Diagnostic value of antegrade pyelography in renal transplants: a comparison of imaging modalities.
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Biomedical subjects
Publications and source records attributed to B Grabensee.
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In a prospective randomized open multicenter study, 107 anemic (Hct < = 28%) peritoneal dialysis (PD) patients were treated with s.c. rhEPO daily. The mean observation period was 299 days (range 14-479 days). Patients were randomly assigned to 3 groups with different initial doses: 5 U/kg (G5), 10 U/kg (G10), 20 U/kg (G20). Initial doses were maintained for at least 8 weeks unless the target Hct (30-35%) was achieved earlier. The weekly increase of Hct was significantly (p < 0.05) dose-dependent: 0.19% in G5, 0.5% in G10 and 0.94% in G20. In case of insufficient response (< 0.5% per week), the dose was doubled every 4 weeks. Final doses on achieving the target Hct ranged from 5 to 40 U/kg (median 20 U/kg). The dose was then reduced to 50% and adjusted individually. The median maintenance dose was 9.9 U/kg/day. No tendency towards higher blood pressure or intensification of antihypertensive treatment was observed. When rhEPO is administered daily, 10 U/kg/day (70 U/kg weekly) is the recommended starting dose. The need for higher doses used in unsatisfactory response, should lead to further examination to rule out iron deficiency and other reasons for non-response. The median maintenance dose reported here is the lowest published in the literature for PD patients and seems to be linked to the daily injections.
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30 patients with an acute build-up of renal transplant were examined comparatively via antegrade pyelography (AP), computed tomography (CT) and sonography (SONO). In the proof of obstructions and compressions of the ureter of renal transplant, antegrade pyelography was superior to sonography and computed tomography. Perirenal collections of fluids were recognised correctly via sonography by 73% (11/15) and computed tomography by 87% (13/15). The computer tomogram is superior in the differentiation of perirenal collection of fluids. In establishing proof of the cause of an acute build-up of renal transplant it was evident that computed tomography with a sensitivity of 64% and a specificity of 94% was slightly superior.
The aim of the study was to determine the influence of ciclosporin (Cs) on prostacyclin and thromboxane generation. Four groups of patients were studied. Group 1: Controls, n = 10. Group 2: Patients without kidney disease treated with Cs, n = 10. Group 3: Patients after transplantation treated with azathioprine, n = 10. Group 4: Renal transplant recipients receiving Cs, n = 10. Parameters investigated: CIn, CPAH, TxB2 in plasma, serum and urine; 6-oxo-PGF1 alpha in plasma and urine, urinary 2,3-dinor-TxB2 excretion. CPAH and CIn were significantly decreased during Cs treatment. Plasma TxB2 levels were enhanced in patients without kidney disease receiving Cs (group 2) amounting to 189 +/- 106 pg/ml as compared to 12 +/- 4 pg/ml in controls (group 1). In patients without kidney disease (group 2), plasma 6-oxo-PGF1 alpha was increased (20 +/- 9 pg/ml) as compared to controls in group 1. Plasma TxB2 and plasma 6-oxo-PGF1 alpha were increased in renal graft recipients without any difference due to different immunosuppressive drugs. Treatment with Cs was associated with impaired renal function and resulted, in patients without kidney disease, in elevated plasma TxB2 and plasma 6-oxo-PGF1 alpha. This effect could not be proven in renal graft recipients. We suggest that the deleterious effect of Cs on kidney function is presumably not paralleled by corresponding changes in prostaglandin and thromboxane formation.
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The clinical clues of sudden arterial hypertension, acute pain in the side, proteinuria, hematuria, abdominal bruits and renal failure are suspicious for spontaneous dissection of the renal arteries, even in the absence of one or more of the above-mentioned symptoms. To confirm the diagnosis and to provide appropriate therapy, immediate renal arteriography is mandatory, otherwise acute loss of renal tissue may occur. We report on one patient with spontaneous dissection of the renal arteries.
Aggressive immunosuppression in kidney transplantation increases the risk of opportunistic infections. We report ten cases of pneumocystis carinii pneumonia in a group of 420 kidney recipients (2.1%). All patients showed a severe--hyperacute--course of the infection. One patient required mechanical ventilation. In all cases the diagnosis could be established applying fibreoptic bronchoscopy with lavage and partly using transbronchial biopsy. The therapy consisted of intravenous cotrimoxazole and inhalation of pentamidine. All patients survived even after severe course of the disease. Graft explantation for saving patients was not necessary.
