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Biomedical subjects

B Grabensee

Publications and source records attributed to B Grabensee.

At least 73 records · Page 4Linked to original sources
PubMed1999

Anticoagulation with r-hirudin in a patient with acute renal failure and heparin-induced thrombocytopenia.

After a Caesarean section subcutaneous bleeding with a secondary infection occurred accompanied by acute renal failure. Additionally the diagnosis of a heparin-induced thrombocytopenia type II could be made. Therefore, haemodialysis treatments were performed with r-hirudin as an alternative anticoagulation. Even in dialysis dependent acute renal failure a safe anticoagulation with r-hirudin is possible if aPTT and plasma r-hirudin are closely monitored.

Acute Kidney Injury↗
PubMed1999

Etiology and pathogenetic mechanisms of optic disc swelling with visual loss. An interdisciplinary prospective pilot study of 102 cases.

A nonrandomized, prospective, interdisciplinary pilot study of 102 patients with noncompressive optic disc swelling with visual loss (ODSWVL) was performed in order to investigate etiologic and pathogenetic mechanisms. Forty-six patients suffered from underlying inflammatory disease. Seventeen patients suffered from highly probable cardiogenic embolization, 16 patients from multiple vascular risk factors. The remaining patients of the noninflammatory disease group suffered from leukemia, previously unknown or severely decompensated diabetes mellitus, acute arterial hypertension, different kinds of coagulopathies and others. Ninety-six of the 102 patients required medical treatment according to general medical standards. Inhomogeneity of the underlying disease processes explains the ineffectiveness of different monotherapies in previous studies. Interdisciplinary search for the underlying causes allows causative treatment. ODSWVL and anterior ischemic optic neuropathy in particular seem to be a common final pathway of various pathogenetic mechanisms due to different etiologies rather than a disease entity by itself.

Adult↗
PubMed1999

Nitric oxide production in peritoneal macrophages from peritoneal dialysis patients with bacterial peritonitis.

Nitric oxide (NO) is produced by various cell types, and it is an important mediator in many biological processes, including macrophage-mediated cellular host defense. The relevance and amount of NO production in peritonitis during peritoneal dialysis (PD) treatment is still not clear. We studied whether human peritoneal macrophages (PMphi) isolated from healthy PD patients or PD patients with peritonitis showed different spontaneous or lipopolysaccharide (LPS)/interferon gamma (IFN-gamma)-induced NO production (LPS, 1 ng/mL-10 microg/mL; IFN-gamma, 10-1000 U/mL; incubation between 6-48 hours; measured by Griess reagent). Results were compared with human blood monocytes (HBM) isolated from buffy coats. Inducible nitric oxide synthetase (iNOS) mRNA expression was looked for in PMphi by reverse transcriptase polymerase chain reaction (RT-PCR). Furthermore, plasma (P) and peritoneal dialysate effluent (D) nitrite concentrations were measured in vivo. The dialysate-to-plasma ratio (D/P) of nitrite concentration was inverse in the case of peritonitis compared to infection-free patients (peritonitis D/P = 1.3, non peritonitis D/P = 0.4; p < 0.01). PMphi from peritonitis patients produced higher amounts of NO than did those from infection-free patients (0.040+/-0.044 nmol per microgram cell protein versus 0.018+/-0.015 nmol per microgram cell protein, p < 0.05). NO release could not be further enhanced by stimulation with LPS plus IFN-gamma (1 ng/mL, 250 U/mL, respectively). However, NO production in PMphi from infection-free patients increased during in vitro stimulation (0.044+/-0.031 nmol per microgram cell protein versus 0.018+/-0.015 nmol per microgram cell protein, p < 0.01). An increase of iNOS mRNA expression could be demonstrated by RT-PCR. Blood monocytes from healthy donors also increased NO release during cytokine stimulation (0.032+/-0.015 nmol per microgram cell protein versus 0.019+/-0.009 nmol per microgram cell protein, p < 0.05). Our results indicate that significant amounts of NO are released intraperitoneally in the case of bacterial peritonitis. PMphi represent a site of NO production, though the absolute amounts released in vitro are only moderate. NO production can be induced in PMphi and HBM by LPS/IFN-gamma stimulation in vitro.

