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Biomedical subjects

B Grabensee

Publications and source records attributed to B Grabensee.

At least 55 records · Page 3Linked to original sources
PubMed1999

Percutaneous renal biopsy: three years of experience with the biopty gun in 761 cases--a survey of results and complications.

From 1.1.1993 to 12.31.1995 we performed 761 consecutive biopsies on 509 non-selected patients. The most frequent diagnoses in 351 biopsies (39.4%) on native kidneys were 262 cases of glomerulonephritis (74.6%) and 167 of so-called benign nephrosclerosis (47.6%). With 410 biopsies (60.6%) on allograft kidneys 219 cases (78%) showed signs of interstitial rejection, 14 cases (5%) vascular and 49 cases (17%) interstitial as well as vascular rejection. Only after 5 biopsies (0.66%) clinical relevant complications (3 perirenal haematomas, 1 AV fistula, 1 vesical tamponade) appeared. Again percutaneous renal biopsy is proven to be a diagnostically efficient and safe tool at the same time even when used in a large number of non-selected patients, so that an ambulant performance may be discussed. The relatively frequent diagnosis of a so-called benign nephrosclerosis seems to indicate the need for an intensified examination of this disease.

Adult↗
PubMed1999

Effect of flosulide, a selective cyclooxygenase 2 inhibitor, on passive heymann nephritis in the rat.

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) induce an inhibition of cyclooxygenase (COX), an enzyme that makes prostaglandins. Two isoforms of COX exist: COX-1 represents the constitutively expressed enzyme, whereas COX-2 is the inducible isoform. This study investigated the role of COX-2 in the inflammatory processes of the kidneys of rats with passive Heymann nephritis (PHN), and focused of the effect of a selective COX-2 inhibitor, flosulide. COX-2-selective inhibitors are thought to represent potent anti-inflammatory agents without major renal side effects. METHODS: PHN was induced by injecting heterologous Fx1A antiserum into female Wistar rats. Two treatment groups, each consisting of 12 rats with PHN, received either 3 or 9 mg of flosulide/kg body wt/day and were compared with untreated controls. After four weeks, the generation of thromboxane B2 (TxB2) and 6-keto-PGF1alpha were determined in renal tissue and in urine. COX-2 protein expression was investigated by Western blotting using a selective antibody. RESULTS: Rats with PHN exhibited a marked proteinuria of 71 +/- 8 mg/24 hr as compared with 2.0 +/- 0.3 mg/24 hr in healthy controls (P < 0.01). Treatment with flosulide reduced the proteinuria to 26.1 +/- 9 mg/24 hr at 3 mg flosulide/kg body wt/day and 35.5 +/- 6 mg/24 hr at 9 mg/kg body wt/day, which was equivalent to a reduction of proteinuria by a maximum of 65% (P < 0.05). This was accompanied by an increase in glomerular TxB2 from 3073 +/- 355 to 5255 +/- 1041 pg/mg glomerular protein and 6-keto-PGF1alpha from 1702 +/- 161 to 2724 +/- 770 pg/mg glomerular protein in rats with PHN. COX-2 protein expression was also highly elevated in comparison to healthy controls. Low-dose flosulide treatment had no effect on COX protein expression and renal prostaglandin formation. High-dose flosulide treatment reduced renal prostaglandin production and caused a marked decline in COX-1 and COX-2 protein expression. Urine prostanoid excretion remained unchanged in all therapeutic groups. There was a small though significant reduction in renal creatinine clearance from 0.86 ml +/- 0.2/min in untreated controls to 0.6 ml +/- 0.1/min in flosulide-treated rats with PHN (P < 0.01) after four weeks. CONCLUSIONS: Under the influence of flosulide, a highly COX-2-selective inhibitor, we observed an antiproteinuric drug effect. The inflammation in PHN induced COX-2 protein expression that was not affected by low-dose flosulide. COX-1 and COX-2 protein expression was affected by high-dose flosulide, which therefore might lose its selectivity. High-dose flosulide induced a decrease in glomerular prostanoid production possibly because of COX-1 inhibition. Our results suggest that the therapeutic use of flosulide in proteinuria seems advantageous and deserves further studies because the basal prostaglandin levels remain unchanged in the low-dose-treated group, indicating that the compensatory capacity of prostaglandin production, which is essential for the regulation of renal hemodynamics, is maintained.

Animals↗
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↗