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T Sauerbruch

Publications and source records attributed to T Sauerbruch.

At least 55 records · Page 3Linked to original sources
PubMed2004

Intravenous treatment of hyperhomocysteinemia in patients on chronic hemodialysis--a pilot study.

BACKGROUND: Treatment of hyperhomocysteinemia in patients with end-stage renal disease (ESRD) can be performed with the oral application of vitamins. However, this therapy rarely normalizes total homocysteine (tHcy) levels. Frequently, a rebound is observed after the end of treatment. Currently, no data are available about intravenous combination therapy with folic acid, pyridoxine (B6), and cyanocobalamin (B12). METHODS: We conducted a prospective pilot study comprising 13 patients on chronic hemodialysis treatment (63.7+/-4.9 years; 6 female, 7 male) for 27 weeks. The patients received 10 mg folic acid and 100 mg pyridoxine intravenously (IV) after each dialysis plus 1000 microg vitamin B12 IV once a week for 9 weeks. Between weeks 10 and 18 the patients received 10 mg folic acid, 100 mg vitamin B6 once a week, and 1000 microg vitamin B12 bimonthly IV. RESULTS: The therapy regimen decreased tHcy concentration (baseline: 30.5+/-2.2 micromol/L) significantly to 17.4+/-1.2 micromol/L, 15.6+/-1.0 micromol/L, and 16.4+/-0.1 micromol/L after 3, 6, and 9 weeks, respectively (p<0.01 vs. baseline concentration). The maximum reduction (-47.5+/-3.3%) of tHcy concentration was measured after 6 weeks of therapy. During the following maintenance therapy, tHcy-levels did not increase and no rebound of tHcy was detected during follow-up (week 27:16.5+/-1.97 micromol/L). CONCLUSION: The concept of a short, high-dose induction therapy with intravenous folic acid, pyridoxine, cyanocobalamin, and a subsequent low-dose maintenance regimen is effective in the treatment of hyperhomocysteinemia in patients with ESRD.

Aged↗
PubMed2004

Binding of HCV E2 to CD81 induces RANTES secretion and internalization of CC chemokine receptor 5.

Hepatitis C virus (HCV) infection has been shown to be associated with reduced expression of the CC chemokine receptor (CCR) 5, and reduced responsiveness of lymphocytes to chemokines. However, the mechanism by which HCV alters CCR5 expression remains unclear. Here, we investigated whether altered CCR5 expression in hepatitis C results from interactions of CD81 with the HCV E2 protein. Peripheral blood mononuclear cells (PBMC) from HCV-negative individuals were prepared by Ficoll density gradient separation. PBMC subpopulations (CD4+, CD8+ lymphocytes, CD19+ B cells, natural killer (NK) cells and monocyte-derived dendritic cells) were isolated and stimulated with immobilized HCV E2, and changes in CCR5 expression and CC-chemokine secretion were determined. Migration assays were performed using a 5-microm nitrocellulose filter microchamber system according to the manufacturer's recommendations. Exposure of PBMC to HCV E2 induced a dose-dependent release of regulated on activation normal T-cell-expressed and secreted (RANTES), down-regulation of CCR5 expression and intracellular accumulation of CCR5. This effect was blocked by preincubation of PBMC with anti-CD81. RANTES release following exposure to HCV E2 was mainly attributable to CD8+ cells. After exposure to HCV E2 markedly fewer CD8-positive lymphocytes were attracted by RANTES when compared with CD8+ cells that were studied in the absence of HCV E2. Our results suggest that interaction of HCV E2 with CD81 leads to increased RANTES secretion by CD8+ lymphocytes which induces down-regulation of CCR5 surface via receptor internalization resulting in altered lymphocyte migration.

Adult↗
PubMed2004

Tumour suppression induced by the macrophage activating lipopeptide MALP-2 in an ultrasound guided pancreatic carcinoma mouse model.

