Kidneys transplanted in Göteborg, 1985 to 1990.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
L Karlberg
Publications and source records attributed to L Karlberg.
Modal DNA values and estramustine-binding protein (EMBP) as prognostic markers in prostatic cancer.
In this study, we have investigated the model DNA values and the expression of estramustine-binding protein (EMBP) in formalin-fixed and paraffin-embedded TUR specimens from 76 untreated patients with prostatic cancer. In addition, specimens from 13 patients were analyzed for tumour EMBP expression only. Ploidy was measured as diploid, tetraploid and non-tetraploid aneuploid or aneuploid in the near-diploid region. All patients had been referred during 1978-1981, and were subjected to TUR due to urinary obstruction. Survival data were obtained for all patients through March 1988. Statistical analyses were performed using a Cox's regression model with respect to survival and cause specific survival and correlated to the DNA pattern and the expression of EMBP. The existence of a near-diploid aneuploid cell population as well as poor differentiation grade were both statistically significantly correlated with poor survival. Near-diploid aneuploid cell lines were seen in 9/76 (12%) of the patients and were also seen in well differentiated cancers (4/17). The expression of EMBP was most abundant in the moderately differentiated cancers. However, all prostatic cancer specimens investigated were positive for the antigen. Patients with poorly differentiated carcinomas and high EMBP expression showed a tendency towards better prognosis than those with poorly differentiated carcinomas and low EMBP expression. The present patient material was, however, too small to show a statistically significant correlation between EMBP and survival.
Aged↗
[Cholesterol screening in a healthy father of 4 children--an ethical dilemma for the district physician].
Explore the source record for details and available documents.
Adult↗
Expression of estramustine-binding protein (EMBP) and the proliferation-associated antigen Ki-67 in prostatic carcinomas.
The expression of EMBP and the proliferation-associated antigen Ki-67 was studied in in vitro cultured prostatic carcinoma cells and in tumor tissues removed by transurethral electroresection (TUR). EMBP was found to be expressed predominantly in the moderately differentiated carcinomas. A technique based on the immunohistochemical analysis of fine needle specimens was also evaluated. This technique is of potential interest in prospective studies and in monitoring the effect of therapy. Ki-67 was found to be expressed in the prostatic carcinoma cell line (DU-145) studied, as well as in TUR specimens. This antigen reflects the proliferative characteristics of the tumor and may prove useful with respect to prognostic information and choice of appropriate therapy.
Antibodies, Monoclonal↗
Renal vasodilation after unilateral renal ablation.
Renal blood flow was studied in rats 120 minutes after unilateral renal ablation. The influence of endogenous prostaglandin formation was evaluated by indomethacin treatment prior to the ablation. Radioactive microspheres were used for estimation of the total renal and cortical blood flow, and the renal medullary blood flow was determined with the 86-Rb chloride extraction method. The total blood flow in the remaining kidney was increased by 80% following contralateral ablation, with augmentation in all areas, particularly in the deep medullary region. Indomethacin treatment in intact rats evoked increased blood flow as compared with the indomethacin control group. The results indicated that the renal blood vessels respond to ablation of the contralateral kidney with dilation in all kidney regions, and that this vascular dilation may be prostaglandin-mediated.
Animals↗
Total and regional renal blood flow during complete unilateral ureteral obstruction.
Regional renal blood flow was investigated after 1, 2, 12 and 24 h of unilateral ureteral obstruction in rats. Total renal and cortical blood flow rates were determined by the microsphere technique and regional medullary blood flow by the 86-Rb extraction method. The kidneys were microdissected into cortex and medulla, which was further divided into the outer stripe and the inner stripe of the outer zone, and the inner zone. In the obstructed kidneys cortical blood flow increased by 33% after 1 h of obstruction, but was normalized after 2 h. After 12 and 24 h this flow was significantly decreased (55% and 65% of control respectively). The pattern of total renal blood flow was similar to that of cortical blood flow. In the outer stripe there was an initial increase (44%) after 1 h, but later no significant deviations from control values were found. After 1 h of obstruction the blood flows in the inner stripe and the inner zone were not significantly different from control values. A significantly decreased blood flow was seen in the inner stripe after 2 h (57% of control) and in the inner zone after 12 h (58% of control). A significant recovery of the blood flow had occurred in the inner stripe and the inner zone after 24 h of obstruction. In the contralateral, non-obstructed kidney no significant changes were found, besides an increased innerstripe blood flow after 24 h of UUO.
