successfully reversed by antirejection treatment. However, late rejections diagnosed by impaired endocrine function were seen in 6 of the 15 (40%) patients, and the prognoses for these rejections were worse: 4 patients (27%) lost their grafts because of chronic rejections, and 2 patients still had impaired endocrine function.

Amylases↗
PubMed1989

Long-term metabolic control in recipients of segmental-pancreas grafts with pancreaticoenterostomy or duct obstruction.

Metabolic control in recipients of segmental-pancreas grafts with pancreaticoenterostomy (performed in Stockholm) or duct obstruction by polymer injection (performed in Oslo) were compared. The recipients were uremic diabetic patients and also received a kidney from the same donor. Because the patient population in the two Scandinavian countries is very similar and the immunosuppressive protocols used are almost identical, such a comparison seemed reasonable. The number of patients available for study at 1, 2, and 3 yr was 22, 10, and 4, respectively, with duct injection and 28, 10, and 3 with pancreaticoenterostomy. The mean age of the patients was somewhat higher in the Oslo series. There were no significant differences regarding immunosuppression or kidney-graft function as estimated by serum creatinine at 1, 2, and 3 yr. No significant differences were found in fasting blood glucose, glycosylated hemoglobin, and intravenous glucose tolerance between the two groups at 1, 2, and 3 yr.

Adult↗
PubMed1988

Mitotic response to high protein intake in different renal cell types in weanling rats.

We examined the effect of high protein intake on the mitotic response (3H-thymidine incorporation) in the glomerulus, proximal tubule (PT), thick ascending limb of Henle (TAL), distal tubule (DT) and collecting duct (CD) in kidneys from 16- to 24-day-old rats that received an isocaloric diet containing 21% (NP) and 50% (HP) protein from 16 days of age. Nephron filtration rate was also determined. After two days of HP diet, thymidine incorporation (TI) was significantly increased in PT and TAL. After two days on HP diet TI was most pronounced in TAL. After eight days on HP diet TI remained elevated in PT, but not in TAL. HP did not increase TI in DT or CD. The glomerular TI was the same in HP as in NP rats after two and four days on the diet, but was significantly elevated after eight days on HP diet. The nephron filtration rate was increased after two days and remained significantly elevated after eight days on HP diet. The proximal tubule fractional reabsorption was the same in 24-day-old NP and HP rats. We conclude that the results are compatible with the hypothesis that the Na load is a major factor triggering tubular growth after HP intake. Glomerular growth is secondary to increase in nephron filtration rate.

Animals↗
PubMed1988

Experimental depletion of different renal interstitial cell populations.

To define different populations of renal interstitial cells and investigate some aspects of their function, we studied the kidneys of normal rats and rats with hereditary diabetes insipidus (DI, Brattleboro) after experimental manipulations expected to alter the number of interstitial cells. DI rats showed an almost complete loss of interstitial cells in their renal papillae after treatment with a high dose of vasopressin. In spite of the lack of interstitial cells, the animals concentrated their urine to the same extent as vasopressin-treated normal rats, indicating that the renomedullary interstitial cells do not have an important function in concentrating the urine. The interstitial cells returned nearly to normal within 1 week off vasopressin treatment, suggesting a rapid turnover rate of these cells. To further distinguish different populations of interstitial cells, we studied the distribution of class II MHC antigen expression in the kidneys of normal and bone-marrow depleted Wistar rats. Normal rats had abundant class II antigen-positive interstitial cells in the renal cortex and outer medulla, but not in the inner medulla (papilla). Six days after 1000 rad whole body irradiation, the stainable cells were almost completely lost, but electron microscopic morphometry showed a virtually unchanged volume density of interstitial cells in the cortex and outer medulla, as well as the inner medulla. Thus, irradiation abolished the expression of the class II antigen but caused no significant depletion of interstitial cells.

Animals↗
PubMed1988

Back-leak of pelvic urine to the bloodstream.