BACKGROUND AND AIM: Carcinoma of the exocrine pancreas has a particularly poor prognosis. Therefore, novel therapeutic strategies such as immunotherapy are required. Here we investigated the immunomodulatory capacity of macrophage activating lipopeptide 2 (MALP-2), which binds to toll-like receptors 2 and 6 and induces activation of nuclear factor kappaB in monocytes. This causes the release of early stage leucocyte attracting chemokines and proinflammatory cytokines. METHODS: MALP-2 was tested in a new orthotopic ultrasound guided pancreatic cancer mouse model. This model is close to the biological situation and avoids the stress and immunostimulation caused by laparotomy. Cells from the syngeneic, highly aggressive, and metastatic cell line Panc 02 were administered orthotopically, by ultrasound guidance, to C57bl/6 mice. MALP-2 was administered intratumorally or intraperitoneally and tumour growth, immune status, and leucocyte infiltration at the tumour site were determined. RESULTS: We showed a tumour suppressive effect induced by a single injection of MALP-2. Median survival increased from 21 to 30 days (p<0.002). Combining chemotherapy (gemcitabine) with MALP-2 treatment caused further prolonged survival (median survival 27 days with chemotherapy alone v 37 days for combined treatment; p<0.0002). The life prolonging effect was paralleled by a significant increase in cytotoxic T cells, restoration of beta2 integrin expression on lymphocytes, and high expression of CD45RB on T helper cells. Immunohistochemical stains showed strong cytotoxic T lymphocyte and natural killer cell infiltration. CONCLUSIONS: In conclusion, in a model of orthotopic pancreatic cancer in mice, we induced a tumour suppressive effect by treatment with a synthetic lipopeptide. Treatment with MALP-2 could be an option for immunotherapy in pancreatic cancer.

Adenocarcinoma↗
PubMed2004

Influence of rifampin on serum markers of cholesterol and bile acid synthesis in men.

OBJECTIVE: It has been demonstrated in preliminary studies that rifampin, a semisynthetic antibiotic and known inducer of hepatic cytochrome P450 3A4, reduces serum concentrations of total bile acids only in individuals with liver disease and elevated serum bile acid levels. METHODS: We studied the effect of rifampin on concentrations of surrogate serum markers of cholesterol and bile acid synthesis as well as of cholesterol absorption in 10 male subjects before and after administration of rifampin (600 mg/day) for 6 days. Cholesterol and its precursors were analyzed by gas-liquid chromatography (GLC), bile acid intermediates and individual bile acids by isotope-dilution methods using GLC-mass spectrometry (MS) or by high-performance liquid chromatography (HPLC). RESULTS: Treatment with rifampin resulted in a 70% increase (p = 0.008) of the serum concentration of the bile acid precursor 7alpha-hydroxy-4-cholesten-3-one, which is a marker for bile acid production. Serum total cholesterol was not altered, however, treatment with rifampin elevated the ratio of lathosterol to cholesterol, an indicator of cholesterol synthesis, by 23% (p = 0.037). Interestingly, serum concentration of total bile acids decreased slightly by 29% (p = 0.022), mainly due to a lowering of the secondary bile acid, deoxycholic acid (-60%; p = 0.005). CONCLUSION: A 6-day treatment with rifampin induces a reduction of deoxycholic serum concentrations in healthy men associated with a moderate increase of serum markers of bile acid and endogenous cholesterol synthesis.

Adult↗
PubMed2003

Prognostic value of CA 19-9 levels in patients with inoperable adenocarcinoma of the pancreas treated with gemcitabine.

Serum carbohydrate antigen 19-9 (CA 19-9) has been identified as a useful tumour marker for diagnosis of exocrine pancreatic carcinoma, but its value for evaluating the response to chemotherapy with gemcitabine is not clear. Tumour regression in pancreatic carcinoma is hard to determine due to massive desmoplastic tissue. Furthermore, objective tumour response does not automatically transcribe into better survival. Therefore, clinical benefit response, a composed parameter consisting of factors like performance status, pain, and body weight was integrated in evaluating tumour response. The aim of this prospective study was to evaluate the usefulness of serial CA 19-9 measurements as a biochemical response marker and an outcome prognostic parameter in patients with advanced pancreatic cancer receiving gemcitabine treatment. A total of 46 consecutive patients (median age 66 years) suffering from histologically proven locally advanced or metastatic adenocarcinoma of the exocrine pancreas were analysed. Gemcitabine was applied for a median of 23 courses (range 6-76). Two patients achieved an objective complete remission, five an objective partial remission (overall response, OR=15.2%), while objective stable disease was documented in 19 and objective progressive disease in 20 patients. Patients with a decrease of >20% of the baseline CA 19-9 level after 8 weeks of chemotherapy had a significantly better median survival than patients with a rise or a decline <20%. The response of CA 19-9 >20% during chemotherapy was the only independent predictor of survival in a multivariate analyses. In contrast, neither objective tumour response nor clinical benefit response showed this level of significance. In conclusion, kinetics of CA19-9 serum concentration serves as an early indicator of response to gemcitabine chemotherapy in advanced pancreatic cancer.

