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R A Koene

Publications and source records attributed to R A Koene.

At least 19 recordsLinked to original sources
PubMed2000

Evaluation of clinical guidelines for the management of end-stage renal disease in europe: the EU BIOMED 1 study.

BACKGROUND: There are wide national and international variations in the management of patients with end-stage renal disease (ESRD). The aim of this study was to develop, harmonize, implement, and evaluate consensus-based clinical guidelines for the management of renal anaemia and renal bone disease in patients with ESRD, and for the prevention and management of cytomegalovirus disease in renal transplant recipients across six renal centres in Europe. METHODS: The trial was a prospective, multicentre, randomized balanced incomplete block design. Nephrologists from the six European renal units were randomized to develop and implement guidelines for two out of the three conditions and to act as a control for the third condition. Data were collected pre- (1 year) and post- (9 months) intervention on aspects of patient monitoring, management, and outcome. RESULTS: Eight hundred and twenty-nine dialysis patients from the six European dialysis centres were included in the study. Multivariate analysis (adjusting for case-mix and secular trends) showed a significant increase in the number of monitoring events in the guideline group compared with control group (6%, 95% CI, 1-11%). There was no concomitant increase in either appropriate management or the number of favourable patient outcomes. CONCLUSIONS: In the first European collaboration on renal guidelines, the introduction of the guidelines improved the monitoring of the patients, but did not improve patient management or outcome. This study suggests the potential for creating clinical guidelines with the aim of standardizing treatment protocols across international boundaries, and improving the quality of the medical care provided.

Adolescent↗
PubMed1999

The impact of recurrent glomerulonephritis on graft survival in recipients of human histocompatibility leucocyte antigen-identical living related donor grafts.

BACKGROUND: Graft loss due to rejection is uncommon after human histocompatibility leukocyte antigen-identical living related donor (LRD) transplantation, resulting in an excellent long-term graft survival. Data on the impact of recurrence of the original disease on graft survival after LRD transplantation are scarce. METHODS: We have studied the influence of recurrent glomerulonephritis in adult recipients of a human histocompatibility leukocyte antigen-identical LRD graft transplanted in our center in the period from 1968 to 1996. To that end, the data of 33 patients with proven or suspected primary glomerulonephritis and 27 patients with nonglomerular diseases were analyzed. RESULTS: The patient survival was similar in both groups at 5, 10, and 20 years. The functional graft survival, i.e., graft survival after censoring for death, was, however, significantly worse for patients with glomerulonephritis as underlying disease (P<0.01). At 5 years graft survival was 100% vs. 88%, at 10 years 100% vs. 70%, and at 20 years 100% vs. 63%, respectively. Thus none of the patients with nonglomerular diseases lost a graft, whereas eight grafts were lost in the group of patients with glomerulonephritis. The main cause of graft loss in this patient group was recurrent glomerulonephritis (n=5), whereas chronic vascular rejection caused graft loss in two patients and occlusion of a transplant artery was the cause in one. A clinically significant proteinuria was detected in six more patients in the glomerulonephritis group: a recurrent glomerulonephritis was diagnosed in four patients and in two patients there was no biopsy. The cumulative incidence of recurrence was as high as 45% at 12 years after transplantation. CONCLUSION: Recipients of a human histocompatibility leukocyte antigen-identical LRD kidney have a good prognosis with respect to graft survival. After censoring for death, recurrent glomerulonephritis is the main cause of graft failure in these patients and the impact of recurrent disease on graft survival will become even more prominent with longer follow-up.

Adult↗
PubMed1999

Discriminant component pruning. Regularization and interpretation of multi-layered back-propagation networks.

Neural networks are often employed as tools in classification tasks. The use of large networks increases the likelihood of the task's being learned, although it may also lead to increased complexity. Pruning is an effective way of reducing the complexity of large networks. We present discriminant components pruning (DCP), a method of pruning matrices of summed contributions between layers of a neural network. Attempting to interpret the underlying functions learned by the network can be aided by pruning the network. Generalization performance should be maintained at its optimal level following pruning. We demonstrate DCP's effectiveness at maintaining generalization performance, applicability to a wider range of problems, and the usefulness of such pruning for network interpretation. Possible enhancements are discussed for the identification of the optimal reduced rank and inclusion of nonlinear neural activation functions in the pruning algorithm.

Algorithms↗
PubMed1999

[The magnitude of the 'anion gap'].