Animals↗
Impaired medullary circulation in postischemic acute renal failure.
Acute renal failure was induced in heparinized rats by clamping the renal artery for 45 min. Ten minutes after recirculation the intrarenal blood flow distribution was measured. For this purpose labelled microspheres were injected together with 86-Rb chloride. The microspheres were used for determination of cardiac output, total renal and cortical blood flow, and 86-Rb for calculations of medullary blood flow. Total renal blood flow was reduced from 7.6 to 3.8 ml . min-1 . g-1 and cortical blood flow was reduced from 11.7 to 7.0 ml . min-1 . g-1. In the outer stripe of the medulla there was a reduction from 2.5 to 1.4 ml . min-1 . g-1. In the inner stripe there was a more pronounced reduction from 1.8 to 0.2 ml . min-1 . g-1 and in the inner zone from 0.8 to 0.1 ml . min-1 . g-1. The marked reduction in the blood flow to the renal medulla after recirculation is suggestive for a medullary ischemia, which might be responsible for the characteristic dysfunctions in acute renal failure.
Acute Kidney Injury↗
Postischemic renal failure. Intrarenal blood flow and functional characteristics in the recovery phase.
Intrarenal blood flow, nephron function and whole kidney function were studied in the recovery phase of acute failure induced by 45 min of warm ischemia. Analyses were made 24 h, 7 days and 28 days after the ischemic insult. At 24 h the total renal blood flow was 4.0 ml . min-1 . g-1, decreasing to 1.2 within one week. After four weeks it was normalized to 3.4 ml . min-1 . g-1. The intrarenal blood flow distribution, studied with the 86-Rb extraction method, showed the same pattern of response, with no signs of a persistent heavy reduction in the deeper parts, as was found 10 min after recirculation (Karlberg et al. 1982 a). The contralateral, nonischemic kidney responded with hyperemia in all areas 24 h after the trauma, but after 7 days the values were normal. The function of the superficial nephrons was studied with the micropuncture technique. In the initial phase mainly obstructed nephrons were found, but after four weeks the nephrons were essentially normal. After 24 h the postischemic kidneys were anuric but at 7 days urine production had started and the GFR was 0.1 ml . min-1; this improved to 0.55 ml . min-1 after 4 weeks.
Acute Kidney Injury↗
Renal medullary blood flow studied with the 86-Rb extraction method. Methodological considerations.
The 86-Rb extraction method was applied for a study of regional renal blood flow. In the cortex, a sampling time of 30 s led to an underestimation by about 15% as compared with the microsphere method. This was due to incomplete cortical cellular extraction of rubidium with subsequent rapid wash-out the tracer. In the renal medulla, a sampling of 30-60 s gave valid data with almost complete extraction. A sampling time of only 10 s, i.e. a time similar to the intravascular transit time, gave rise to a 50% underestimation of the inner medullary blood flow. Errors due to transport of rubidium by the tubular fluid were investigated in detail. A theoretical analysis based on equilibrium data revealed a maximal error of about 5%. Studies with micropuncture of distal tubules and studies of the urinary transport showed no or negligible contamination from tubular urine. Under control antidiuretic conditions the blood flow in the cortex was 5.2 +/- 0.2 ml . min-1 . g-1 (mean +/- SE, n = 16), in the outer stripe of the outer zone 2.2 +/- 0.1, in the inner stripe 1.5 +/- 0.1 and in the inner zone 0.69 +/- 0.06.