Adult↗
PubMed1999

Acid-base balance and substitution fluid during continuous hemofiltration.

Critically ill patients with acute renal failure usually present with an unstable acid-base balance, often leading to cardiovascular complications and multi-organ failure. Therefore, to prevent metabolic acidosis, acid-base balance must be normalized and maintained; these patients are primarily treated with continuous hemofiltration techniques using different replacement fluids to influence the acid-base values. Dialysate solutions can be an acetate-based, lactate-based, citrate-based or bicarbonate-based buffer. This article discusses the strengths and weaknesses of each type of hemofiltration replacement fluid.

Acid-Base Equilibrium↗
PubMed1999

Congestive heart failure as an indication for continuous renal replacement therapy.

Continuous venovenous hemofiltration (CVVH) is the most widely used renal replacement therapy for the treatment of critically ill patients with acute renal failure on the intensive care unit. Whether or not congestive heart failure is an indication for CVVH is controversial and needs to be discussed. Therefore, we present a patient with congestive heart failure who was treated successfully with CVVH.

Acute Kidney Injury↗
PubMed1999

The "point of no return" and the rate of progression in the natural history of IgA nephritis.

BACKGROUND: Based on the observation of 7 patients with chronic IgA nephritis and on a course to end-stage renal failure after several years, D'Amico et al. [1993] reported on a "point of no return" at 2.5 to 3 mg/dl serum creatinine. After exceeding this limit all 7 patients exhibited an irreversible progressive renal failure. PATIENTS AND METHODS: Therefore, 115 patients with IgA nephritis from the "German Glomerulonephritis Therapy Study" were examined in order to look for the existence of such a "point of no return". RESULTS: Three different courses could be distinguished: a stable chronic course with constantly normal or only minor elevated serum creatinine lasting for years (91 patients), a progressive course with continuously increasing serum creatinine (22 patients), and a rare (only 2 patients) early acute course with a short-term increase of serum creatinine followed by a rapid return to the normal range. After exceeding 3 mg/dl serum creatinine no remissions were observed in the progressive cases. Sixteen patients showed a rapid, continuously progressive course until end-stage renal failure with exactly the same progression as the 7 patients of D'Amico et al. Six patients of the 22 progressors were not observed long enough. The serum creatinine level doubled on average from 3 to 6 mg/dl within 10 months. CONCLUSION: Our study confirmed the existence of a "point of no return" at 3 mg/dl (265 micromol/l) during the natural course of chronic IgA nephritis.

Adolescent↗
PubMed1998

Cardiovascular risk factors and diseases after renal transplantation.

UNLABELLED: Cardiovascular disease is a leading cause of death after renal transplantation (tpx), and the incidence is considerably higher than in the general population. OBJECTIVE: To evaluate the incidence of atherosclerotic cardiovascular complications after tpx, the prevalence of cardiovascular risk factors, prior to and following tpx, and the association between the risk factors and complications. PATIENTS AND METHODS: Analysis of atherosclerotic cardiovascular diseases (coronary artery disease, cerebral and peripheral vascular disease) and cardiovascular risk factors before and after transplantation in 427 renal transplant recipients between 1987 and 1992 (mean age at transplantation 45+/-12 years, 58% male, 7% diabetics) with a mean post-transplant follow-up of 29+/-20 months. RESULTS: Following tpx 11.7% developed atherosclerotic cardiovascular diseases, the majority coronary artery disease (9.8%). The comparison of risk factors 12 months before and 24 months following transplantation showed: prevalence of systemic hypertension (from 73% to 85%), diabetes mellitus (from 7% to 16%) and obesity with a body mass index >25 kg/m2 (from 26% to 48%) had increased significantly whereas the number of smokers halved to 20%. Triglycerides decreased significantly (from 235 mg/dl to 217 mg/dl). Total and HDL cholesterol rose significantly (from 232 mg/dl to 273 mg/dl and from 47 mg/dl to 56 mg/dl, respectively). LDL cholesterol increase was significant (from 180 mg/dl to 189 mg/dl). In the univariate analysis, cardiovascular diseases were significantly associated with male gender, age over 50 years, diabetes mellitus (DM), smoking, total cholesterol > or=200 mg/dl, LDL cholesterol >180 mg/dl, HDL cholesterol < or =55 mg/dl, fibrinogen > or =350 mg/dl, body mass index >25 kg/m2, serum uric acid >6.5 mg/dl and with more than two antihypertensive agents per day. The Cox proportional hazards model revealed DM with a relative risk (RR) of 4.3, age >50 years (RR=2.7), body mass index >25 kg/m2 (RR=2.6), smoking (RR=2.5), LDL cholesterol >180 mg/dl (RR=2.3) and uric acid >6.5 mg/dl as independent risk factors. CONCLUSIONS: The high incidence of cardiovascular disease following renal transplantation is mainly due to a high prevalence and accumulation of classical risk factors before and following transplantation. Future prospective studies should evaluate the success of treatment regarding reduction of cardiovascular morbidity and mortality in this high risk population.

