A co-relation of the eye and kidney-in diabetes mellitus and hypertension

The study was undertaken to observe the co-relation between microangiopathic changes in diabetic retinopathy and microvascular changes in diabetic nephropathy. Included in the study were 64 patients with chronic renal failure who were on maintenance dialysis, 40 had hypertension alone, 21 hypertension and diabetes and 3 had diabetes alone. On examination of retina, of 40 hypertensive patients, 14 had positive findings, while in the hypertensive and diabetic group, 20 patients out of 21, had positive findings. Nine patients in the hypertensive group had delayed choroidal filling on fluorescein angiography which was not very accurately reflected on Funduscopy. In the diabetic and hypertensive group, 13 patients having proteinuria of more than 1 gm, also had exudates and haemorrhages in the fundus. It was concluded that a correlation exists between the arterial changes in the fundus of the eye and the glomeruli of the kidney.     

Early electrocardiographic abnormalities in Trypanosoma cruzi-seropositive children

OBJECTIVE: The incidence of diabetic nephropathy in type 2 diabetes differs widely by race. Although clinical proteinuria is reportedly more common in East Asian type 2 diabetic patients than in their Caucasian counterparts, data on the incidence of microalbuminuria are not available. This study was undertaken to investigate the incidence and the determinants of microalbuminuria in Korean type 2 diabetic patients. RESEARCH DESIGN AND METHODS: A cohort of 188 Korean type 2 diabetic patients with initial normoalbuminuria were followed prospectively for 5.5 +/- 0.9 years in an outpatient clinic of a university hospital. The incidence of elevated urinary albumin excretion (UAE) (> 20 micrograms/min) and its relationship with baseline characteristics and follow-up data were determined. RESULTS: Of the 146 patients who finished the study, 37 showed persistently elevated UAE during follow-up, giving an incidence of 52/1,000 person-years. Age, duration of diabetes, and baseline UAE were significantly higher in the progressors than in the nonprogressors. More patients in the progressor group had retinopathy at baseline and at the end of follow-up. The mean values of fasting plasma glucose, HbA1, and systolic and diastolic blood pressure during the follow-up period were significantly higher in the progressors than in the nonprogressors. Cox proportional hazards analysis revealed that presence of retinopathy, duration of diabetes, mean fasting plasma glucose, and mean systolic blood pressure during follow-up are independent variables that have a statistically significant influence on the development of microalbuminuria. CONCLUSIONS: The incidence of microalbuminuria in Korean type 2 diabetic patients is lower than that reported in Pima Indians with type 2 diabetes but is as high as that in Caucasians with type 1 diabetes. Presence of diabetic retinopathy, poor glycemic control, and high blood pressure are risk factors for development of microalbuminuria in Koreans with type 2 diabetes.     

The C825T polymorphism in the human G-protein beta3 subunit gene is not associated with diabetic nephropathy in Type I diabetes mellitus

In Type I (insulin-dependent) diabetes mellitus a genetic predisposition exists to nephropathy and is related to parental hypertension. Enhanced G-protein activation, a cellular phenotype observed in cultured cells from patients with essential hypertension, was recently documented in Type I diabetic subjects with nephropathy. This enhanced G-protein activation has been associated with a genetic variant in the G-protein beta3 subunit, GNB3. A C-->T polymorphism at position 825 in exon 10 is associated with G-protein activation, the T allele associated with enhanced activity. Furthermore the T allele was observed more frequently in a group with essential hypertension. In this report we have analysed the role of the C825T polymorphism in the predisposition to diabetic nephropathy in Type I diabetes. We have investigated the frequency of this polymorphism in a large case-control study and found no association of the T allele with diabetic nephropathy. Specifically carriage of the T allele as CT or TT was observed in 49% of 200 Type I diabetic control subjects with normoalbuminuria (diabetes duration 24 years) compared with 53% of 216 Type I diabetic subjects with nephropathy (overt proteinuria or end-stage renal failure). Within this group we have also examined the inheritance of C825T alleles in a family study and found no evidence for excess transmission of the T allele to Type I diabetic offspring with nephropathy (T allele transmitted to 51% of nephropathy offspring, C allele transmitted to 49% of nephropathy offspring, p = 0.79). In none of the Type I diabetic datasets examined was there any effect of genotype on variation in systolic or diastolic blood pressure. In conclusion we can find no evidence for the C825T polymorphism of the beta3 G-protein subunit as a major gene in the susceptibility to diabetic nephropathy in Type I diabetes.     

Renogram deconvolution in the management of diabetic nephropathy: utility of the measurement of initial tracer uptake

Our objective was to assess mean transit time (MTT) and initial uptake, both parameters derived from the renal retention function (RRF), in the study of renal function in patients with diabetic nephropathy. We studied 25 patients, 7 with type I diabetes mellitus and 18 with type II diabetes mellitus, all of whom fulfilled the criteria for diabetic nephropathy with proteinuria and/or retinopathy. We found a statistically significant correlation between initial uptake and the other biochemical and renographic parameters studied except proteinuria: serum creatinine (r = 0.66, P < 0.002), creatinine clearance (r = 0.61, P < 0.003), glomerular filtration rate (r = 0.74, P < 0.003) and effective renal plasma flow (r = 0.66, P < 0.003). The other renographic parameters studied (maximal activity of the conventional renogram and MTT of the deconvoluted renogram) did not show any correlation. Initial uptake is a semi-quantitative renographic parameter that can provide complementary information to biochemical data and it may be useful in the management of diabetic nephropathy, especially in patients with high serum creatinine or creatinine clearance.     

