[Diagnosis and therapy of life-threatening disorders of water and electrolyte balance].
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Biomedical subjects
Publications and source records attributed to B Grabensee.
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In order to investigate the behaviour of atrial natriuretic peptide (ANP) in untreated mild to moderate essential hypertension and the influence of blood pressure normalisation by a beta 1-receptor blocker a study was conducted in groups of normotensive and hypertensive middle aged subjects. 10 normal subjects and 10 patients with essential hypertension (WHO I-II) without any medication and on betaxolol monotherapy were studied at rest and during graded exercise. In addition the response of ANP, cyclic guanosine monophosphate (cGMP) and the renin-aldosterone-system was investigated. Normal subjects and hypertensive patients did not differ in ANP levels at rest and also responded with a comparable exercise dependent increase at all workload levels. A steady decrease of ANP was noticed during the recovery period in both groups. After beta-blocker treatment in the hypertensive patients ANP concentrations significantly rose, both at rest and more pronounced during exercise. cGMP reacted in a similar way but showed a more inert response. A counter-regulatory behaviour between ANP and PRA or aldosterone, as seen under volume shifts, could not be detected. These findings demonstrate that plasma ANP is not altered in untreated essential hypertension. Increased ANP levels in beta 1-blocker treatment may contribute to its blood lowering effect.
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Patients with end stage renal failure have elevated plasma levels of atrial natriuretic peptide (ANP) which seems to be a sensitive parameter of body fluid status. A prospective study comparing patients on hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) was still missing. Six identical patients (59 +/- 10 yrs, residual diuresis 1.3 +/- 0.61, 1 data expressed as means +/- SEM) were studied in the predialysis phase and under steady state conditions on HD and on CAPD. Plasma levels of ANP, cyclic guanosine monophosphate (cGMP), adrenaline, noradrenaline and dopamine were determined. Blood and dialysate samples were repeatedly taken. Ultrafiltration-volume, dry weight and blood pressure were not different between HD and CAPD. ANP and cGMP reached the highest plasma levels in the predialysis phase with 421 +/- 180 pg/ml and 19.8 +/- 6.4 pmol/ml and decreased after the onset of dialysis treatment. On HD mean ANP levels of 279 +/- 175 pg/ml were not significantly different from those on CAPD (320 +/- 213 pg/ml). However, cGMP concentrations on CAPD (15.7 +/- 5.4 pmol/ml) surpassed the values measured on HD (10.5 +/- 3.4 pmol/ml, p less than 0.05). Plasma noradrenaline was markedly elevated in the predialysis phase (421 +/- 180 pg/ml) and decreased under dialysis treatment. Differences between HD and CAPD were not found. Adrenaline and dopamine concentrations fell within the normal range.
Peritoneal equilibration tests (PETs) in patients on CAPD show wide variations. To find out whether these are correlated with time on CAPD, we investigated changes in PET in 97 tests in 86 patients. 46 PETs were performed with a 1.36% glucose solution and 40 PETs with a 3.86% glucose solution at different time intervals. Neither did the intra-individual comparison of 11 patients with 1.36% glucose solution following 1 year of treatment show any significant change nor the inter-individual comparison following a treatment time of 1 and 2 years. There was also no difference using a 3.86% glucose exchange, when the results at the beginning and after 1 year were compared. However, alterations in equilibration ratios were significant after 24 and 36 months of treatment for creatinine (36 months versus 0: p less than 0.005), glucose absorption (36 months versus 0: p less than 0.01) and UF (36 months versus 0: p less than 0.01). No correlation exists between these changes either with the number of peritonitis episodes or with the time of treatment. Though, no single factor could be identified, patients had an increase in peritoneal permeability especially after long-term treatment. Further investigations are necessary to evaluate the reasons for these changes.
