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The prevalence of diabetes mellitus among patients treated for end-stage renal failure was studied using a questionnaire mailed to all dialysis units of mainland France in 1989. With a response rate of 80.8%, the study population amounted to 12,903 dialysed patients of whom 884 were declared diabetic (6.9%). In a second phase, the study focused on the diabetic patients treated in the 63 largest units (those with at least four diabetic patients). Seven specially trained physicians completed questionnaires after having interviewed the patients and checked their medical records. All this material was reviewed by the same diabetologist. The conflict of diabetes type declared by both sources of information (the nephrologists and the diabetologist) showed a misclassification rate of 31.2%. Using these new data, the prevalence of type 1 diabetes mellitus was estimated at 1.4% of patients on dialysis therapy in mainland France, and 5.5% for type 2 diabetes mellitus. A north-south declining trend was suggested for type 2 diabetes mellitus. Diabetic nephropathy was the only primary renal diagnosis among 93.9% of type 1 diabetic patients, but only for 36.8% of type 2 diabetic patients. Of the latter, 51.6% had a non-diabetic cause of renal failure. These data show that the proportion of diabetics among patients receiving dialysis, while steadily increasing in France, remains lower than in other countries in Europe and in North America. However, the validity of international comparisons depends on diabetes ascertainment. Heterogeneity in selection of patients and in diabetes type classification by dialysis units may account to a considerable degree for the differences between diabetes mellitus prevalence across countries.
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PMID:Diabetes mellitus prevalence among dialysed patients in France (UREMIDIAB study). 133 35

The plasma membrane Na+/H+ exchanger is a ubiquitous system which plays a role in the regulation of intracellular pH and the control of cell growth. In order to assess the potential role of this system in the pathogenesis of diabetic nephropathy, we investigate 42 normotensive insulin-dependent diabetic patients with or without microalbuminuria. We tested the platelet Na+/H+ exchange as the rate of amiloride sensitive and sodium dependent volume gain of cells suspended in sodium propionate. Urinary albumin excretion (UAE) was assayed by radioimmunoassay on a 24 h sample; the glomerular filtration rate (GFR) and the renal plasma flow were determined by 99 m Tc-DTPA and 1231 l-hippuran respectively. Thirty patients (group 1) had EUA > 30 mg/24 h (m +/- sd: 11 +/- 7 mg/24 h), 12 patients (group 2) had microalbuminuria (62 +/- 30 Mg/24 h, range from 35 to 136 mg/24 h). The platelet Na+/H+ exchange rate was significantly increased in patients of group 2: 0.34 +/- 0.01 versus 0.26 +/- 0.06 s-1 x 10(-2) (p < 0.005). There was no significant difference between these two groups regarding blood pressure (116 +/- 14/71 +/- 7 versus 119 +/- 12/73 +/- 5 mmHg), age, diabetes duration, glycated hemoglobin or fructosamine levels. On the whole population, we found a significant positive correlation between the platelet Na+/H+ exchange rate and the UAE (r = 0.57, p < 0.001) and with the glomerular filtration fraction (r = 0.43, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Activity of platelet sodium-proton exchanger, microalbuminuria and insulin-dependent diabetes]. 133 55

A double blind crossover trial was performed on the effect of enalapril on urinary albumin excretion (UAE) in normotensive insulin dependent diabetics. Nineteen normoalbuminuric (UAE < 30 mg/24 h) and 17 microalbuminuric patients (UAE > 30 and < 300 mg/4 h) were studied; all patients had post prandial blood glucose levels < 180 mg/dl, HbA1 < 11% and none had chronic diabetic complications. Both groups had similar age, years of diabetes, body mass index and protein ingestion (70 g/day). Fifty percent of patients in each group received 5 mg/day of enalapril or placebo during one year, and during the second year the therapy was switched. No changes were observed in blood pressure, post prandial blood glucose, HbA1 and plasma electrolytes during the study period. A reduction in creatinine clearance, within normal limits, in both groups of patients treated with enalapril and no modifications with placebo were observed. UAE decreased significantly in normo and microalbuminuric patients initially treated with enalapril from 19 +/- 8 to 8 +/- 2 and from 71 +/- 19 to 39 +/- 12 mg/24 h respectively. These values increased during the placebo period to 23 +/- 6 and 47 +/- 13 mg/24 h respectively. Among those initially treated with placebo, UAE increased only in normoalbuminurics from 19 +/- 7 to 28 +/- 9 mg/24 h. During subsequent treatment with enalapril, UAE decreased in both groups. It is concluded that, in this group of patients, enalapril decreases UAE, possibly preventing the progression to severe forms of diabetic nephropathy.
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PMID:[Reversibility of early stage diabetic nephropathy]. 134 Sep 38

