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The underlying risk factors, presenting features, and outcome of 22 children with sacral agenesis and associated neuropathic bladder were studied retrospectively. The age of children at presentation was bimodally distributed, with peaks below 1 year and between 4 and 5 years of age. Ten patients presented after 1 year. The oldest was diagnosed at 12 years of age. In 12 children there was maternal diabetes, orthopaedic anomalies in 14, skin defects in 11, and anorectal/tracheooesophageal anomalies in three. Most children had persistent dribbling of urine on presentation associated with frequency, urgency, recurrent urinary tract infections, failure to respond to medication, and/or constipation. Twenty-one children had abnormal neurology in the lower limbs. Videourodynamics showed neuropathic vesicourethral dysfunction in all children and vesicoureteric reflux in 10. Nineteen had a history of urinary tract infections. Seven had renal scarring, with renal impairment in three at presentation. Clean intermittent catheterization was recommended for 20 of the children. Bladder or bowel surgery has been carried out in seven and neurosurgery performed in two. Twenty of the 22 children underwent operative procedures. Ten operations were performed before sacral agenesis was diagnosed. Over a third of the children have required psychological support. The combination of urinary symptomatology and any of the above risk factors should give rise to a high level of suspicion and low threshold to perform investigations to exclude sacral agenesis. All these children have abnormal bladder and urethral function which not only causes incontinence but puts the kidneys at risk. Early detection allows effective multidisciplinary input specifically aimed at continence, preservation of renal function, and adequate psychological support.
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PMID:Presentation and outcome of sacral agenesis: 20 years' experience. 1103 61

Renal impairment is a recognized risk factor for prolonged hypoglycemia, but predisposing characteristics in patients with advanced renal impairment have not been studied. We observed prolonged hypoglycemia in a number of patients with end-stage renal disease (ESRD) and conducted a case-control study at two Canadian centers to identify such risk factors. Through hospital, pharmacy, and dialysis program records, we retrospectively identified 7 case patients and 31 controls with ESRD and type 2 diabetes using oral hypoglycemic monotherapy. Control patients had no history of hospital admission for prolonged hypoglycemia. All case patients and 28 controls were receiving glyburide (glibenclamide in Europe); the remainder were treated with tolbutamide. Duration of intravenous treatment for hypoglycemia ranged from 28 to 256 hours, with 83 g to 2 kg of glucose administered per episode. Preceding treatment with glyburide varied from 2 days to 13 years. Univariate analyses showed a recent decline in oral intake (odds ratio [OR], 81; 95% confidence interval [CI], 3.6 to 1,840), previous hypoglycemic episodes (OR, 15; 95% CI, 0.77 to 297), longer duration of diabetes (22 versus 12 years; P = 0.008), and a history of cerebrovascular disease (OR, 7. 0; 95% CI, 1.0 to 47) to be associated with prolonged hypoglycemia. No association between prolonged hypoglycemia and age, sex, beta blockers, angiotensin-converting enzyme inhibitors, oral hypoglycemic dose, or duration of treatment was identified. This study describes the potentially devastating effect of sulfonylurea-based oral hypoglycemic therapy in ESRD. Patients at greatest risk appear to be those with reduced intake, previous hypoglycemic episodes, and longer duration of diabetes. We describe the mechanisms for observed hypoglycemia and suggest that alternative drugs may be considered in this patient group.
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PMID:Prolonged sulfonylurea-induced hypoglycemia in diabetic patients with end-stage renal disease. 1069 77

Clinical trials have shown the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in delaying the progression of diabetic renal disease. There is less evidence from primary clinical trials of nondiabetic renal disease. We performed an updated meta-analysis to determine the efficacy of ACE inhibitors in slowing the progression of renal disease over a broad range of functional renal impairment. We included published and unpublished randomized, placebo-controlled, parallel trials with at least 1 year of follow-up available from January 1970 to June 1999. In nine trials of subjects with diabetic nephropathy and microalbuminuria, the relative risk for developing macroalbuminuria was 0.35 (95% confidence interval [CI], 0.24 to 0.53) for individuals treated with an ACE inhibitor compared with placebo. In seven trials of subjects with overt proteinuria and renal insufficiency from a variety of causes (30% diabetes, 70% nondiabetes), the relative risk for doubling of serum creatinine concentration or developing end-stage renal disease was 0.60 (95% CI, 0.49 to 0.73) for individuals treated with an ACE inhibitor compared with placebo. Treatment of individuals with chronic renal insufficiency with ACE inhibitors delays the progression of disease compared with placebo across a spectrum of disease causes and renal dysfunction.
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PMID:Effect of ACE inhibitors in diabetic and nondiabetic chronic renal disease: a systematic overview of randomized placebo-controlled trials. 1073 92