There have been only a few investigations that have considered renal disease or any disturbance of renal function in the calculation of risk in cardiac surgery. Risks of cardiac surgery have to be considered for renal disease without direct connection to heart disease (e.g., infections of the kidney and of the urinary tract, primary and secondary glomerulonephritis, parenchymal renal disease, and impaired renal function of unknown origin), as well as in renal disease with concomitant influence on heart and kidney (e.g., infective endocarditis, arterial hypertension, systemic disease of heart and kidney such as with diabetes mellitus, disturbance of kidney function or electrolyte balance due to heart failure). In most cases, the problem is solved by therapeutic intervention and postponement of cardiac surgery. A limited or negative operative indication is found with untreatable infection of the kidney or urinary tract, with untreatable nephrotic syndrome, in advanced renal disease with heart transplantation, as well as in case of severe arterial hypertension with possible organ complications, and in advanced diabetes mellitus with ESRD and multiorgan involvement. After cardiac surgery, acute renal failure represents a critically important complication. Primary therapeutic procedures must include prophylaxis of hemodynamic unstable situations, as well as prophylaxis of infectious complications. Cardiac surgery in dialysis patients and post-transplant patients is basically possible and only has a slightly increased risk compared to patients with normal renal function. Seventy-seven dialysis patients were operated (49 aorto-coronary bypass operations, 19 single-valve and multiple-valve replacements, five patients with valve replacement and aorto-coronary bypass, and four other cardiac surgical operations). Only in valve replacement, was mortality significantly higher than in renal healthy persons, the main causes of death being cerebrovascular complications and septicemia.
Plasma levels of human atrial natriuretic peptide (ANP) were measured in 10 patients with mild essential hypertension (EH) (WHO I). The renin-angiotensin-aldosterone-(RAA) system and ANP were investigated in a sequential study without treatment and under administration of a cardioselective beta-blocker (betaxolol). We analyzed the RAA system and ANP under conditions of volume loading induced by 2000 ml saline and volume depletion induced by 40 mg furosemide iv. Volume depletion induced a stimulation of the RAA-system but the ANP levels decreased from 87 +/- 13.6 to 55 +/- 7.6 pg/ml. Volume loading induced a suppression of the RAA-system but caused a rise of ANP from 47 +/- 12 pg/ml to 133 +/- 30 pg/ml. Under application of betaxolol the RAA system was suppressed and ANP levels were increased, but physiological volume regulation was maintained. Although blood pressure and heart rate were lowered under administration of betablockers, the ANP levels were increased. These results suggest that increased ANP in plasma under administration of betaxolol may play a role in compensatory mechanisms in response to beta-adrenergic blockade.
Therapeutic plasmapheresis is an effective therapy in the management of CIDP. A varying percentage of patients, approximately 30 to 60%, may benefit from the treatment. The optimal frequency and volume of PE need to be clarified, but, taking into account the heterogeneity of the disease, a too rigid approach should be avoided. According to our experience, neither morphological findings on sural nerve biopsy, nor conduction slowing, conduction block, or the amount of spontaneous activity on needle electromyography in a weak muscle correlated clearly with the later outcome of PE. Possibly our patient number is too small to provide any statistically significant predictor of outcome. In our opinion it is essential to combine plasmapheresis with effective immunosuppression to avoid a rebound with overshooting synthesis of putative pathogenic antibodies or factors. Finally, IA with T-PVA columns has proven effective in single, case-controlled patients with CIDP. It may be a promising supplement to PE avoiding the need and risks of protein replacement.
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To check the reliability of the captopril test and of quantitative radioisotope techniques for the primary diagnosis of renovascular hypertension the data from 41 patients suspected of this disease were retrospectively analysed. In all cases plasma renin activity (PRA) was assayed in peripheral blood and in renal vein blood before and after 25 mg captopril. Double tracer studies with 131I-hippuran and 99mTc-DTPA were also performed, as was renal arteriography. The postoperative blood pressure plots of 23 patients with unilateral renal artery stenosis (who had subsequently been operated upon) were included in the evaluation. Renovascular hypertension was diagnosed in 21 patients and essential hypertension in 20. Twelve of the 20 patients with essential hypertension had renal artery stenosis, but this had not produced renovascular hypertension. The diagnostic significance of the tests as markers of renovascular hypertension was as follows: captopril test P less than 0.001, glomerular filtration fraction P less than 0.02, hippuran clearance P less than 0.001. The captopril test and the quantitative radioisotope techniques were in agreement in identifying patients with renal artery stenosis and renovascular hypertension. False-positive results due to methodological shortcomings can be avoided by applying both methods in succession.