Cardiovascular Diseases↗
PubMed1998

Effect of alternative peritoneal dialysis solutions on cell viability, apoptosis/necrosis and cytokine expression in human monocytes.

BACKGROUND: Cellular function, cell viability and the cytokine network of human monocytes are influenced by the specific composition of peritoneal dialysis (PD) fluids. In an in vitro study using isolated human blood monocytes, we investigated the effect of peritoneal dialysates containing amino acids (Amino) or glucose polymer (Glu-poly) instead of glucose (Glu) as the osmotic agent, and bicarbonate (Bic) or PBS instead of lactate (Lac) as a buffer. METHODS: The following parameters were studied: mitochondrial dehydrogenase activity (using the MTT assay), interleukin (IL)-6 and IL-8 release (ELISA) and cellular IL-6 mRNA expression after lipopolysaccharide (LPS) stimulation (using RT-PCR). FACS flow cytometry with annexin V and propidium iodide as markers and fluorescence microscopic methods were used to study the effects of the test fluids on cell necrosis and apoptosis. RESULTS: Glu/Lac pH 5.5 and Glu-poly/PBS pH 7.4 both significantly reduced mitochondrial dehydrogenase activity by more than 50% after 60 minutes of incubation (30.5 +/- 7.6%, 42.5 +/- 6.5%, referred to RPMI 1640 as 100%). Amino/Bic and Glu/Bic were both superior (Mtt assay > 63%). The rate of necrotic cells after 15 minutes of incubation measured by FACS was mostly increased with Glu/Lac pH 5.5 (29.9 +/- 4.0%). The rate of apoptotic cells, however, was not significantly different between the test solutions. The concentration of IL-6 in the supernatant of stimulated monocytes was highest with Glu/Bic (1023 +/- 278 pg/ml) and Amino/Bic (776 +/- 296 pg/ml) an lowest with Glu/lac pH 5.5 (46 +/- 22 pg/ml) and Glu-poly/PBS (32 +/- 13 pg/ml). IL-8 release from stimulated monocytes showed a similar pattern. Glu-poly/PBS showed a suppressive effect on IL-6 mRNA expression (ratio IL-6/beta-Actin, 0.4 +/- 0.25 vs. RPMI 1.5 +/- 3.6). CONCLUSIONS: Bicarbonate buffered solutions both with glucose or amino acids as osmotic agents were superior when regarding cell metabolism, viability and cytokine release, while lactate buffered solutions and Glu-poly/PBS showed some reduced biocompatibility pattern for monocytes in vitro.

Actins↗
PubMed1998

Point mutations of the human parathyroid calcium receptor gene are not responsible for non-suppressible renal hyperparathyroidism.

The calcium-dependent secretion of parathyroid hormone (PTH) is mediated through an extracellular G protein-coupled calcium receptor (CaR). Inactivating point mutations of this receptor have been found in familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism. These diseases feature a decreased calcium sensitivity of the parathyroid glands, resulting in a rightward shift of the Ca2(+)-PTH relationship. Severe non-suppressible renal hyperparathyroidism (rHPT) is often characterized by similar setpoint shifts to the right. Thus, point mutations of the CaR gene could contribute to non-suppressible rHPT. We examined genomic DNA of hyperplastic or mainly nodular tissues of 39 parathyroids from 25 rHPT-patients with resistance to calcitriol therapy. Amplification of the six exons of the CaR gene was followed by single-strand conformation polymorphism (SSCP) analysis. DNA sequencing was performed where band shifts were observed. No point mutations in the coding sequence of the CaR gene were detected using the PCR-SSCP strategy. Point mutations in the coding regions of the CaR gene probably play no role in the evolution of renal HPT and are not responsible for the calcitriol resistance of PTH secretion.