Nephropathy is a complication of diabetes mellitus that can affect women in their reproductive years. This article reviews the effects on treatment on the main factors associated with short- and long-term complications in pregnant women with diabetic nephropathy. Tight glycemic control, adequate treatment of elevated blood pressure, and renal function in early pregnancy are the most significant predictors of maternal and perinatal outcomes. Contemporary methods of perinatal care and adequate treatment of blood pressure allow fetal survival rates of 95%. Furthermore, pregnancy per se does not appear to worsen the natural progression to end-stage renal disease for most women with renal insufficiency. However, patients with moderate to severe renal impairment may experience acceleration of renal disease.
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PMID:Effect of medical therapy on progressive nephropathy: influence of pregnancy, diabetes and hypertension. 1075 40

The gastrointestinal motility stimulants, cisapride and erythromycin, have been used in the management of diabetic gastroparesis. However, drug interactions may result in prolongation of the electrocardiographic QT interval with the risk of ventricular arrhythmias. These drugs should, therefore, not be used in combination. We report two cases that illustrate inappropriate use of these agents. Moreover, patients with recurrent severe hypoglycemia or renal impairment may be at increased risk from cisapride-related cardiotoxicity. Thus, even as monotherapy, cisapride may pose dangers for high-risk diabetic patients.
J Diabetes Complications
PMID:Should cisapride be avoided in patients with diabetic gastroparesis? 1076 8

We assessed the renal and cardiac benefits of cicletanine (CIC), a furopyridine derivative drug with diuretic and antihypertensive properties, in diabetic spontaneously hypertensive rats with renal impairment. Uninephrectomized streptozotocin (STZ)-diabetic spontaneously hypertensive Izmo rats (SHRIzm) (10 weeks old) were randomly assigned to receive vehicle or CIC (100 mg/kg/day, orally), and age-matched, uninephrectomized STZ diabetic Wistar-Kyoto Izmo rats (WKYIzm) were assigned to receive vehicle for up to 12 weeks. Blood pressure increased progressively in diabetic SHRIzm but not in diabetic WKYIzm. Urinary albumin excretion increased significantly in both diabetic SHRIzm and diabetic WKYIzm throughout the experiment. The antihypertensive effect of CIC was not significantly observed in diabetic SHRIzm. However, the subdepressor doses of CIC significantly decreased urinary albumin excretion, serum creatinine, and blood urea nitrogen in diabetic SHRIzm. These results were confirmed by morphological analysis of kidneys in each group of rats. The index of focal glomerular sclerosis (FGS) in diabetic SHRIzm was significantly higher than that in diabetic WKYIzm. The CIC treatment significantly and effectively protected against an increase in the index of FGS in diabetic SHRIzm. Moreover, CIC treatment significantly attenuated the increase in the heart weight to body weight ratio in diabetic SHRIzm. Treatment with CIC did not affect urinary and blood glucose concentrations at this dose. These results suggest that CIC has a renal-protective action, which is not related to improvement of diabetes or improvement of high blood pressure in diabetic rats with hypertension. The action might be due to the reduction of intraglomerular capillary pressure or protection of the renal glomerular vascular endothelial cell injury and mesangial cell injury through stimulation of PGI2 generation or elimination of free radicals, although the mechanism remains to be further investigated.
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PMID:Renal-protective effect of nondepressor dose of cicletanine in diabetic rats with hypertension. 1077 35

NORDIL--the Nordic Diltiazem Study (NORDIL)--is a prospective, randomized, open blinded-endpoint (PROBE), multicenter, parallel-group morbidity/mortality outcome study in hypertensive patients designed to compare an intervention strategy based on the calcium antagonist diltiazem with a strategy based on conventional antihypertensive drug treatment (diuretics or beta-adrenergic blockers). Patient recruitment was started in Norway and Sweden in September 1992, and ended on December 15, 1996, when 10.896 male and female patients, aged 50-74 years, with essential hypertension had been randomized. In this paper we describe the baseline data of the patient cohort and blood pressures achieved in the two treatment groups during the early part of the study. The patient cohort consists of 5294 males and 5602 females with a mean age of 59.6 and 60.3 years, respectively. Concomitant disorders and risk factors in the cohort are: smoking 22%, ischemic heart disease 3.0%, previous myocardial infarction (MI) 2.0%, previous stroke 1.5%, diabetes mellitus 7.0%, and renal impairment 0.3%. There were no differences between the treatment groups in these respects. The blood pressure treatment goal is a target diastolic blood pressure of < or =90 mmHg or a 10% diastolic blood pressure reduction from the inclusion pressure. In the treatment group randomized to a diltiazem-based treatment strategy, blood pressure was 174/106 mmHg at baseline and 156/90 mmHg after 12 months of follow-up on active treatment. In the group randomized to a conventional treatment strategy, baseline blood pressure at randomization was 173/106 mmHg and 153/90 mmHg after 12 months on active therapy. The NORDIL study will terminate on October 31, 1999 and the final results should be available by mid-2000.
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PMID:Progress report on the Nordic diltiazem study (NORDIL): an outcome study in hypertensive patients. 1080 90