The anion gap is used to evaluate disturbances in the acid-base balance, in particular metabolic acidosis. Due to the introduction of new clinical chemical techniques and modern analysers the reference range of the anion gap has changed. Clinical chemical laboratories should establish or verify their own anion gap reference range. Better communication between the laboratory and the clinician with regard to the anion gap is desirable.

Acid-Base Equilibrium↗
PubMed1999

Acute haemodynamic and proteinuric effects of prednisolone in patients with a nephrotic syndrome.

BACKGROUND: Administration of prednisolone causes an abrupt rise in proteinuria in patients with a nephrotic syndrome. METHODS: To clarify the mechanisms responsible for this increase in proteinuria we have performed a placebo controlled study in 26 patients with a nephrotic syndrome. Systemic and renal haemodynamics and urinary protein excretion were measured after prednisolone and after placebo. RESULTS: After i.v. administration of 125-150 mg prednisolone total proteinuria increased from 6.66+/-4.42 to 9.37+/-6.07 mg/min (P<0.001). By analysing the excretion of proteins with different charge and weight (albumin, transferrin, IgG, IgG4 and beta2-microglobulin) it became apparent that the increase of proteinuria was the result of a change in size selectivity rather than a change in glomerular charge selectivity or tubular protein reabsorption. Glomerular filtration rate rose from 83+/-34 ml to 95+/-43 ml/min (P<0.001) after 5 h, whereas effective renal plasma flow and endogenous creatinine clearance remained unchanged. As a result filtration fraction was increased, compatible with an increased glomerular pressure, which probably contributes to the size selectivity changes. Since corticosteroids affect both the renin-angiotensin system and renal prostaglandins, we have evaluated the effects of prednisolone on proteinuria after pretreatment with 3 months of the angiotensin-converting enzyme inhibitor lisinopril or after 2 weeks of the prostaglandin synthesis inhibitor indomethacin. Neither drug had any effect on prednisolone-induced increases of proteinuria. CONCLUSIONS: Prednisolone increases proteinuria by changing the size selective barrier of the glomerular capillary. Neither the renin-angiotensin axis nor prostaglandins seem to be involved in these effects of prednisolone on proteinuria.

Adolescent↗
PubMed1999

Renal transplantation in patients with dense deposit disease: morphological characteristics of recurrent disease and clinical outcome.

BACKGROUND: Dense deposit disease (DDD) is an uncommon cause of end-stage renal disease (ESRD). As a consequence, information on the outcome of renal transplantation in patients with DDD comes from series with a limited number of patients. METHODS: We present the histological and clinical data of 13 adult patients with DDD, who received their first allograft in our centre in the period between 1983 and 1994. RESULTS: Renal transplant biopsies were performed in 11 patients, at 2.9 months after transplantation (median; range 0.4-13.8 months). The indication for taking the biopsy was in all instances a raised serum creatinine level. Five patients also had a significant proteinuria. In only one patient, light microscopy showed alterations in the capillary walls suggestive of a recurrence of DDD. However, by immunofluorescence or electron microscopy, we found glomerular deposits compatible with a recurrence of DDD in all 11 patients. Three patterns of glomerular C3 deposition were found: globular depositions only in the mesangium; mesangial accumulation with linear deposits in the capillary wall; and prominent linear presence in the capillary wall with only a few mesangial granules. The findings by electron microscopy matched the immunofluorescence results. The linear C3 accumulation in the capillary wall was visible ultrastructurally as electron-dense ribbon-like transformation of the glomerular basement membrane. Mesangial C3 deposits were seen ultrastructurally as local electron-dense deposits in the mesangium. Four patients showed a pronounced glomerular influx of neutrophils, accompanied by crescents in three patients. In these three latter patients, the recurrence of DDD was the only histological lesion. In the other patients, the recurrence was merely a coincidence, the biopsy demonstrating an additional histological lesion (three chronic vascular rejection, two acute rejection, one ischaemic necrosis and two cyclosporin A toxicity). Eight patients with a recurrence of DDD have progressed to ESRD at an average of 14 months (range 0.2-38 months) after transplantation. The recurrence was the sole cause of graft loss in the three patients with crescents. The patients in whom the C3 deposits were confined to the mesangium appeared to have a better prognosis. CONCLUSIONS: The histological recurrence rate of DDD is high. The histological picture is quite diverse, and in most patients abnormalities are only found by immunofluorescence and electron microscopy. Up to one-quarter of the patients with DDD lost their grafts because of a recurrence.

Adolescent↗
PubMed1998

[Kidney donation by a 'non-heart-beating' donor from an ethical perspective].