Animals↗
Hemodynamic alterations in ischaemic acute renal failure.
It is concluded that the condition of 'acute renal failure' starts in the first minutes after restoration of the circulation, following the ischemic period. The aggregation of red blood cells in the renal medulla with the subsequent cessation of medullary blood flow represents an important factor causing both the reduced urinary concentrating ability and the depressed urinary potassium concentration. The persisting medullary ischemia leads to cellular swelling and eventually to cell necrosis, which in turn results in a mechanical obstruction of the tubular lumen in the region of the loops of Henle and the medullary collecting ducts. In contrast, the anuria which is evident weeks after the primary damage, seems to be caused by the release of vasoconstrictor principles, whose origin is unclear, but it seems not to be mediated via the renal nerves, since the same symptoms are found in transplanted kidneys. Therapeutic endeavors using heparin, saline expansion and mannitol to improve the rheological characteristics of the blood seems to be of limited value. Infusion of hyperoncotic albumin during the ischemic period, however, seems to be of some benefit, since glomerular filtration is better preserved. The addition of ATP and magnesium, glucose or adjustment of the acid base status with buffers has not been encouraging in the present models, in which glomerular filtration rate is reduced to only a few percent of control.
Acute Kidney Injury↗
Nephron function in postischemic acute renal failure.
Acute renal failure was induced in rats by clamping the renal artery for 45 min. After reestablishing renal blood flow, tubular heterogeneity was observed, with (1) seemingly normal tubules, (2) dilated tubules and (3) collapsed tubules. Micropuncture techniques were used to examine the hydrostatic pressures in the different nephrons and superficial vessels, and also to determine single nephron glomerular filtration rate. The dilated tubules showed minimal filtration, due to an elevated intratubular pressure probably caused by obstructions; in these nephrons filtration could be induced by lowering the intratubular pressure. In the "normal" nephrons there was some filtration, as the proximal tubular pressure was only moderately increased. No filtration took place in the collapsed type, probably as a result of glomerular ischemia and consequently decreased glomerular capillary pressure. The kidneys also exhibited isosthenuric polyuria with a reduced potassium secretion. It is suggested that a medullary ischemia will lead to interstitial and intracellular edema and eventually cell necrosis with subsequent formation of obstructions in the loops of Henle. The obstructions would explain the increase in proximal tubular pressure and the decrease in total kidney filtration to about 5% of the normal. It is proposed that the deficient urine concentration ability and the inhibited potassium secretion are caused by the ischemic damage to the renal medulla.
Acute Kidney Injury↗
Erythrocyte and albumin distribution in the kidney following warm ischemia. A study in rats.
A dark zone of probably stagnant erythrocytes, localised primarily to the inner stripe of the outer medulla, is always found in acute renal failure caused by clamping of the renal artery for 45 min. To test the possible accumulation of red cells, the regional renal red cell content was investigated with 51Cr labelled red cells injected before, during and 10 min after the recirculation. Analyses were made of the volumes of (1) cells remaining from the period of clamping, (2) cells aggregated 0--10 min after recirculation and (3) cells still circulating 10--20 min after recirculation. In the inner stripe the total red cell volume was 21.8 +/- 2.2 microliter . 100 mg-1 (control value 9.3 +/- 0.6), where 26% remained from the period of clamping, 46% had accumulated 0--10 min after recirculation, and only 28% had entered the region 10--20 min after recirculation. The same pattern of response, though less pronounced, was also found in the inner zone. In the cortex the total red cell volume was 6.3 +/- 1.2 microliter . 100 mg-1 (control value 4.4 +/- 0.3), where 24% remained from the period of clamping, 32% were accumulated and 44% remained circulating. The plasma volume as investigated from 131I-labelled albumin was markedly increased in all zones, probably due to extravasation of the tracer. It is suggested that red cell accumulation plays an important role for the medullary ischemia found in ischemic acute renal failure.
Acute Kidney Injury↗