Adenocarcinoma↗
PubMed2003

Effect of propranolol and depot lanreotide SR on postprandial and circadian portal haemodynamics in cirrhosis.

BACKGROUND: Long-acting somatostatin analogues have been suggested as an alternative to propranolol for the prevention of variceal rebleeding. AIM: To compare the effectiveness of lanreotide SR, a new depot formulation injected once-weekly, and propranolol in reducing circadian portal blood flow (PVF) and meal-stimulated hepatic venous pressure gradient (HVPG) in patients with liver cirrhosis. METHODS: Patients were randomized to receive either lanreotide SR intramuscularly (30 mg once weekly, n=12) or propranolol (n=12) orally. Hemodynamic measurements were performed on day 0 and on day 21 after a 3-week period of drug administration, while patients received three standard oral liquid test meals. On each study day 27 PVF measurements were performed over 24 h and eight measurements of HVPG during the first postprandial period. RESULTS: Propranolol was more effective than lanreotide SR in reducing baseline HVPG (-21.9 vs. -13.6%, P=0.04) and meal-stimulated HVPG (-16.6 vs. -3.8%, P=0.04). Propranolol reduced circadian PVF significantly by 9.3% (P=0.03) but not lanreotide SR. CONCLUSIONS: Long-term treatment with propranolol reduced baseline and postprandial HVPG and circadian PVF, while lanreotide SR did not. The results of our study do not encourage clinical testing of lanreotide SR 30 mg for the prevention of variceal haemorrhage.

Antihypertensive Agents↗
PubMed2003

Piperacillin-tazobactam is more effective than ceftriaxone plus gentamicin in febrile neutropenic patients with hematological malignancies: a randomized comparison.

GOALS: Efficacy and costs of empirical antibacterial therapy in febrile neutropenic patients are important issues. Several strategies have been reported to be similarly effective: monotherapy with cefepime, ceftazidime or a carbapenem or duotherapy with an antipseudomonal beta-lactam antibiotic or ceftriaxone in combination with an aminoglycoside. Piperacillin-tazobactam monotherapy is promising, but its role in this setting still has to be defined. PATIENTS AND METHODS: Of 212 consecutive febrile episodes in 130 neutropenic patients with hematological malignancies randomized to receive either piperacillin-tazobactam (4.5 g every 8 h; group A) or ceftriaxone (2 g once daily plus gentamicin 5 mg/kg once daily; group B), 183 episodes (98 group A, 85 group B) were evaluable for response. RESULTS: Defervescence within 72 h without modification of the antibiotic therapy was achieved in 56/98 episodes (57.1%) in group A and in 30/85 (35.3%) in group B (P=0.0047). If fever persisted, teicoplanin plus gentamicin (group A) or teicoplanin plus ciprofloxacin (group B) were added. All patients still febrile then received meropenem, teicoplanin and amphotericin B. With these modifications of antibiotic therapy, 89.8% of patients in group A had responded at 21 days but only 71.8% in group B (P=0.005). The mean total antibiotic drug cost in group A was only 39.4% of that in group B (euro 445 versus euro 1129; P=0.010). CONCLUSION: Piperacillin-tazobactam monotherapy is significantly more effective and cost-efficient than ceftriaxone plus gentamicin as first-line therapy in febrile neutropenic patients with hematological malignancies.

Adolescent↗
PubMed2003

Superior virological efficacy of ritonavir-boosted protease inhibitor regimens compared to single protease inhibitor therapy.

Low dose-ritonavir boosted protease inhibitors are increasingly being used for the first-line antiretroviral treatment, though their virological efficacy has just poorly been compared to alternative antiretroviral therapies. Here, we retrospectively investigated the virological responses of 316 protease inhibitor-naive HIV patients receiving highly active antiretroviral treatment based on a single (n = 256) or a ritonavir-boosted protease inhibitor (n = 60), both in the background of two nucleoside analogues. - By intent-to-treat analysis, a complete initial virological response was achieved in 71.8% of all patients in the single protease inhibitor group (indinavir: 76%, ritonavir: 67.5%, nelfinavir: 70.6%) and in 88.3% (p = 0.008) of patients treated with a boosted protease inhibitor (saquinavir/r: 71.4%, indinavir/r: 92.1%, lopinavir/r: 86.6%). The multivariate risk analysis identified boosted PI treatment as an independent predictor of a complete virological response (OR = 2.8, p=0.02). Viral rebound after an initial complete virological response was observed in 28% and 17% (p = 0.06) of patients receiving a single or a dual protease inhibitor, respectively. The rate of durable viral suppression over 12 months was 44.5% and 56.7% (p = 0.09) in the respective study cohorts. Ritonavir-boosted protease inhibitors therefore seem to induce a superior virological response rate and a higher degree of sustained virological suppression.