210 patients receiving antihypertensive treatment underwent non-invasive ambulatory blood-pressure monitoring for the first time. 44 suffered from chronic renal failure, 51 had been renal transplanted, 36 had chronic glomerulonephritis, 36 had renovascular hypertension, and 43 had essential hypertension with severe end-organ damage. We analyzed the Circadian rhythm and the rate of insufficient antihypertensive treatment. While mean daytime systolic and diastolic blood pressure were not different between groups, patients with chronic renal failure, renal transplant or glomerulonephritis showed a very high rate (95-72%) of absent nighttime blood-pressure reduction. In patients with renovascular hypertension or complicated essential hypertension there was a lower rate (69-40%) of absent nighttime blood pressure reduction. The ambulatory blood-pressure monitoring led to a modification of antihypertensive treatment in 78% of patients because of nighttime hypertension. We think that ambulatory blood-pressure monitoring is an essential tool for physicians treating patients with renal disease or complicated essential hypertension.
Long-term administration of ciclosporin has been complicated by side-effects, the predominant being nephrotoxicity. We performed renal function studies on 20 patients treated with ciclosporin (group 1) and on 12 patients serving as controls (group 2). Only patients with serum creatinine less than 1.3 mg/dl entered the study. The renal function studies consisted of: Inulin clearance, PAH clearance, sodium sulphate loading, sodium bicarbonate loading. Plasma renin activity (PRA), inactive renin (IR) and aldosterone (ALDO) were measured basally and after stimulation with 40 mg furosemide i.v. Serum creatinine was not significantly impaired under ciclosporin with 1.1 +/- 0.1 mg/dl vs 0.9 +/- 0.1 mg/dl in the control group (ns). Glomerular filtration rates as measured by creatinine and inulin clearance were significantly impaired in group 1 as compared to group 2. Inulin clearance was impaired by ciclosporin with 93.5 +/- 4.4 ml/min/1.73 m2 as compared to 121 +/- 6.6 ml/min/1.73 m2 (p less than 0.05) in patients of group 2. The PAH clearance in ciclosporin treated patients was impaired, with 379 +/- 22.1 ml/min/1.73 m2 in group 1 as compared to 605 +/- 39 ml/min/1.73 m2 (p less than 0.001) in group 2. Mean arterial pressure and renovascular resistance were significantly increased in ciclosporin treated patients. We demonstrated, by means of sodium sulphate and bicarbonate loading, incomplete distal tubular acidosis in 3 patients from group 1 but in none of group 2. There was no difference in basal plasma renin activity (PRA), but during volume contraction induced by furosemide there was only blunted response by PRA in patients receiving ciclosporin with 2.7 +/- 0.3 ng/ml/h as compared to 7.7 +/- 0.5 ng/ml/h in controls.(ABSTRACT TRUNCATED AT 250 WORDS)
A patient, born in 1968, was found at the age of 9 years to have Alport's syndrome. In his 20th year, when in terminal renal failure, his father's kidney was transplanted into him. 14 months later there was a sudden worsening of his renal function after a varicella infection; for the first time antibodies against the glomerular basal membrane (GBM) were detected. Despite an increase in prednisolone dosage and 6 plasmaphereses chronic haemodialysis again became necessary. Renal biopsy revealed necrotizing intra- and extracapillary glomerulonephritis. Simultaneously there was a raised anti-NC-1-antibody titre (1:80) in the serum. After removal of the transplant the titre fell to normal. The NC-1 antigen, a component of the GBM in healthy persons, may be absent in Alport's syndrome. An analysis of the few cases of anti-GBM glomerulonephritis in renal transplants of patients with Alport's syndrome may make it possible to recognize factors which precipitate or favour this form of glomerulonephritis.
