PubMed Health⌕ Search

Biomedical subjects

M Zeier

Publications and source records attributed to M Zeier.

At least 37 records · Page 2Linked to original sources
PubMed2003

[Uremic patients--late referral, early death].

BACKGROUND AND OBJECTIVE: A number of reports from various countries document that patients with renal failure who are referred late to renal units, have more complications e. g. lack of vascular access when dialysis has to be started as well as longer hospitalisation and have also a higher risk of early death. No data on these points are available from Germany. PATIENTS AND METHODS: In a retrospective analysis the timing of referral to the nephrologists was studied in two Departments of Medicine, e. g. Heidelberg and Vienna, for all patients who started renal replacement therapy. For patients in Heidelberg the relation between timing of referral and survival on dialysis was analysed using the Kaplan-Maier-technique. RESULTS: In Heidelberg 280 patients were analysed, 174 men, 106 women, age 61.8 +/- 14.5 years; 136 diabetic patients (9 type 1). They had been referred from GPs (n = 131), specialists (diabetologists, cardiologists; n = 20), emergency departments (n = 33), other hospitals (n = 90) or other institutions (n = 16). The measured median creatinine clearance at the time of referral was 14 ml/min (5-34). The median interval between referral and start of dialysis was 17 weeks. 137 patients had been referred < 17 weeks and 143 patients > or = 17 weeks prior to the start of dialysis. 97 of the 111 patients referred < or = 4 weeks prior to dialysis and 59 of the 169 patients referred > 4 weeks had to be dialysed with a central catheter. There were clear differences in patient survival. In patients referred < 17 weeks before the start of dialysis, the actuarial risk of death during the first 12 month was 34.2 % compared to 5.5 % (p < 0.0001) in patients referred > or = 17 weeks. Even the mortality in the interval between 12 and 24 months after the start of dialysis was clearly higher (15.3 %) in patients with late compared to early referral (11.4 %). CONCLUSION: Late referral of patients with impaired renal function to renal units causes more frequent problems of vascular access, longer hospitalisation, more medical complications, higher costs and higher mortality. Early referral of patients with renal failure is indispensable to improve dialysis outcomes.

Adult↗
PubMed2003

Underdiagnosis of diabetes mellitus in chronic dialysis patients on the renal transplant waiting list.

In diabetic patients long-term patient and graft survival after renal transplantation is reduced compared to nondiabetic graft recipients. Incidence and prevalence of diabetic patients on dialysis is rising continuously; however, there is a surprisingly low prevalence of patients with known diabetes mellitus on our local renal transplant waiting list. In a retrospective study we clarified the underestimation of diabetic dialysis patients on the transplant waiting list. Our local waiting list includes 46 diabetic patients among 377 (12.2%) candidates. Nine patients had type 1 diabetes and 37 type 2 diabetes. Surprisingly, only 20 of 37 patients (ie, 54%) were initially (at the time of wait-listing) classified as (type 2 diabetes mellitus). Primary renal disease in these 17 diabetic patients was classified in only eight patients, whereas the remaining nine were considered as chronic glomerulonephritis (not biopsy-proven and diabetic nephropathy not excluded). We conclude that among uremic patients on the renal transplant waiting list, the prevalence of diabetes mellitus and the number of patients with diabetic nephropathy are notably underdiagnosed.

Diabetes Mellitus↗
PubMed2003

Review of the antiproliferative properties of mycophenolate mofetil in non-immune cells.

