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Biomedical subjects

B Grabensee

Publications and source records attributed to B Grabensee.

At least 19 recordsLinked to original sources
PubMed1992

[The imaging diagnosis of acute renal transplant obstruction with special reference to antegrade pyelography].

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.

Acute Disease↗
PubMed1992

The role of thromboxane and prostacyclin in ciclosporin-induced nephrotoxicity.

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.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

[Spontaneous renal artery dissection].

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.

Aortic Dissection↗
PubMed1992

[Pneumocystis carinii pneumonia: a life threatening complication after kidney transplantation].

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.

Administration, Inhalation↗
PubMed1992

[The value of noninvasive 24-hour blood pressure measurement in patients with renoparenchymal, renovascular or severe essential hypertension].

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.

Antihypertensive Agents↗
PubMed1991

[Kidney function of patients with healthy kidneys during cyclosporin treatment].

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)

Acid-Base Equilibrium↗
PubMed1991

Atrial natriuretic peptide in dialysis patients under various conditions of volume homeostasis.

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.

Adult↗
PubMed1991

Influence of ciclosporin A on renal tubular function after kidney transplantation.

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.

Adult↗
PubMed1991

Influence of betaxolol on renal function and atrial natriuretic peptide in essential hypertension.

The hypotensive action of beta-adrenoreceptor blockers is not fully understood, there being a lack of studies focusing on possible relationships between beta-blockers and the secretion of atrial natriuretic peptide (ANP). In 10 patients with essential hypertension, we investigated the influence of betaxolol, a selective beta 1-adrenergic blocking agent, on renal function and on plasma levels of ANP during exercise, volume depletion and volume expansion. Chronic therapy with betaxolol (mean 14.5 mg/day) did not alter glomerular filtration rate and renal blood flow although blood pressure was reduced. Renal vascular resistance decreased from 12795 +/- 1064 dyn/s per cm5 to 10614 +/- 833 dyn/s per cm5 (P less than 0.005). Under betaxolol, basal ANP levels increased from 39 +/- 10 pg/ml to 80 +/- 19pg/ml (P less than 0.01). ANP increased during exercise and volume expansion but was decreased during volume depletion. ANP values observed under betaxolol treatment showed significantly higher values while preserving their dynamic features. We believe that the stimulating effect of betaxolol on ANP may at least partly account for its hypotensive action.

Adolescent↗
PubMed1991

Clinical and pathophysiological effects of piretanide treatment in the nephrotic syndrome.

12 patients with the nephrotic syndrome (N.S.) and normal serum creatinine (less than 1.5 mg/dl) were investigated in a follow-up study over 10 days under diuretic treatment with piretanide (29 +/- 24 pg/ml). Clinical effects, parameters of renal clearance and hemodynamics, metabolic changes and the influence on vasoactive and volume dependent hormonal systems were studied. Piretanide markedly increased urine volume and electrolyte excretion (Vu +53%, UNa +24%, p less than 0.05, after 10 days treatment) but did not significantly alter glomerular filtration rate or renal blood flow. While baseline plasma renin activity was in the normal range and regularly stimulated (2.55 ng/ml x h to 7.7 ng/ml x h) plasma ANP values were elevated (152 +/- 107 pg/ml) at the start of the study and did not significantly change under piretanide treatment. This may be an indicator of sodium retention and a high plasma volume in the primary form of the nephrotic syndrome. Thereby piretanide did not significantly alter the intravascular space.

Adolescent↗
PubMed1979

[Interaction of quinidine and digoxin in humans (author's transl)].

After full digitalisation, 11 healthy subjects received 0.375 mg digoxin daily as maintenance dose. Under steady-state conditions and determination of serum concentration and renal clearance of digoxin, they were then given 500 or 1000 mg quinidine daily in addition to the digoxin. While serum concentration of digoxin rose significantly from 0.75 +/- 0.2 ng/ml after one week on 500 mg quinidine, and to 1.8 +/- 0.6 ng/ml after 1000 mg of quinidine, renal digoxin clearance fell from 186.2 +/- 67.4 to 125.4 +/- 61.8 ml/min after 500 mg of quinidine. Raising quinidine dosage to 1000 mg daily caused no further digoxin clearance reduction. During the total experimental period endogenous creatinine clearance remained unchanged. The results indicate that the rise in serum digoxin concentration on simultaneous quinidine administration is largely due to reduction in renal digoxin clearance. A clinical observation confirms the considerable practical importance of this interaction.

Digoxin↗