Adolescent↗
PubMed1998

Haemolytic-uraemic syndrome and thrombotic-thrombocytopenic purpura in adults: clinical findings and prognostic factors for death and end-stage renal disease.

BACKGROUND: Left untreated, haemolytic-uraemic syndrome (HUS) and thrombotic-thrombocytopenic purpura (TTP) in adults have a poor prognosis with mortality rates reaching 90%. Patients who survive often develop end-stage renal disease. Because of similarities in clinical and morphological findings, both diseases are considered as one entity referred to as HUS-TTP syndrome. METHODS: From 1974 to January 1995, 45 adult patients received treatment for HUS-TTP at our clinic. By stepwise logistic regression analyses, we examined how known risk factors and plasma exchange with fresh-frozen plasma (PE) influenced mortality and end-stage renal disease. RESULTS: Three of 45 patients died (7%). Though we were not able to find significant predictors of mortality, low haemoglobin levels (5.93 +/- 0.32 vs 9.10 +/- 2.16 g/dl) and high leukocyte counts on admission (15.830 +/- 3.690 vs 11.150 +/- 4.580 microliters-1) appeared to indicate an unfavourable outcome. Regarding the development of end-stage renal disease, PE proved to be the only favourable indicator (P = 0.0001). PE was performed in 30 patients 3-20 times (9.2 +/- 4.8, mean +/- SD). Of 28 surviving patients treated with PE, only four developed end-stage renal disease, whereas dialysis was necessary in 11 of 14 patients not treated with PE. Application of PE led to an 81.8% reduction of the relative risk of developing end-stage renal disease. An additional prognostic influence of other potential risk factors such as age, sex, platelet count on admission, lactate dehydrogenase serum levels, serum creatinine, blood pressure, prodromal disease, and renal histology was not found. CONCLUSION: This retrospective clinical study confirms the therapeutic value of plasma exchange with fresh-frozen plasma to maintain renal function in patients with HUS-TTP.

Adolescent↗
PubMed1998

Different actions of the cyclooxygenase 2 selective inhibitor flosulide in rats with passive Heymann nephritis.

The prostaglandin cyclooxygenase (Cox) exists in two isoforms with different genetic representation. The isoform, which is constitutively expressed (Cox 1), and mediates physiological functions of prostaglandins, and the inducible isoform (Cox 2) which is upregulated by inflammatory stimuli. This study attempts to determine whether a Cox 2 selective inhibitor, flosulide, differs from the mixed type Cox 1 and Cox 2 inhibitor aspirin in respect of renal function and eicosanoid excretion in experimental nephritis. The effects of flosulide and aspirin were studied during the autologous phase of passive Heymann nephritis (PHN) in rats. Female Wistar rats were injected i.v. with 1 ml of Fx1A antiserum at day 1. From day 7 to day 14 they received either aspirin (aspirin, 50 mg/day), flosulide, (0.75 mg/day) or vehicle p.o. The kidney function was evaluated and the animals sacrificed. The kidneys were removed and glomeruli isolated. The glomeruli were incubated in physiological buffer solution. Basal prostaglandin generation was determined in the supernatant. Treatment with flosulide significantly reduced proteinuria as compared to aspirin treatment (64+/-15 vs. 109+/-14 mg/24 h, p < 0.05). Plasma protein and albumin levels were significantly lower in the aspirin-treated group than in flosulide-treated animals (4.7+/-0.26 vs. 5.48+/-0.08 mg/dl, p < 0. 05 and 0.96+/-0.04 vs. 1.25+/-0.10 mg/dl, p < 0.05). Glomerular prostaglandin production (6-keto-PGF1alpha, TxB2, Bicyclo-PGE2) was significantly reduced in aspirin-, but not in flosulide-treated animals. This was mainly due to a reduction of glomerular TxB2 production by aspirin. Our data demonstrate that a Cox 2 selective inhibitor of prostaglandin formation, flosulide, has beneficial effects on preservation of kidney function in rats with PHN, whereas aspirin has not. These beneficial effects of flosulide possibly result from preservation of the physiological glomerular prostaglandin production. Thus, selective Cox 2 inhibitors might be interesting substances for treatment of nephrotic syndrome.