Studies of two post-mortem pancreata of children at the onset of type I diabetes have suggested activation and expansion of islet infiltrating T cells by a superantigen. We present the first reported case of a superantigen mediated disease, toxic shock syndrome (TSS), occurring at the diagnosis of type I diabetes. A 12-year-old girl presented with TSS and newly diagnosed diabetes with ketoacidosis. At presentation she was unconscious, febrile and hypotensive, with a desquamating erythematous rash and Kussmaul breathing. During resuscitation, her renal impairment, diarrhoea, thrombocytopaenia and ketoacidosis resolved. Vaginal discharge and blood cultures grew Staphylococcus aureus. T cell studies at 2 weeks after diagnosis detected a high level of spontaneous and islet antigen-specific proliferation with associated interleukin-10 production compared to human leucocyte antigen DR matched controls.
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PMID:Toxic shock syndrome associated with newly diagnosed type I diabetes. 1084 34

Rilmenidine is an antihypertensive agent with selectivity for I1 imidazoline receptors that acts both centrally by reducing sympathetic overactivity and in the kidney by inhibiting the Na+/H+ antiport. Rilmenidine provides antihypertensive efficacy comparable with that of diuretics, beta-blockers, calcium channel blockers, and angiotensin-converting enzyme (ACE) inhibitors. Experience from trials and clinical practice highlights rilmenidine's clinical and metabolic acceptability in hypertensive populations, including those at special risk because of old age, renal impairment, diabetes mellitus, or dyslipidemia. In the at-risk hypertensive, rilmenidine reduces left ventricular hypertrophy to a similar degree to other reference agents. New studies show a significant improvement in glucose metabolism in metabolic syndrome patients treated with rilmenidine, and a significant reduction in microalbuminuria during rilmenidine treatment of hypertensive type 2 diabetics. Thus the efficacy/tolerance ratio of rilmenidine supports its role as a first-line antihypertensive option for all groups of hypertensive patient, with specific advantages in some at-risk populations.
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PMID:Rilmenidine: a clinical overview. 1092 29

Progressive impairment of kidney function is one of the major problems in diabetic patients. Control of glycaemia and blood pressure is the main strategy for preventing or slowing impairment in renal function in this condition. However, contributing factors such as hyperlipidaemia and high protein intake have now been identified, and their control can be regarded as a complementary measure. The role of lipid abnormalities and hypercholesterolaemia in the pathogenesis of glomerular injury has been demonstrated in animal models, and a link between hypercholesterolaemia and diabetic nephropathy has been established in humans. To date, few intervention studies in diabetic patients have shown a slower decline in renal function. Nonetheless, in every study in which follow-up was long enough, cholesterol lowering had a beneficial effect on renal function. Although hypercholesterolaemia may not be the cause of renal injury, it represents an aggravating factor. High serum cholesterol seems to have a similar action on glomerular mesangial cells and endothelial cells. This appears to be analogous to the process of atherosclerosis, as mesangial cells possess binding sites for LDL and oxidised LDL, help recruit macrophages and secrete proliferative factors. Protein intake is another factor that can influence renal deterioration. Two meta-analyses have confirmed the beneficial effect of a low-protein diet in diabetic nephropathy, showing no adverse effects on the glycaemic control. Protein intake even seems to enhance the sensitivity of tissues and liver to insulin. Thus, there appear to be no contraindications to such diets in well-controlled diabetic patients. In short, although glycaemic and blood pressure control are still the main lines of treatment for diabetic patients, lowering blood cholesterol and restricting protein intake represent complementary measures that can help slow renal impairment.
Diabetes Metab 2000 Jul
PMID:Lipids, protein intake, and diabetic nephropathy. 1092 73


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