Mycophenolate mofetil (MMF), the prodrug ofmycophenolic acid (MPA), is a selective, non-competitive and reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH) and of the type II isoform in particular. IMPDH is the rate-limiting enzyme in the de novo biosynthesis of guanosine nucleotides. MMF strongly inhibits both T- and B lymphocyte proliferation and has been used in the prevention of acute and chronic allograft rejection since the mid 1990s. Recent evidence, however, suggests that MMF is also capable of inhibiting the proliferation of non-immune cells. In various cell lines, i.e. smooth muscle cells, renal tubular cells and mesangial cells, MPA reduced or even abrogated proliferation in response to proliferative stimuli. Furthermore, data from our own laboratory demonstrate a dose-dependent inhibition of dermal fibroblast proliferation by MPA. In animal studies, MMF ameliorated renal lesions in immune-mediated disease, i.e. in the anti-thy 1.1 model and experimental lupus nephritis, but was also effective in non-immune-mediated renal damage in the rat remnant-kidney model. These observations prompted several investigators to study the effects of MMF in proliferating (renal) disease of non-immune origin in humans. MMF significantly reduced proteinuria in minimal-change disease and focal segmental glomerulosclerosis. In addition, MMF showed beneficial effects in the treatment of chronic allograft nephropathy and calcineurin inhibitor toxicity through reduction of immune- and non-immune-mediated renal damage. MMF is well tolerated and has proven to be a relatively safe drug causing only minor bone marrow suppression. Taken together, there is a growing body of evidence pointing to therapeutic applications of MMF other than immunosuppression, in particular the prevention of fibrosis.

Animals↗
PubMed2003

Hypertension after renal transplantation.

With current immunosuppression elevated blood pressure is found in almost 90% of renal graft recipients. Major causes of this finding are impairment of renal function, secondary to chronic allograft nephropathy or (less frequently) recurrence of primary renal disease, the use of calcineurin inhibitors as immunosuppresants, uncontrolled renin secretion by the shrunken kidneys of the recipient, stenos- ing lesions of the transplant artery (or the upstream arteries of the recipient), polycytemia and (genetic predisposition to) hypertension of the graft donor. Even minor degrees of blood pressure elevation have a significant impact on survival of the recipient and on graft survival, presumably by amplifying vascular injury to the graft. In this respect, elevation of systolic blood pressure and an abnormal circadian blood pressure profile are of particular relevance. In contrast to previous opinion, ACE inhibitors are indicated in the treatment, but, given the causal role of sodium retention in graft vasoconstriction, diuretics and calcium channel blockers remain main stays of antihypertensive treatment in the renal allograft recipient.

Antihypertensive Agents↗
PubMed2002

Treatment of life-threatening multiresistant staphylococcal and enterococcal infections in patients with end-stage renal failure with quinupristin/dalfopristin: preliminary report.

BACKGROUND: Life-threatening infections with multiresistant gram-positive bacteria are increasing. Treatment with quinupristin/dalfopristin (Q-D) has turned out to be effective against such resistant pathogens. PATIENTS AND METHODS: We report on treatment of six patients on dialysis (four with additional liver injury) and of one renal graft recipient with normal renal function who had severe infections caused by multiresistant Staphylococus epidermidis (1/7), methicillin-resistant Staphylococcus aureus (4/7) and vancomycin-resistant Enterococcus faecium (2/7). RESULTS: Six out of seven patients were cured by therapy with Q-D in adjusted doses lasting for 10 to 34 days. Pharmacokinetics of Q-D and its metabolites were determined and remained within the therapeutic range, despite a modest increase of all compounds at the presumed steady state. The concentrations of the metabolites of Q-D were clearly lower than the parent drugs, including those of quinupristin-conjugated derivatives, which has not been reported previously. CONCLUSION: These preliminary results suggest that: a) neither quinupristin nor dalfopristin or its metabolites accumulated despite the long duration of treatment; b) no adjustment of the standard dosage regimen (three times 7.5 mg/kg/day) is necessary in end-stage renal disease.

Aged↗
PubMed2002

Risk of mortality in patients with end-stage renal disease: the role of malnutrition and possible therapeutic implications.

The mortality rate of dialysis patients is still considerably high. Beside the traditional risk factors, specific uremia-related risk factors are identified. Among them, hypoalbuminemia and malnutrition have a strong association to mortality in chronic dialysis patients. Various studies document a strong relation between reduced calorie and protein uptake and mortality in uremic patients. Several factors responsible for malnutrition in dialysis patients have been identified. These factors may be dialysis-associated, due to intercurrent illnesses or are associated with uremic complications (e.g. hyperparathyroidism, anemia, acidosis, etc.). Malnutrition is treatable and can be avoided by several means. Beside the increase in the dose of dialysis and adequate protein and calorie intake, intradialytic nutrition is an additional choice. The combination with specific drugs (e.g. growth hormone) may potentiate the success of the modified treatment modalities, particularly in patients who need nutritional support during an intercurrent illness. Further studies are required to measure the impact of for example growth hormone supplementation on mortality rate and quality of life in malnourished patients on chronic dialysis.