Adult↗
PubMed2003

[Chronic diarrhea in a 43-year-old patient].

A 43-year old patient came to our clinic with chronic diarrhea. Determination of the faecal alpha 1-antitrypsin-clearance led to the diagnosis of exsudative enteropathy. Blood counts showed pronounced lymphocytopenia. Histopathological findings from intestinal and colorectal biopsies showed diffuse lymphangiectasis. Following exclusion of secondary types, our diagnosis was primary intestinal lymphangiectasis. Additional distinctive morphological and anamnestic features strongly suggested presence of Noonan's syndrome. Characteristic manifestations of Noonan's syndrome include changes in the lymphatic vessels in accordance with primary lymphangiectasis. Frequently, these changes are localized in the lungs. To date, only rare cases of intestinal lymphangiectasia in Noonan's syndrome have been reported. Treatment consisted of a protein-rich diet, with reduced fat content enriched by middle-chain fatty acids, as well as twice-daily injections of 200 micrograms octreotide. With this therapy, the symptoms improved.

Adult↗
PubMed2003

[Acute biliary colic. Etiology, diagnosis and therapy].

Acute biliary pain represents the main symptom of gallbladder stones, less frequently of common bile duct stones or functional disorders of the biliary tract. The pain lasts at least 15 minutes, is typically localized to the epigastrium or the right upper quadrant of the abdomen and my radiate to the right shoulder. Diagnosis of biliary pain is primarily based on clinical criteria, ultrasound allows detection of causative gallstones with high sensitivity and specificity. Analgesics and laparoscopic cholecystectomy are widely accepted as standard therapy for the majority of patients.

Biliary Tract Diseases↗
PubMed2003

IgA class antineutrophil cytoplasmic antibodies in primary sclerosing cholangitis and autoimmune hepatitis.

Antineutrophil cytoplasmic antibodies (ANCA) of IgG class have been described at high prevalence in autoimmune hepatitis (AIH) and primary sclerosing cholangitis (PSC). Data on IgA class ANCA in these diseases are limited. The aim of this study was to determine the prevalence and fluorescence patterns of IgA class ANCA in AIH and PSC and to examine a relationship between the presence of IgA ANCA and clinical characteristics in these patients. Sera from 35 patients with PSC (21 with concomitant inflammatory bowel disease), 40 patients with AIH and 10 healthy controls were studied. ANCA were detected on ethanol-fixed neutrophils using an indirect immunofluorescence technique. ANCA of the IgA class were found in 20% of sera from patients with PSC and in 50% of AIH sera. The majority of AIH patients with IgA class ANCA showed a 'classical' perinuclear staining pattern, whereas the 'classical' and 'atypical' perinuclear fluorescence patterns were distributed equally in PSC. In sera containing IgG and IgA class ANCA simultaneously, IgG class ANCA showed an 'atypical' pANCA fluorescence pattern whereas IgA class ANCA produced a 'classical' perinuclear staining. The presence of IgA class ANCA was not associated with disease-specific clinical characteristics. IgA class ANCA are more frequently detected in sera of patients with AIH than PSC. The diversity of fluorescence patterns points to different target antigens of IgA class ANCA with distinct subcellular localizations.

Adolescent↗
PubMed2003

Portal hypertension is associated with increased mRNA levels of vasopressor G-protein-coupled receptors in human hepatic arteries.

