[Glomerular hematuria: an atypical presentation of anti-glomerular basement membrane nephritis]. / Glomerulaire hematurie.

BACKGROUND: Urologic diseases can cause hematuria, but dysmorphic erythrocytes directs to a glomerular disease. The latter might occur isolated or in the presence of systemic complaints, proteinuria or kidney failure. These factors determine the differential diagnosis that ranges from an innocent IgA nephropathy to a fatal anti-glomerular basement membrane (GBM) nephritis. CASE: A 30-year old patient attended the outpatient clinic because of glomerular hematuria and normal kidney function with working diagnosis IgA nephropathy. Three months later he presented to the emergency department with a severe acute kidney injury duo to an anti-GBM nephritis. In retrospect, the anti-GBM titer was already high during the outpatient clinic phase, but due to the preserved kidney function, anti-GBM nephritis was not added to the differential diagnosis. CONCLUSION: Glomerular hematuria with a preserved kidney function could in a rare instance be caused by a subclinical anti-GBM nephritis. Follow-up of the kidney function and comprehensive laboratory testing - or even a kidney biopsy - could potentially lead to an early diagnosis of anti-GBM nephritis.

GUIDE, a structured pre-dialysis programme that increases the use of home dialysis.

BACKGROUND: Despite the many advantages it offers, the percentage of dialysis patients that receive home dialysis [peritoneal dialysis (PD) or home haemodialysis (HHD)] in the Netherlands has declined over the last decade. Pre-dialysis education could stimulate the use of home dialysis. This article presents the results of the pre-dialysis programme GUIDE, with regard to the following question: Does the implementation of a structured pre-dialysis programme with a home-focused approach increase the number of pre-dialysis patients that choose and receive home dialysis? METHODS: The GUIDE process starts when a patient has an eGFR of 15 mL/min/1.73 m2. The process begins with a home visit from a case manager and the completion of questionnaires by the patient, the case manager and the nephrologist. A multidisciplinary meeting (MDM) is held to determine a specific patient profile (or treatment recommendation). This is followed by patient education, a second MDM and finally the selection of the treatment by the patient and the nephrologist. This retrospective observational study describes the selection process of all patients that received a treatment recommendation between 12 September 2013 and 18 December 2014 at Meander Medical Centre. Data were collected by file research and analysis of questionnaires. RESULTS: One hundred and two patients were included. They started the process at a mean eGFR of 12.3 mL/min/1.73 m2. Home dialysis was recommended for 62.8% of the patients who were advised to have dialysis treatment. Of the patients that opted for dialysis, 34.2% chose PD and 8.2% chose HHD; 22.9% started home dialysis as their first therapy, compared with 17.6% in the months before implementation of GUIDE. Finally, 32.1% of the patients that received dialysis therapy received home dialysis. In the months before GUIDE, an average of just 19.5% of the patients that received dialysis received home dialysis. CONCLUSIONS: In comparison to historical data, the pre-dialysis programme GUIDE increases the number of patients that choose and receive home dialysis.

Angiotensin I-converting enzyme: a pathogenetic role in diabetic renal damage?

The renin-angiotensin aldosterone system (RAAS) is well-established to be involved in diabetic nephropathy. Several abnormalities in the RAAS have been described in diabetes mellitus, including an abnormal aldosterone to renin ratio, elevated angiotensin I-converting enzyme (ACE) levels, and altered angiotensin II sensitivity. Whereas the renoprotective properties of ACE-inhibition in diabetic nephropathy have been demonstrated more than a decade ago, somewhat surprisingly, the role of ACE-activity in the pathogenesis of diabetic nephropathy is not well established. This paper addresses the possible functional impact of genetic and environmental increased in ACE activity in the pathogenesis of diabetic renal damage, in the context of the various other abnormalities in the RAAS in diabetes. Human and experimental data on circulating and tissue ACE in diabetes are reviewed, as well as the associations of ACE with angiotensin I conversion, with pathophysiological responses, and with renal end organ damage. New data from our laboratory provide evidence for interaction between genetical regulation of ACE activity by the ACE (I/D) genotype and diabetes as an environmental factor. Moreover, for functional effects of the elevated ACE activity in terms of increased conversion of angiotensin I to angiotensin II. The effects of enhanced generation of angiotensin II are modulated by the angiotensin II-subtype I receptor (AT1R). Altered AT1R sensitivity has been reported in diabetes that may further modu-late the eventual effects of elevated ACE. Epidemiological data on the association of genetically elevated ACE activity with diabetic nephropathy provide support for a pathogenetic role of elevated ACE activity in diabetic nephropathy. Together, the data suggest that differences in ACE expression and activity, resulting from both genetic and environmental factors and their interaction can modulate the pathogenesis of diabetic nephropathy. Unravelling the nature of this interaction, with focus on modifiable environmental factors, may help to ameliorate the risk for nephropathy in diabetes.