The aim of the present investigation was to measure the back-leak of pelvic urine to the blood circulation. In normopenic hydronephrotic, dehydrated hydronephrotic and dehydrated control kidneys the back-leak was estimated from a servocontrolled machine which regulated infused saline to keep a present pelvic pressure constant. The disappearance of fluid from the renal pelvis could be measured at different pressure levels, and a pressure-dependent outflow of fluid was found. From these measurements a back-leak conductance could be calculated which proved to be independent of pressure. In the lower pressure range (15-20 mmHg) there was a significantly lower conductance in the dehydrated controls compared with the dyhydrated hydronephrotic kidneys, while in the higher pressure range (25-30 mmHg) no difference was found. From electron microscopical studies the pyelorenal back-leak of fluid in both hydronephrotic and control animals seemed to be most pronounced in the fornix region, as documented by a heavy presence of horseradish peroxidase in the intracellular spaces there. Other experiments with radioactively labelled inulin, which was injected into the pelvic cavity, indicated that most of the back-leak occurred via the renal blood vessels and not through the lymphatic system. The importance of this back-leak was evident from the measurements of the total kidney glomerular filtration rate (GFR) at a slightly increased pelvic pressure, where some of the urine with radioactive tracer flows back to circulation. The back-leak of pelvic urine could also affect the concentration mechanism by removing diluted urine which had flowed over the renal papilla, and through water and urea diffusion increased papillary interstitial osmolarity.

Animals↗
PubMed1988

Focal glomerulosclerosis and nephron atrophy in rats on long-term cyclosporine treatment.

Although acute cyclosporine nephrotoxicity has been extensively studied both in humans and in experimental animals, little has been written about experimentally-induced chronic renal changes after cyclosporine treatment. Groups of rats were therefore given cyclosporin A (CyA), 10 mg/kg pelleted food, for 21, 32 and 66 weeks. This corresponds to a daily CyA dose of 5-6 mg/kg body weight which is comparable to both the minimal immunosuppressive dose in rats and the doses given to patients. Kidney tissue was investigated using light microscopic morphometry and electron microscopy. After 32 wk, mild renal lesions in the form of focal glomerulosclerosis and nephron atrophy were present in the CyA-treated animals but nearly absent in the controls (p less than 0.05). At 66 wk, the changes were extensive in the CyA-treated animals. Similar but much less pronounced changes known as "chronic nephropathy of the rat" were found in the untreated rats. The proportion of glomeruli with segmental lesions was 33% in the CyA-treated animals and 7.5% in the controls (p = 0.014). No significant vascular lesions were found in either group. Electron microscopy confirmed the light microscopic observations but no ultrastructural changes specific for CyA treatment were identified. In conclusion, as with humans, chronic irreversible renal lesions can be induced in the rat by administering moderate doses of CyA over a long period.

Animals↗
PubMed1988

Loss of renomedullary interstitial cells in Brattleboro rats after vasopressin treatment.

Previous studies have shown a disappearance of interstitial cells from the renal medulla of rats with hereditary diabetes insipidus (Brattleboro) when the animals were treated with vasopressin in high doses. The present study was undertaken to elucidate the mechanisms behind this cell loss. The disappearance of interstitial cells from the renal medulla of Brattleboro rats was quantitatively determined by electron microscopic stereology after various types of treatment. A considerable decrease in the volume density of interstitial cells was induced by the administration of either 8-arginine vasopressin or 1-desamino-8-D-arginine vasopressin. This lesion of the interstitial cells was not prevented by the simultaneous administration of oxytocin. Even a 48-hour period of water deprivation also resulted in a slight decrease in the volume density of interstitial cells. The results indicate that the observed loss of renal medullary interstitial cells is not a direct effect of the hormone on the cells but probably secondary to the marked increase in the renal medullary solute (urea) concentration. The fact that animals with hardly any renomedullary interstitial cells concentrated their urine to a virtually normal level shows that these cells cannot play an important role in the concentrating mechanism. The interstitial cells recovered rapidly when the vasopressin treatment was discontinued, but it could not be determined whether this was due to local proliferation or to the immigration of cells from extrarenal tissue.

Analysis of Variance↗
PubMed1987

Development of focal glomerulosclerosis after unilateral nephrectomy in infant rats.

Rats unilaterally nephrectomized in infancy (Nx5) or in adulthood (Nx55) and fed a normal (21%) protein diet were studied at 2, 3 and 6 months after surgery with regard to glomerular filtration rate (GFR) and the development of both albuminuria and focal glomerulosclerosis (FGS) in the remnant kidney. Nx rats were compared with sham-operated animals (S) of corresponding age. The incidence of FGS never exceeded 1.4% in S rats. In Nx5 rats the incidence of FGS was not increased at 2 and 3 months after surgery whereas it was significantly higher (range 10%-27%) than in S rats 6 months after surgery. Urinary albumin excretion was significantly increased in Nx5 rats 2 months after surgery and was even higher 6 months after surgery. In Nx55 rats the incidence of FGS was the same as in Nx5 rats 2, 3 and 6 months after surgery, but urinary albumin excretion was significantly lower than in Nx5 rats 6 months after surgery. The GFR expressed per unit of body weight decreased in both Nx5 and S5 rats from 2 to 6 months, but the decrease was more pronounced in Nx5 rats than in S5 rats. The GFR factored by kidney weight was significantly lower in Nx5 than in any of the other groups at the 6-month follow-up study. We conclude that, as in adults, when unilateral nephrectomy is performed in infancy, FGS will develop in the remnant kidney. More pronounced albuminuria and reduction of GFR may indicate that the glomerular lesion is more severe in rats nephrectomized in infancy than in adulthood.