Animals↗
PubMed1998

Effects of the angiotensin II antagonist valsartan on blood pressure, proteinuria, and renal hemodynamics in patients with chronic renal failure and hypertension.

Angiotensin II receptor antagonists have become clinically available for the treatment of arterial hypertension. Presently, there is little information about their effects on BP, proteinuria, and renal function in patients with moderate or advanced renal failure. This study examines the effects of the angiotensin II antagonist Valsartan (80 mg/d) on proteinuria and glomerular permselectivity in patients with chronic renal failure during a 6-mo treatment, using a double-blind, randomized, placebo-controlled study (treatment group [V-group]: n = 5, age 57 +/- 7 yr, serum creatinine 365 +/- 122 micromol/L; placebo group [P-group]: n = 4, age 62 +/- 11 yr, serum creatinine 346 +/- 61 micromol/L). Study parameters included BP, 24-h proteinuria, GFR, and effective renal plasma flow (ERPF) as determined by inulin and para-aminohippurate clearance. Changes in glomerular permselectivity were assessed by measuring the fractional clearances of neutral dextrans by HPLC gel-permeation chromatography. Valsartan lowered the mean arterial pressure on average by 13 +/- 7 mmHg during the 6-mo treatment (P < 0.05). GFR and ERPF remained almost unchanged. However, after 6 mo of Valsartan treatment, proteinuria was reduced by 396 +/- 323 mg/24 h (26 +/- 18%) and albuminuria by 531 +/- 499 mg/24 h (41 +/- 21%) with regard to baseline values (P < 0.05). In the P-group, both proteinuria and albuminuria increased slightly with time (by 30 +/- 43% and 30 +/- 54%, respectively, NS). The fractional clearances of high molecular weight dextrans >66 A were significantly reduced after 6 mo of Valsartan treatment (P < 0.05), indicating a reduction of the glomerular shunt volume by 54 +/- 20% (P < 0.05) according to the model of Deen et al. (Am J Physiol 249: 347-389, 1985). The mean pore size radius of the glomerular membrane remained unchanged. This effect was independent of glomerular hemodynamic changes. Valsartan persistently lowered proteinuria in patients with chronic renal failure. Although GFR and ERPF remained nearly stable, this effect could be attributed to an improvement in glomerular permselectivity.

Aged↗
PubMed1998

Renal transplantation in secondary systemic amyloidosis.

When renal amyloidosis has progressed to end-stage renal failure, most patients are severely affected by systemic amyloidosis and nephropathy. An alternative to chronic dialysis is renal transplantation. We present a patient with amyloid nephropathy who developed recurrent transplant amyloidosis. Renal transplantation was performed in 1985 with a living related donor. In 1990 the patient developed amyloidosis of the graft with membranous nephropathy and tubular acidosis due to hyporeninemic hypoaldosteronism. Secondary amyloidosis has been reported to involve glandular organs inducing hypothyroidism, hypocortisolism and hypoaldosteronism. Cyclosporine has been reported to induce hyporeninemic hypoaldosteronism and tubular acidosis, but not hypocortisolism and hypothyroidism. Progression of the amyloidosis of the graft was confirmed by a renal biopsy in 1993. Data published in the literature indicate that the survival rate of amyloidotic graft recipients is worse than those of non-amyloidotic graft recipients. This was confirmed in an analysis of the current CTS data which showed an impaired survival rate at 5-yr of 66 +/- 4% (+/- SE) for patients with amyloidosis (n = 413) as compared with 86 +/- 1% (p < 0.0001) for patients with glomerulonephritis and 84 +/- 1 (p < 0.01) for patients with polycystic kidney disease. Graft survival after 5 years was 55 +/- 4% in patients with amyloidosis as compared with 63 +/- 1% (p = 0.02) in patients with glomerulonephritis and 68 +/- 1% in patients with polycystic kidney disease. Graft survival was improved in amyloidotic patients treated with cylosporine as compared with patients on steroids and azathioprine (55 +/- 4% vs. 38 +/- 8%, p < 0.05). It is concluded that renal transplantation is the renal replacement therapy of choice for patients with AA-type amyloidosis although the overall patient survival is impaired in comparison with patients with other diseases.