BACKGROUND: The contractile response of human splanchnic vessels to different vasoconstrictors is attenuated in cirrhosis. Functional studies indicate a cellular signalling defect upstream of the G-protein level. The aim of the present study was to analyze expression and mRNA levels of the following most relevant vasopressor receptors in the smooth musculature of human hepatic arteries: alpha1 adrenoceptor (AR) subtypes a, b and d, angiotensin II type 1 receptor (AT1), arginine vasopressin receptor type 1a (V1a), endothelin receptor type A (ETA) and B (ETB). MATERIALS AND METHODS: Hepatic arteries were collected from 10 donors (noncirrhotic) and 14 recipients (cirrhotic) at liver transplantations. Real-time-PCR was performed to quantify steady-state levels of receptor mRNAs. RESULTS: alpha 1aAR mRNA levels showed no significant difference between the cirrhotic arteries and the controls while the mRNA levels of the other vasoactive receptors were significantly higher in the cirrhotic hepatic arteries (alpha 1bAR: 4-fold, P = 0.013; AT1: 16-fold, P = 0.024; V1a: 23-fold, P = 0.001; ETA: 4-fold, P = 0.02; ETB: 8-fold, P = 0.008). No mRNA for the alpha 1dAR was detected either in the donor or recipient hepatic arteries. CONCLUSION: We conclude that vascular hyporeactivity to the most relevant endogenous vasoconstrictors of cirrhotic hepatic arteries is not caused by a receptor down-regulation at mRNA levels. In contrast they were up-regulated.

Adult↗
PubMed2003

Acute haemodynamic effects of losartan in anaesthetized cirrhotic rats.

BACKGROUND: Portal hypertension in cirrhosis is the result of increased intrahepatic vascular resistance to portal outflow as well as increased portal tributary blood flow. The angiotensin II type 1 receptor antagonist losartan has been suggested as a portal pressure-lowering drug in patients with cirrhosis. AIM: To investigate the systemic and splanchnic haemodynamic effects of different doses of losartan. METHODS: In 35 anaesthetized rats with secondary biliary cirrhosis, 3, 10 or 30 mg of losartan kg(-1) or solvent were administered intravenously. Ten sham-operated rats served as controls. Mean arterial pressure and portal pressure were measured by catheters in the femoral artery or portal vein. Systemic and splanchnic haemodynamics and mesenterico-systemic shunt rate were determined by the coloured microsphere method. RESULTS: Losartan reduced portal pressure (sham: 9.1 +/- 0.4. cirrhosis: 19.3 +/- 1.1, after 3 mg kg(-1) of losartan 16.4 +/- 0.4, after 10 mg kg(-1) of losartan 15.6 +/- 0.6, after 30 mg kg(-1) of losartan 14.9 +/- 0.6 mmHg) without reducing portal sinusoidal resistance. However, in cirrhotic rats it reduced portal tributary blood flow (sham: 4.3 +/- 0.6. cirrhosis: 8.6 +/- 1.4, after 3 mg kg(-1) of losartan 3.8 +/- 0.7, after 10 mg kg(-1) of losartan 4.7 +/- 0.5, after 30 mg kg(-1) of losartan 5.9 +/- 0.9 mmHg). This was owing either to an increase in splanchnic vascular resistance at the 3 mg kg(-1) dose or to a reduction in the splanchnic perfusion-pressure gradient secondary to a reduction in mean arterial pressure at the 10 and 30 mg kg(-1) doses (mean arterial pressure: sham: 109.7 +/- 4.8. cirrhosis: 109.4 +/- 2.8, after 3 mg kg(-1) of losartan 99.7 +/- 2.9, after 10 mg kg(-1) of losartan 89.9 +/- 3.4, after 30 mg kg(-1) of losartan 81.0 +/- 2.9 mmHg). CONCLUSIONS: Low doses of losartan reduce portal hypertension by an increase in splanchnic vascular resistance without hypotensive side-effects on arterial pressure.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2003

Changes of lymphocyte apoptosis associated with sequential introduction of highly active antiretroviral therapy.

OBJECTIVE: To assess the effect of highly active antiretroviral therapy (HAART) on surrogate markers of lymphocyte apoptosis in HIV 1-infected individuals. METHODS: Ex vivo apoptosis was studied prospectively in 26 antiretroviral naive HIV-positive patients up to 12 weeks after sequential initiation of HAART [phase I: nucleoside reverse transcriptase inhibitor (NRTI), phase II: NRTI + protease inhibitor (PI)]. Apoptosis was assessed via CD95-, Apo2.7-expression and annexin-V-binding in peripheral CD4, CD8, B and NK-cells, and compared to changes in activation markers (HLA-DR, CD38) and viral loads. RESULTS: After introduction of HAART CD4-counts rose significantly mainly through cell redistribution, while activation markers decreased. Although Apo2.7 expression decreased throughout the study period, it was not possible to establish a correlation to the rise in CD4 cells. Unexpectedly, CD95 expression and annexin V binding were elevated during phase I of treatment without PI and began to decline only after the addition of a PI in phase II. Poor responders to antiretroviral therapy had significantly higher CD95 expression and annexin V binding in the initial phase of antiretroviral regimen. CONCLUSION: These data show divergent effects of HAART on surrogate markers of apoptosis, when treatment is initiated sequentially with NRTIs first. Partial suppression of HIV replication during treatment without PI may be associated with increased rates of apoptosis.