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A prospective study of 45 consecutive patients (27 men, 18 women, mean age 42 [22-64] years) who had undergone allogeneic renal transplantation was carried out to ascertain whether rejection of the graft can be detected by routine follow up with colour-coded Doppler ultrasonography even in the presence of acute renal failure requiring dialysis. Conventional diagnostic methods detected 44 episodes of rejection in 33 patients: 26 of these arose in 18 patients with acute renal failure requiring dialysis and 18 in 15 patients who did not require dialysis. Colour-coded Doppler ultrasonography was used to determine the "pulsatility index" (PI) at intervals of 3 to 6 days. 17 of the 18 episodes of rejection occurring in transplant patients with stable serum creatinine levels (3.41 +/- 1.48 mg/dl) were detected by colour-coded Doppler ultrasonography 3.8 +/- 5.6 days earlier than by conventional diagnostic methods, the indicator being the rise in PI (sensitivity 93.8%). 25 of the 26 rejection reactions which arose in patients with oligo-anuria due to post-operative renal failure were detected 2.0 +/- 2.7 days earlier (sensitivity 96%). The rise in PI was greater in episodes of vascular rejection than in purely interstitial rejection episodes (40.9 +/- 73.9% versus 10.0 +/- 8.8% per day). Colour-coded Doppler ultrasonography ia a new, highly sensitive, noninvasive method for the early detection of rejection reactions after renal transplantation. Acute postischaemic renal failure does not reduce its sensitivity.
Atrial natriuretic peptide (ANP) and plasma renin activity (PRA) were studied in 19 patients with end-stage renal disease (ESRD) under haemodialysis (HD). On the basis of clinical findings, patients were divided into three groups: group A, 6 patients, of mean age 41 +/- 15 years, without heart failure and in need of ultrafiltration (658 +/- 282 ml h-1); group B, 6 patients, of mean age 54 +/- 15 years, without heart failure under isovolaemic HD; group C, 7 patients, of mean age 60 +/- 3 years, with heart failure (NYHA III-IV) and in need of ultrafiltration (607 +/- 120 ml h-1). The highest predialysis ANP levels were found in group C (1534 +/- 471 pg ml-1) followed by group A (476 +/- 168 pg ml-1) and group B (236 +/- 138 pg ml-1) (normal range 62 +/- 27 pg ml-1). Systolic and diastolic blood pressure and heart rate did not correlate with ANP levels in either of the groups. However, iso-osmotic reduction of the body weight by ultrafiltration was correlated with decreasing ANP levels during HD (for groups A and C, r = 0.88 and 0.98, respectively). Isovolaemic HD did not alter ANP concentrations (group B). All patients received a volume bolus at the end of HD, and they responded with an instant increase in ANP concentration, which was most pronounced in patients with concomitant heart failure. PRA was not significantly correlated with ANP levels during HD. In conclusion, the results of this study indicate that there is a sensitive response of ANP levels to changes in body fluid status in ESRD.
There are typical morphological indicators of tubular defects during the administration of ciclosporin A (CSA). Distal tubular function remains unclear although hyperkalemia is a common clinical feature in these patients. We performed renal function studies 3 months after renal transplantation on 35 patients (group 1) treated with CSA. The results were compared to those of a control group consisting of 15 patients transplanted earlier and treated with azathioprine (group 2). Only patients with stable renal function (creatinine less than or equal to 2.0 mg/dl) entered the investigation consisting of: inulin (In) clearance; p-aminohippuric acid (PAH) clearance; ammonium chloride loading; sodium sulfate loading, and sodium bicarbonate loading. Plasma renin activity and aldosterone were measured basally and after stimulation with 40 mg i.v. furosemide. Clearances of In and PAH were significantly impaired during the administration of CSA. Group 1: CIn 73.3 +/- 8.7 ml/min/1.73 m2 (p less than 0.01), CPAH 263 +/- 58.3 ml/min/1.73 m2 (p less than 0.01); group 2: CIn 89.6 +/- 19.1 ml/min/1.73 m2, CPAH 338.7 +/- 63.5 ml/min/1.73 m2. Incomplete distal tubular acidosis could be demonstrated in 8 patients from group 1 but none of group 2. Hyporeninemic hypoaldosteronism could be demonstrated in 4 patients during the administration of CSA. CSA in therapeutic doses significantly impairs renal perfusion, glomerular filtration, distal acidification and the renin-aldosterone axis.
Three patients with solar urticaria were treated with plasmapheresis. By intradermal injection of in vitro irradiated serum the existence of a circulating photoallergen was demonstrated in cases 1 and 2 but not in case 3. Plasmapheresis induced complete remission of solar urticaria in case 1 and transient improvement in case 2. In case 3, however, no beneficial effect was observed. It is suggested that some patients with solar urticaria, probably those with a circulating photoallergen, may benefit from plasmapheresis.