Spontaneously hypertensive rats (SHR) were injected with streptozotocin (STZ-SHR) to induce diabetes. The effect of DP-1904, a thromboxane A2 synthetase inhibitor, on diabetic nephropathy was then studied by administering it for 5 months (1 or 10 mg/kg). DP-1904 did not affect renal 6-keto prostaglandin (PG)F1 alpha production in STZ-SHR, but markedly inhibited renal thromboxane (TX) B2 production, so that the 6-keto PGF1 alpha/TXB2 ratio was significantly increased (P less than 0.05). STZ-SHR showed significant uraemia and proteinuria, plus increases in urinary gamma-glutamyl-transpeptidase and urinary N-acetyl-beta-glucosaminidase. DP-1904 significantly decreased (P less than 0.01) the urinary changes. STZ-SHR also showed an increase in mesangial periodic acid-Schiff-positive substance and in relative renal weight, both of which were significantly inhibited by DP-1904 (P less than 0.05). Thus, DP-1904 inhibited both TXB2 production and the progression of renal damage in STZ-SHR.
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PMID:A thromboxane A2 synthetase inhibitor retards hypertensive rat diabetic nephropathy. 135 Sep 91

Characteristic pathological changes in the glomeruli in diabetic nephropathy include expansion of the mesangial matrix and thickening of the glomerular basement membrane (GBM). Using an acellular digestion technique combined with scanning electron microscopy, the three-dimensional ultrastructural changes in glomerular extracellular matrices were studied in rats with diabetic glomerulopathy. Diabetes was induced by the intravenous injection of streptozotocin and morphological analyses were performed 3, 6 and 11 months after the injection. Expansion of mesangial area and GBM thickening became evident with time. After treatment with the series of detergents, all cellular components were completely removed leaving the extracellular matrices intact. In normal controls, the mesangial matrix appeared as fenestrated septa with oval or round stomata between the glomerular capillaries. In diabetic glomerulopathy, expansion of mesangial matrix and narrowing of the mesangial fenestrae were observed. These changes in the mesangial matrices seem to play a vital role in the progression of glomerulosclerosis in rat diabetes. A subendothelial thin layer of the GBM was continuous with the mesangial matrix. One cause of GBM thickening in streptozotocin diabetes may be expansion of the mesangial matrix into the peripheral GBM.
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PMID:Glomerular extracellular matrices in rat diabetic glomerulopathy by scanning electron microscopy. 135 71

Urinary glycylprolyl dipeptidyl aminopeptidase (GP-DAP) concentrations were determined in 36 insulin-dependent diabetic children aged 4-18 years with a duration of diabetes ranging from 1 month to 14 years. Abnormal urinary GP-DAP concentrations were found in 19 of the 36 patients. Twelve of 27 patients without microalbuminuria also had increased urinary concentrations of GP-DAP. There was a significant correlation between urinary GP-DAP and plasma fructosamine (r = 0.52, p < 0.001). Our data suggest that urinary GP-DAP may be used as a marker for diabetic nephropathy. However, there is also a possibility that increased urinary GP-DAP concentrations are functionally related to poor metabolic control. Longitudinal studies are needed to establish the clinical usefulness of urinary GP-DAP.
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PMID:Urinary glycylprolyl dipeptidyl aminopeptidase (GP-DAP) in insulin-dependent diabetic patients. 136 79

A number of risk factors associated with the development of diabetic nephropathy has been described, such as elevated blood pressure, poor metabolic control, hyperlipidemia, and smoking. Abnormal albuminuria also is associated with progression of renal disease, but has until recently been considered principally a marker of disease activity rather than a risk factor. This article discusses the role of elevated blood pressure versus abnormal albuminuria in a genesis and prediction of renal disease in diabetes. Controversy exists regarding parental disposition to hypertension and early blood pressure elevation in the course of diabetes, but all studies agree that elevated blood pressure--in the presence of abnormal albuminuria--constitutes a risk factor. Because abnormal albuminuria is associated with progression disease, it may itself be a risk factor because increased macromolecular traffic over the glomerular membrane may produce glomerulopathy. Problems related to blood pressure measurement are important, and 24-h recordings of blood pressure may be recommended in some situations. Regarding renal structure, preliminary results suggest that structural lesions precede blood pressure elevation. The solid end point for evaluation of renal disease progression is the fall rate of GFR, with abnormal albuminuria as an intermediate end point, also in drug trials. Abnormal albuminuria may constitute a new indication for antihypertensive treatment, being, as it is, a clear indicator of organ damage, whereas elevated blood pressure with normal AER may not increase risk substantially.
Diabetes Care 1992 Sep
PMID:Blood pressure elevation versus abnormal albuminuria in the genesis and prediction of renal disease in diabetes. 139 16