Humans↗
PubMed2001

[Incidence and clinical characteristics of renal insufficiency in diabetic patients].

BACKGROUND: In all Western countries there is a dramatic increase of diabetic patients who need renal replacement therapy. Very different figures for incidence and prevalence have been reported. There is a strong suspicion that the epidemiological dimension of the problem has been underestimated in many of the statistics. METHODS: In a retrospective analysis we assessed all patients admitted to the Department Internal Medicine Heidelberg from January 1(st) 1998 - December 31(st), 2000 for renal replacement therapy, i. e. hemodialysis or CAPD, because of acute or chronic renal failure. We counted the number of known diabetic patients (i) with signs of classical diabetic nephropathy (enlarged kidneys, proteinuria > 1g/24h +/- retinopathy), (ii) with atypical renal changes (contracted kidneys, proteinuria < 1 g/24 h) and (iii) diabetic patients with (coincident) primary chronic renal disease as well as (iv) the proportion of patients in whom the diagnosis of diabetes had been unknown when uremia had supervened. RESULTS: Dialysis treatment was started in 568 patients for acute (ARF; n = 341) or chronic (CRF; n = 227) renal failure. 95/341 (28 %) patients with ARF had diabetes. ARF occured in no less than 12/95 (13 %) of the diabetic patients after cardiological intervention. Diabetes was present in 111/227 patients with CRF (7 type 1, 104 type 2); in 12/111 patients the diagnosis of diabetes was established only after admission. Only 67/111 of the diabetic patients (60 %) had classical signs of diabetic nephropathy, in 14/111 (13 %) patients the classical signs of diabetic nephropathy were absent and in 30/111 (27 %) non-diabetic primary chronic renal disease was present. CONCLUSION: The study illustrates the importance of diabetes for the epidemiology of renal failure. A sizeable proportion of patients with acute renal failure have diabetes, typically patients with pre-existing nephropathy in whom this complication supervenes during diagnosis and treatment of late diabetic complications. In diabetic patients with chronic renal failure the presentation is frequently atypical and non-diabetic primary renal disease is present more frequently than expected by chance. In a sizeable proportion of patients diabetes had not been diagnosed by the time chronic renal failure occurred.

Acute Kidney Injury↗
PubMed2001

Measurement of the high energy two-body deuteron photodisintegration differential cross section.

The first measurements of the d(gamma,p)n differential cross section at forward angles and photon energies above 4 GeV were performed at the Thomas Jefferson National Accelerator Facility (JLab). The results indicate evidence of an angular dependent scaling threshold. Results at straight theta(cm) = 37 degrees are consistent with the constituent counting rules for E(gamma) greater, similar 4 GeV, while those at 70 degrees are consistent with the constituent counting rules for E(gamma) greater, similar 1.5 GeV.

Journal Article↗
PubMed2001

Measurement of the electric form factor of the neutron through d-->(e-->,e(')n)p at Q2 = 0.5 (GeV/c)(2).

We report the first measurement using a solid polarized target of the neutron electric form factor G(n)(E) via d-->(e-->,e(')n)p. G(n)(E) was determined from the beam-target asymmetry in the scattering of longitudinally polarized electrons from polarized deuterated ammonia ( 15ND3). The measurement was performed in Hall C at Thomas Jefferson National Accelerator Facility in quasifree kinematics with the target polarization perpendicular to the momentum transfer. The electrons were detected in a magnetic spectrometer in coincidence with neutrons in a large solid angle segmented detector. We find G(n)(E) = 0.04632+/-0.00616(stat)+/-0.00341(syst) at Q2 = 0.495 (GeV/c)(2).

Journal Article↗
PubMed2001

Characterization and phylogenetic analysis of South African HIV-1 subtype C accessory genes.