Adult↗
PubMed1998

Distal tubular acidosis induced by FK506.

This study was designed to investigate the effect of tacrolimus (FK506) and of cyclosporine (CsA) on tubular function in renal graft recipients. Patients were randomised after renal transplantation to immunosuppressive treatment with FK506 (n = 8) or CsA (n = 8). Patients had a mean age of 45.7 +/- 3.4 yr; there was no difference in age, sex, HLA status or CMV mismatches. Neither was there any difference in the frequency of episodes of acute kidney failure between the groups, nor was there a significant difference in the frequency of episodes of kidney rejection within the first year. The mean FK506 level at the time lay at 14.7 +/- 14.4 ng/mL whole blood, and the mean CsA level at the time of study was 162 +/- 25 ng/mL whole blood. We performed renal function studies 6 months after transplantation: CIn, CPAH, NaHCO3 loading, and Na2SO4 loading. There was no significant impairment of GFR in patients treated with FK506 with 53.6 +/- 2.5 mL/min as compared to 58 +/- 6 mL in group 2. Plasma renin activity (0.6 +/- 0.4 ng/mL vs 2.3 +/- 3; p < 0.01) and aldosterone (69 +/- 17 vs 157 +/- 28.2 pg/mL; p < 0.05) were significantly decreased during treatment with FK506. Fractional HCO3 excretion was low in both groups, indicating that bicarbonate reabsorption in the proximal nephron was unimpaired. Distal renal tubular acidosis was demonstrated in 4 patients of group 1 but in only 1 of group 2. Potassium levels were slightly increased in patients treated with FK506 (5.4 +/- 0.2 mmoL/L) as compared to cyclosporine (4.9 +/- 0.3 mmoL/L; p < 0.05). Distal hydrogen ion secretion, evaluated by the ability to increase urinary pCO2 in a highly alkaline urine, was impaired in patients treated with FK506 (U-B pCO2: 16.1 +/- 4 vs 36 +/- 5.8; p < 0.05) as compared to patients treated with CsA. The maximum acidification capability (NAE) was slightly lowered during therapy with FK506 (67.5 +/- 11.8 versus 86.6 +/- 16.5 mumoL/min, ns). We conclude that FK506 administration results in a decrease in the rate of hydrogen ion secretion by the collecting tubules. This defect was disclosed by the finding of a subnormal pCO2 in a highly alkaline urine. These results show that FK506 is able to induce distal tubular acidosis. Distal tubular acidosis is part of FK506 induced nephrotoxicity, the pathogenesis of this type of hyperkalemic metabolic acidosis found in patients treated with FK506 after renal transplantation has to be further elucidated.

Acidosis, Renal Tubular↗
PubMed1997

[Glomerulonephritis and malignant lymphoma. Mostly men with low-grade lymphoma with various forms of glomerulonephritis].

BACKGROUND: The association of non-Hodgkin's lymphoma with different types of glomerulonephritis is well-known for many years. Whereas in Hodgkin's disease, minimal change glomerulonephritis is mainly observed, in non-Hodgkin's lymphoma various forms of glomerulonephritis are found. PATIENTS AND RESULTS: We describe 3 cases of non-Hodgkin's lymphoma, which were associated with glomerulonephritis. Two cases of glomerulonephritis showed nephrotic syndromes, which improved by medicinal treatment. In 2 cases glomerulonephritis and non-Hodgkin's lymphoma developed simultaneously. In a third lymphoma was followed by glomerulonephritis after 3 years. CONCLUSION: Although the pathogenetic relationship between non-Hodgkin's lymphoma and glomerulonephritis is not fully understood, the high number of reported cases yield interdependence. Lymphoma associated glomerulonephritis is found more often in men than in women. Low-grade non-Hodgkin's lymphomas--especially chronic lymphatic leukemias--seem to develop glomerulonephritis more frequently than high-grade. The majority of non-Hodgkin's lymphoma do not show any predisposition to a special type of glomerulonephritis, only in cutaneous lymphoma IgA-nephropathy predominates.

Aged↗