Not all patients with diabetes develop clinically significant nephropathy and, for this reason, attention has begun to focus on the risk factors for development of this serious complication. These risk factors have not been quantified to the same degree as those factors associated with more common progressive vascular diseases, such as atherosclerosis. However, studies of pathogenesis and clinical and epidemiological surveys of diabetic nephropathy point to numerous risk categories. Glycemic control, genetic and familial predispositions, renal and glomerular enlargement, glomerular hyperfiltration, and capillary and systemic hypertension can be invoked as contributors to this disease process. This review focuses on hemodynamic alterations and their role in the development and progression of diabetic nephropathy. Increases in GFR, largely driven by increases in plasma flow and capillary pressure, appear in early IDDM and NIDDM. This abnormality of renal vascular control probably is derived from alterations in several vasoactive control systems. In addition, the elevations in capillary pressure may be damaging to the glomerular capillaries. Arterial hypertension is not necessarily present before clinical nephropathy appears; however, it is a usual concomitant of progressive diabetic renal disease. The strongest evidences for the roles of altered systemic and renal hemodynamics in the progression of diabetic renal disease are clinical and experimental studies demonstrating attenuation of the disease process by lowering systemic and capillary pressures with antihypertensive agents, and dietary and glycemic modifications. Thus, although multiple factors probably interact to determine risk for the development of diabetic nephropathy, hemodynamic forces are a particularly important contributor and are especially amenable to therapeutic intervention.
Diabetes Care 1992 Sep
PMID:Diabetic nephropathy. Metabolic versus hemodynamic considerations. 139 17

Diabetes mellitus has become the leading cause of ESRF in the United States. Patients with diabetic nephropathy suffer high cardiovascular morbidity and mortality. Because only 40% of diabetic patients eventually develop diabetic kidney disease, it may be possible to devise primary prevention measures targeted at the subset of patients at risk. Recently, a predisposition to hypertension, a family history of diabetic nephropathy, and a family history of CVD disease each have been associated independently with the development of diabetic renal complication in IDDM. Risk factors for macrovascular damage, including raised arterial BP, dyslipidemia, and insulin resistance, can be detected early in the course of progression to diabetic nephropathy. These risk indicators recently have been shown to be already present at the stage of normoalbuminuria in those patients who eventually will progress to microalbuminuria. Treatment of established renal disease can only delay the onset of ESRF, and lowering of microalbuminuria has been shown to retard the onset of persistent proteinuria. However, no study to date has demonstrated prevention of renal disease in these patients. The ultimate aim should, therefore, be the prevention of the transition from normoalbuminuria to microalbuminuria in individuals who are at higher risk of diabetic renal disease and CVD.
Diabetes Care 1992 Sep
PMID:Diabetic nephropathy. Future avenue. 139 18

Diabetic nephropathy is currently the leading cause of new patients requiring dialysis in the United States. Management of the diabetic patient with ESRD is complicated by the frequent coexistence of complications affecting other organ systems, including retinopathy, cardiovascular disease, peripheral neuropathy, or autonomic neuropathy, manifested as gastroparesis, diarrhea or obstipation, cystopathy, or orthostatic hypotension. Associated clinical syndromes must be followed and treated, if possible, while preparing the patient to receive renal replacement therapy. Both the clinical condition and the psychosocial environment are key factors in choice of ESRD therapy for an individual patient. Rehabilitation data are best for patients who undergo kidney transplantation, but these data are confounded by the fact that the healthiest patients are referred for this treatment modality. Living, related kidney transplant is the preferred initial choice for the diabetic patient with kidney disease. At most centers, both in the United States and abroad, the cadaveric transplant is the second choice for uremia therapy. At the appropriate institution, the patient with type I diabetes may also be considered for a simultaneous cadaveric pancreas transplant. While awaiting cadaveric transplantation, or if contraindication to transplantation is present (chronic infection, recent malignancy, or severe cardiac disease), diabetic patients with severe impairment of the glomerular filtration rate (less than 10-15 ml/min) are referred for vascular access placement and/or insertion of a peritoneal catheter. The decision regarding the choice of CAPD vs. hemodialysis must be made on an individual basis. Rehabilitation and survival data for these therapies are similar, although technique survival rates for CAPD decline dramatically as time progresses because of infectious complications. In-center hemodialysis has the worst survival and rehabilitation profile, but the sickest, most debilitated patients with the highest number of comorbid conditions tend to be referred for that therapeutic modality. Most studies of rehabilitation were performed before use of recombinant human erythropoietin, and comparison between ESRD treatment modalities will have to be reevaluated now that the drug is routinely used.
Diabetes Care 1992 Sep
PMID:Diabetic nephropathy. Management of the end-stage patient. 139 19


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