To acquire new knowledge about the genetic diversity and potential impact on vaccine strategies of HIV-1 subtype C in South Africa, we have characterized the vif, vpr, and vpu genes of 15 isolates. Phylogenetic analysis of the genomic fragment encompassing these genes revealed subtype C subclusters, suggesting close relatedness with subtype C strains from other geographic locations and excluded isolation of South African strains. The putative T155 phosphorylation site in the C terminal of Vif was absent in all subtype C sequences. Variation in the predicted amino acid sequences of the three genes further showed strong correlation with other subtype C sequences.

AIDS Vaccines↗
PubMed2001

Advanced glycation endproducts (AGEs) as uremic toxins.

Products of non-enzymatic glycation accumulate both in diabetic and non-diabetic patients with renal failure. The increase in concentration is presumably due to increased generation, secondary to oxidative stress and due to decreased (renal) elimination; whether accumulation of AGEs of dietary origin plays a role is currently under investigation. AGE's have been related to progression of diabetic (and possibly also non-diabetic) renal disease and to a number of complications of the uremic syndrome. These comprise beta-2-microglobulin-derived dialysis-related amyloidosis, dyslipidemia, vascular dysfunction and accelerated atherogenesis. A specific case is AGE related damage to the peritoneal membrane in CAPD patients. Removal of AGE by dialysis is negligible and even high flux dialysis eliminates only a quantitatively limited amount of AGE. In contrast, a rapid decrease of AGE concentrations in plasma is noted after renal transplantation. Dietary AGEs may contribute significantly to the total AGE load of the body, particularly in uremia.

Diabetic Nephropathies↗
PubMed2001

Hypertension after renal transplantation.

With current immunosuppression, elevated blood pressure is found in almost 90% of renal graft recipients. Major causes of this are impairment of renal function (secondary to chronic allograft nephropathy or less frequently recurrence of primary renal disease), the use of calcineurin inhibitors as immunosuppressants, uncontrolled renin secretion by the shrunken kidneys of the recipient, stenosing lesions of the transplant artery (or the upstream arteries of the recipient), polycythemia, and genetic predisposition to hypertension of the graft donor. Even minor degrees of blood pressure elevation have a significant impact on survival of the recipient and on graft survival, presumably by amplifying vascular injury to the graft. In this respect, elevation of systolic blood pressure and an abnormal circadian blood pressure profile are of particular relevance. In contrast to previous opinion, angiotensin converting enzyme inhibitors are indicated in treatment, but given the causal role of sodium retention and graft vasoconstriction, diuretics and calcium channel blockers remain mainstays of antihypertensive treatment in the renal allograft recipient.

Antihypertensive Agents↗
PubMed2001

Blood pressure after renal transplantation.

Hypertension is extremely common in renal allograft recipients, mainly as the result of impaired renal function and cyclosporin A therapy. Blood pressure is a powerful independent predictor of longterm graft outcome. This adverse effect is presumably mediated by both hemodynamic and non-hemodynamic factors. There is also evidence for activation of the renin angiotensin system in the renal allograft. Antihypertensive treatment is of known benefit on graft outcome in experimental models, but this has so far not been documented in clinical trials. Proteinuria is another independent predictor of longterm graft outcome. There is recent documentation of a specific antiproteinuric effect of ACE inhibitors on proteinuria which is of interest since proteinuria is an independent predictor of longterm graft outcome.

Antihypertensive Agents↗
PubMed2001

Hypertension after renal transplantation.

With current immunosuppression, elevated blood pressure is found in almost 90% of renal graft recipients. Major causes of this are impairment of renal function, secondary to chronic allograft nephropathy or less frequently recurrence of primary renal disease, the use of calcineurin inhibitors as immunosuppressants, uncontrolled renin secretion by the shrunken kidneys of the recipient, stenosing lesions of the transplant artery (or the upstream arteries of the recipient), polycytemia and (genetic predisposition) to hypertension of the graft donor. Even minor degrees of blood pressure elevation have a significant impact on survival of the recipient and on graft survival, presumably by amplifying vascular injury to the graft. In this respect elevation of systolic blood pressure and an abnormal circadian blood pressure profile are of particular relevance. In contrast to previous opinion, ACE inhibitors are indicated in the treatment, but, given the causal role of sodium retention and graft vasoconstriction, diuretics and calcium channel blockers remain mainstays of antihypertensive treatment in the renal allograft recipient.

Antihypertensive Agents↗