A Kaposi's sarcoma of the skin with nodular and follicular lesions but no visceral involvement developed in a 44-year-old man nine months after transplantation of an haplo-identical kidney (a relative as donor). He was on an immunosuppressive regimen of daily 10 mg methylprednisolone and 2.5 mg/kg cyclosporin A. No HIV antibodies were demonstrated. After reduction of the dosage to 4 mg methylprednisolone and 1 mg/kg cyclosporin A no further growth of the skin lesions was observed, while transplant function was maintained. The lesions regressed after radiation of two areas in the right lower leg with 48 Gy. Ten months later the sarcoma again progressed and required further radiotherapy, which arrested growth, while there was no change in transplant function.
After six years of home haemodialysis and two years of continuous ambulatory peritoneal dialysis a 59-year-old woman developed an aluminium-induced osteopathy, myopathy and normochromic anaemia. She was at first treated with intravenous, then peritoneal, deferoxamine, 1 g every other day. Before treatment, 15.8 micrograms aluminium (Al) had been eliminated daily, with a peritoneal clearance of 0.3 ml/min; after intravenous deferoxamine a mean of 774.3 +/- 102.3 micrograms Al was eliminated per day, after peritoneal deferoxamine 646.7 +/- 89.6 micrograms of Al per day, with a peritoneal clearance of 2.2 +/- 0.9 (intravenous) and 1.9 +/- 0.7 ml/min (intraperitoneal). After four months of deferoxamine administration, mostly intraperitoneally as an out-patient, the osteomalacia clearly improved, as did the myopathy and anaemia.
Aluminum concentrations in the dialysate and serum of 14 patients on CAPD were measured every six months. Additionally, in ten of the patients Al elimination was measured after a bolus ingestion of 1800 mg aluminium-chloride-hydroxide-complex. There was no significant difference between serum Al concentrations initially (47.3 +/- 8.2 micrograms/l), at six months (55.4 +/- 9.5 micrograms/l), and after 12 months (44.3 +/- 10.1 micrograms/l) although the Al concentration in the dialysate had been decreased from 16.6 +/- 2.3 micrograms/l to 1.5 +/- 0.2 in the last six months. The Al concentrations in the effluent dialysate were 14.5 +/- 1.3 micrograms/l initially, 15.6 +/- 1.2 micrograms/l after six months and 11.9 +/- 2.6 micrograms/l after 12 months. During kinetic studies a constant rise of serum Al concentration was found until the fifth hour, from 29.9 +/- 2.5 to 42.5 +/- 4.0, and a decline after 24 hours to 32.4 +/- 3.0 micrograms/l. The quantity of Al eliminated was 41.1 +/- 8.7 micrograms/24 h, equivalent to 1.2% of the ingested dose. In patients with residual renal function, renal Al clearance was almost double the peritoneal one. These results indicate that Al elimination by CAPD is not efficient and ingestion of Al-containing phosphate binders can result in Al accumulation.
Renal transplantation was performed in 2 patients with end-stage renal disease due to AA-type amyloidosis. One patient with amyloidosis of rheumatoid arthritis (RA) origin died twelve months after renal transplantation in cardiogenic shock. AA-amyloid deposits were demonstrated in the graft even though there were excellent function and no proteinuria. The second patient with amyloid nephropathy due to familial Mediterranean fever (FMF) showed no impairment of graft function 24 months after transplantation. These 2 cases are compared to an additional 31 cases of renal transplantation for amyloid nephropathy described in the literature. Proteinuria was reported in 32.3% and amyloid was detected in the functioning graft in 41.4%. The function was excellent even when small amyloid deposits were present in the graft. Renal transplantation is indicated in cases of amyloid nephropathy of the AA-type, provided life threatening amyloid involvement of other organs is not present.
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