In asystolic patients, kidney donation is possible by using a non-heart-beating (NHB) donation procedure. This involves in situ perfusion of the kidneys by inserting a catheter into the femoral artery and flushing cold fluid through the kidneys. The introduction of an NHB donation programme leads to ethical questions concerning the guarantees for prudent procedure: How should death of a patient be defined in case of NHB donation? Is there a strict separation of responsibilities of the medical teams in the different phases of the procedure (patient treatment and actual donation procedure)? Are sufficient attention and care given to the relatives? Does the NHB donation procedure not interfere with the care of a patient who is expected to die soon? Extensive discussion with the Medical Ethics Committee of the University Hospital Nijmegen, the Netherlands, has led to a protocol for NHB kidney donation that meets the required guarantees.

Cadaver↗
PubMed1998

Hyponatremia due to sodium valproate.

We describe a 50-year-old male patient with hyponatremia (serum sodium level, 128 mEq/L) discovered during routine follow-up for Henoch-Schönlein nephritis. The patient was known to have a generalized idiopathic epilepsy and was on 2,000 mg/day of sodium valproate. After exclusion of other causes such as hypothyroidism and adrenal insufficiency, we considered sodium valproate as the cause of the hyponatremia. Repeated water loading tests performed at different dosages of this drug confirmed that the ability to excrete water was reduced in a dose dependent manner. We conclude that sodium valproate can cause an SIADH-like syndrome with hyponatremia and that serum sodium levels have to be monitored during treatment with high dosages of this drug.

Anticonvulsants↗
PubMed1998

A randomised, prospective study on the conversion from cyclosporine-prednisone to cyclosporine-azathioprine at 6 months after renal transplantation.

In a randomised prospective trial, we studied the effects of replacement of prednisone (Pred) by azathioprine (Aza), 6 months after transplantation, in stable renal allograft recipients on cyclosporine and prednisone (CsA + Pred). Out of 83 patients, 42 started treatment with CsA + Aza and 41 continued therapy with CsA + Pred. CsA was dosed to achieve a level of 150 ng/ml, the Aza dose was 3 mg/kg per day and the Pred dose was 0.15 mg/kg per day. Eighteen months after randomisation, in the CsA + Aza group 18 of the 42 patients were effectively treated with CsA + Aza. In the main, anaemia, leuco- and thrombocytopenia, and hypocorticism necessitated the reintroduction of Pred in the remaining 24 patients. Compared to the continuation of CsA + Pred, conversion of Pred to Aza resulted in a reduced number of antihypertensive drugs needed, and in lower serum total, LDL and HDL cholesterol levels; the incidence of acute rejections and graft losses was no different. In conclusion, conversion of CsA + Pred to CsA + Aza is a safe option in renal transplant patients with contraindications to long-term corticosteroid treatment.

Adult↗
PubMed1998

Immunohistological and ultrastructural differences between recurrent type I membranoproliferative glomerulonephritis and chronic transplant glomerulopathy.

In renal transplant recipients with type I membranoproliferative glomerulonephritis (MPGN), the posttransplantation course can be complicated by a recurrence of the original disease. However, it is well known that a recurrence of type I MPGN and chronic transplant glomerulopathy (CTG) cannot easily be distinguished. It has been suggested that the two entities can be differentiated by using electron microscopy (EM) and immunofluorescence (IF) techniques. However, studies are lacking that compare biopsy specimens from patients with either a recurrence of type I MPGN or CTG. We have studied renal biopsy specimens from 10 patients with CTG and compared the ultrastructural and IF findings with biopsy specimens from 12 patients with a possible recurrence of type I MPGN. All the patients with CTG showed an electron-lucent zone of finely flocculent material in the subendothelial space, whereas all patients with a recurrence of type I MPGN showed subendothelial electron-dense deposits on EM. On IF, all patients with CTG showed Immunoglobulin M (IgM) with greater intensity than C3. For the patients with recurrent type I MPGN, the opposite was true. Eleven specimens showed C3 deposits with greater intensity than IgM, and in one patient, C3 and IgM were found in equal intensity. In conclusion, when IF and EM studies are available, CTG and recurrence of type I MPGN can reliably be distinguished.

Chronic Disease↗
PubMed1998

Prognostic factors in idiopathic membranous nephropathy.