Aging↗
PubMed1986

Renal interstitial fibrosis and vascular changes. Occurrence in patients with autoimmune diseases treated with cyclosporine.

Histologic examinations of kidney biopsy specimens from six patients with relapsing polychondritis (n = 1), Behçet's syndrome (n = 3), and chronic uveitis (n = 2) were performed after four to 36 months of treatment with cyclosporine. Five of the patients had a variable degree of focal interstitial fibrosis and tubular atrophy, with and without minimal interstitial inflammation. Arteriolar hyalinization was noted in four and glomerular sclerosis in two patients. These renal lesions could not be attributed to underlying autoimmune disease or previous drug therapy but were similar to those recently reported in kidney and heart recipients receiving long-term cyclosporine. The initial cyclosporine doses were 15 mg/kg body weight in one patient and 10 mg/kg in the others. The maintenance cyclosporine doses ranged from 2.5 to 7.5 mg/kg with appropriate trough cyclosporine plasma levels (60 to 130 ng/mL). A rough correspondence between the extent of the histologic renal changes and the cumulative cyclosporine was seen, whereas serum creatinine increase or the development of hypertension during treatment did not predict the degree of interstitial fibrosis or the presence of arteriolar changes. Neither did a rapid fall in the serum creatinine level after withdrawal of cyclosporine exclude focal irreversible renal lesions. Since the histopathologic changes found in the kidneys are potentially progressive, we believe that, until more is known, long-term cyclosporine treatment should be reserved for situations where more established immunosuppression has failed to control an autoimmune process threatening the function of vital organs.

Autoimmune Diseases↗
PubMed1985

Prevention of kidney graft diabetic nephropathy by pancreas transplantation in man.

Kidney graft biopsies were performed 2-3 yr after transplantation in eight type I (insulin-dependent) diabetic patients who had previously been subjected to kidney transplantation (six patients) or combined kidney and segmental pancreas transplantation (two patients). In five of the six patients that had undergone only kidney transplantation, light microscopic examination of the graft biopsy revealed changes compatible with diabetic nephropathy, and electron microscopic morphometry showed a thickening of the glomerular basement membrane (GBM). In the two patients who had been subjected to combined pancreas and kidney transplantation, the kidney graft biopsy showed no light microscopic changes suggestive of diabetic nephropathy, and electron microscopy showed no thickening of the GBM. Thus, it appears to be possible to prevent the recurrence of diabetic nephropathy in human kidney allografts by simultaneous pancreas transplantation.

Adolescent↗
PubMed1984

Interstitial fibrosis in renal allografts after 12 to 46 months of cyclosporin treatment: beneficial effect of low doses in early post-transplantation period.

To investigate whether cyclosporin (CsA) causes chronic renal damage 38 renal allograft biopsies were performed 1 to 4 years after transplantation in 28 CsA-treated patients, in the absence of rejection or acute CsA nephrotoxicity. Blind, semi-quantitative light microscopic examination showed that interstitial fibrosis plus tubular atrophy occurred more often in CsA-treated patients than in patients treated with azathioprine. The degree of interstitial fibrosis correlated with high cumulative CsA dose during the first 6 months of treatment, as well as with the number of acute CsA nephrotoxic episodes, which suggests that the findings are an effect of chronic CsA nephrotoxicity. Maintenance doses of CsA (2.3-10.7 mg/kg/day) seemed to contribute little to the renal damage. The pathogenesis of the observed lesions is not known. A high trough CsA level at the time of biopsy correlated with the degree of interstitial mononuclear cell infiltrate in the renal tissue. The results thus demonstrate chronic morphological changes in renal allografts from CsA-treated patients. Avoiding high CsA doses may be a way of preventing this side-effect. Until this has been confirmed, the risk of chronic renal damage must be taken into consideration when new clinical trials of CsA are being planned.

Acute Disease↗