ADP-ribosyl Cyclase↗
PubMed2003

Benign hepatic tumours.

Benign hepatic tumours include a broad spectrum of regenerative and true neoplastic processes. Due to advances in imaging procedures like MRI, Cf-scan and ultrasound as well as progress in immunohistochemistry, the appropriate diagnosis is made ina high percentage of patients without laparotomy and resection. Most important in clinical practice is the differential diagnosis of focal nodular hyperplasia and hepatocellular adenoma because of the risk of rupture and bleeding in the latter. Cavernous haemangioma, the most common benign hepatic tumour, rarely needs treatment. The diagnosis of nodular regenerative hyperplasia is often missed and patients present with secondary complications and signs of portal hypertension that necessitate treatment. The main problem in angiomyolipoma is to distinguish it from malignant processes which do require treatment. Because of its clinical presentation, inflammatory pseudotumour is also sometimes confused with a malignant tumour. Therapeutic options are drug therapy or surgical resection. Benign haemangioendothelioma of the infant is rare but may cause life-threatening complications. Bile duct adenoma is an incidental finding that is not known to cause any symptoms whereas biliary cystadenoma is often symptomatic and may progress to cystadenocarcinoma and therefore needs resection.

Adenoma, Liver Cell↗
PubMed2003

[Drug- and toxin-induced hepatotoxicity].

The liver is essential for metabolism of drugs and exogenous toxins. Therefore, liver toxicity due to natural, domestic and industrial toxins or drugs is common but rarely recognised. Although thorough epidemiological data are missing, the number of cases with drug-induced liver toxicity is increasing, parallel to the growing number of drugs. Adverse hepatic reactions may present as acute or chronic liver damage. Independent from the cause and mechanism of liver damage, the clinical presentation may be either cytolytic or cholestatic. In addition, liver damage may be accompanied by a systemic hypersensitivity reaction against the applied agent. Drug- or toxin-induced liver damage includes vascular damage, induction of liver tumours and development of liver cirrhosis. The prerequisite for specialised treatment of drug-induced adverse hepatic reactions is establishing the diagnosis which is obtained by a thorough medical history taken by an experienced physician with a special emphasis on drug or toxin exposure. The diagnosis may be confirmed by additional diagnostic measures (e. g. liver biopsy) or the clinical course after exposure to the causing agent has been stopped. Only in a minority of cases a definite treatment may be available. Therefore, the main aim is to prevent chronic liver damage through early and correct diagnosis. Due to the extensive variety of possibly liver toxic drugs and chemical agents this aspect is a major challenge to physicians.

Antidotes↗
PubMed2003

Cystatin C as an endogenous marker of glomerular filtration rate in renal transplant patients.

BACKGROUND: Serum creatinine is the most common endogenous marker used to estimate the glomerular filtration rate (GFR). However, creatinine depends considerably on muscle mass, and its tubular secretion increases, especially in chronic renal failure. Cystatin C is a 13-kD protease inhibitor which is produced by all nucleated cells and is independent of muscle mass and sex. Cystatin C is eliminated by glomerular filtration and metabolized by proximal tubular cells. Its measurement has been proposed as an alternative and more sensitive marker of GFR than creatinine in patients with slight to moderately decreased GFR. METHODS: We investigated serum cystatin C levels in comparison with creatinine as a single measurement for estimation of GFR in 173 patients after renal transplantation. GFR was calculated as creatinine clearance according to standard equations. RESULTS: Serum creatinine correlated well with cystatin C (r = 0.84; p < 0.0001). No significant differences were obtained for the comparison of the linear correlation of 1/creatinine with creatinine clearance (r = 0.77; p < 0.0001) and for the linear correlation of 1/cystatin C with creatinine clearance (r = 0.73; p < 0.0001). However, we found a significant advantage of cystatin C in detecting a clinical relevant reduction of kidney function (GFR <70 ml/min; p = 0.0047, McNemar test). CONCLUSION: Cystatin C is an alternative marker for the assessment of GFR in renal allograft recipients that may be superior to creatinine.

Adult↗