Membranous nephropathy is the most frequent cause of glomerulonephritis in adults with nephrotic syndrome. Approximately one quarter of the patients develop end-stage renal disease. Another quarter enters complete remission during follow-up. Treating all patients with membranous nephropathy with immunosuppressive drugs would unnecessarily expose at least one quarter of the patients to these toxic drugs. Identifying patients at highest risk would allow tailor-made treatment. Many risk factors have been found, such as male sex, HLA type DR3+/B8+, white race, advanced age, and tubulointerstitial changes or focal sclerosis found with renal biopsy. In addition, nephrotic syndrome, elevation of immunoglobulin G excretion or beta2-microglobulin excretion, low serum albumin, high serum cholesterol, an elevation of urinary excretion of complement activation products, impaired renal function at diagnosis, and, finally, hypertension are associated with a higher risk of renal function deterioration during follow-up. We have critically reviewed the literature and summarized the clinical significance of the above-mentioned risk factors in predicting subsequent renal function deterioration in patients with membranous nephropathy.

Adolescent↗
PubMed1998

Comparing outcomes in renal replacement therapy: how should we correct for case mix?

The need to evaluate the effectiveness of clinical practice to justify expensive therapy in the face of financial constraints in all areas of health care delivery makes it necessary to identify groups of patients who are likely to benefit most from treatment. Various risk stratification methods have been used for analyzing survival probabilities for patients receiving renal replacement therapy. Complicated risk stratification methods produce large numbers of risk groups of small sizes, which makes comparison between individual centers difficult. We compared three simple methods of risk stratification, that divided patients into low-, medium-, and high-risk groups, in a cohort of 1,407 patients who commenced renal replacement therapy in five European countries during a 7-year period. Method 1 considered age (>55 years) and diabetes alone; method 2 used a higher age limit (>70 years) and comorbid illnesses, including those other than diabetes; and method 3 used only the number of comorbidities (none, 1, or > or =2) for stratification. Kaplan-Meier survival curves were constructed for comparison between risk groups and Cox's regression model used to assess strength of relationship with mortality. Although patient survival was significantly different between the low-, medium-, and high-risk groups using all three methods, Cox's regression analysis showed that method 2 provided the greatest discrimination between risk groups. In predicting mortality, method 2 (based on comorbidities and age) showed the highest sensitivity and specificity (84% and 80%, respectively) compared with method 1 (80% and 74%) and method 3 (64% and 82%). Validation of this approach in other populations in a prospective study is required before this method, which takes into account the influences of both age and comorbidity for risk stratification, can be used for comparing survival data and for presenting results of renal replacement therapy.

Adolescent↗
PubMed1998

Effects of low-dose nifedipine on urinary protein excretion rate in patients with renal disease.

BACKGROUND: The observation that proteinuria is an important determinant of the progression of renal disease has prompted numerous studies on the effects of antihypertensive agents on protein excretion. Reports on the proteinuric effects of calcium-channel blockers are quite controversial. It has been suggested that the short-acting dihydropyridine calcium-channel blocker nifedipine increases protein excretion by interference with tubular protein reabsorption. METHODS: In a randomized controlled trial 10 patients with renal disease and proteinuria were treated with a dose of 10 mg nifedipine o.d. (slow release formulation) for 1 week. The acute effects on renal and systemic haemodynamics and on urinary albumin, IgG, and beta2-microglobulin excretion were investigated during a clearance study in the supine position after the first dose. After 1 week of treatment urinary protein excretion rates were measured in 24-h urine samples collected in the ambulatory patient in consecutive fractions of 4-8 h during normal daily activities. RESULTS: After the first dose nifedipine lowered mean arterial blood pressure in the supine position by 7+/-1 mmHg (<0.01), attenuated proximal tubular sodium reabsorption (fractional excretion of sodium 3.48+/-0.49 vs 2.62+/-0.35% during control, P<0.02), but did not affect proximal tubular protein reabsorption (fractional urinary excretion of beta2-microglobulin 0.97+/-0.30 vs 0.98+/-0.32% during control, NS). The decrease in blood pressure was not accompanied by decreases in urinary albumin or IgG excretion rates. The selectivity index as well as GFR, RPF, and FF did not change. Continued treatment for 1 week with nifedipine did not influence 24-h protein excretion. However, we observed a rise of proteinuria during daily activities in the first 4 h after drug intake compared to the start of the study with the patients in supine position. During control measurements there was a slight increase in proteinuria. During nifedipine the increase in proteinuria was more marked and correlated with the selectivity index. CONCLUSIONS: (1) Nifedipine 10 mg orally did not impair tubular protein reabsorption. (2) Nifedipine had no immediate antiproteinuric effect despite the observed blood pressure reduction. (3) Nifedipine increased proteinuria in ambulatory urine collections. This latter observation might explain the seemingly different effects of dihydropyridine calcium-channel blockers as reported in previous studies.

Adult↗