Clinical predictors of non-diabetic renal disease in patients with non-insulin dependent diabetes mellitus

BACKGROUND: Several studies had suggested that non-diabetic renal disease (NDRD) was common among non-insulin dependent diabetes mellitus (NIDDM) patients with renal involvement. METHODS: We prospectively studied the prevalence of NDRD among a Chinese NIDDM population. Renal biopsy specimens were evaluated with light-, immunohistological and electron-microscopy. The cohort consisted of 51 patients who had NIDDM and proteinuria > 1 g/24 h. RESULTS: Patients with both isolated diabetic nephropathy (DN, n = 34) and NDRD (n = 17) had comparable duration of DM, creatinine clearance, serum creatinine, albumin and glycosylated haemoglobin levels, as well as incidences of retinopathy, neuropathy and hypertension. Significantly more patients with NDRD had microscopic haematuria (P = 0.043) or non-nephrotic proteinuria (P = 0.004). IgA nephropathy accounted for 59% of the NDRD identified. CONCLUSIONS: In this study, microscopic haematuria and non-nephrotic proteinuria predicted the presence of NDRD among NIDDM patients presenting with renal disease.     

Diabetic nephropathy and end-stage renal disease in Mexican Americans

Hispanics are the second largest minority group in the United States. Mexican Americans (MAs) are the largest subgroup at 14 million in 1990. MAs have a two- to threefold increased prevalence of non-insulin-dependent diabetes mellitus. Population-based studies of MAs with non-insulin-dependent diabetes have shown that these patients may be more likely than non-Hispanic whites to develop proteinuria and are more likely to develop end-stage renal disease. The reasons for this excess risk are yet to be completely elucidated, but may be due to worse glycemic control, worse blood pressure control when hypertension does occur, worse access to medical care, and/or genetics. When MAs are treated for diabetic end-stage renal disease, they have better survival. Much less data are available for other Hispanic subgroups. From a public health perspective, higher incidence and longer survival as well as relatively young and rapidly growing population predict an increasing burden for MAs if prevention measures are not instituted soon.     

Type II diabetic nephropathy: its clinical course and therapeutic implications

Type II diabetes is responsible for more end-stage renal disease in the United States than any other single condition. Until recently, the majority of research in diabetic nephropathy has focused on patients with type I diabetes despite the fact that type II nephropathy is a more prevalent condition. The notion that there are major differences between the nephropathy of these two types of diabetes is not supported by recent literature. The biggest difference appears to be related to ethnic risk. Histopathologic differences are now being described as well. Clinical interventional trials are few compared to type I diabetes; however, it seems that maneuvers that improve renal prognosis in patients with type I diabetes (blood pressure control, blood glucose control, and the use of angiotensin-converting enzyme inhibitors) apply to the type II population as well. Some of the calcium channel blockers lower proteinuria to a degree that suggests renoprotection and may further improve outcome.     

A polymorphism in the gene for the atrial natriuretic peptide and diabetic nephropathy. Diabetic Nephropathy Study Group

BACKGROUND: Atrial natriuretic peptide is involved in blood pressure regulation via its vasodilating and natriuretic actions. Since diabetic nephropathy and hypertension are closely related, ANP is a reasonable candidate gene for diabetic nephropathy (DN). METHODS: We genotyped 410 patients with type I diabetes (without DN n = 307; with DN n = 103) and 658 patients with type II diabetes (without DN n = 464; with DN n = 194). In the patients the duration of diabetes was at least 10 years. Diabetic nephropathy was defined as urinary albumin excretion of > or = 30 mg/24 h. The HpaII polymorphism in intron 2 of the ANP gene was determined using PCR amplification followed by restriction digest. Alleles were separated on agarose gels stained with ethidium bromide. RESULTS: We compared genotype distribution and allele frequencies between patients with and without nephropathy. No significant difference was observed either in type I (allele frequency without DN H1, 0.02/H2, 0.98 vs with DN H1, 0.05/H2, 0.95; P = 0.132) or in type II diabetes (allele frequency without DN H1, 0.04/H2, 0.96 vs with DN H1, 0.05/H2, 0.95; P = 0.551). CONCLUSIONS: The polymorphism in the gene for the atrial natriuretic peptide does not seem to play a major role in the development of diabetic nephropathy in either type I or in type II diabetes.     

Pardaxin, a new pharmacological tool to stimulate the arachidonic acid cascade in PC12 cells

BACKGROUND: Calcium channel blockers (CCBs) are known to have differential effects on both changes in proteinuria as well as progression of diabetic nephropathy. No clinical study, however, has evaluated whether the differential antiproteinuric effects of CCBs may be explained by their effect on glomerular membrane permeability. We, therefore, tested the hypothesis that certain subclasses of CCBs reduce proteinuria by changing size selectivity of the glomerular membrane, hence changing its permeability. METHODS: Twenty-one patients with type 2 diabetes and the presence of nephropathy with hypertension were randomized to receive either diltiazem CD or nifedipine GITS after baseline data for mean systolic and diastolic pressure, urinary protein excretion, glomerular filtration rate, renal plasma flow, neutral dextran and IgG clearances were obtained. Glomerular filtration rate, renal plasma flow, neutral dextran and IgG clearance were measured every three months, arterial pressure and heart rate every month. Patients were followed for 21 months. RESULTS: At 21 months, both patient groups had similar levels of blood pressure control, however, only the diltiazem group had a change in proteinuria (4+/-10%delta, nifedipine vs. -57+/-18%delta, diltiazem; P < 0.001) with improvement in glomerular size selectivity and change in IgG clearance. CONCLUSIONS: These data support the hypothesis that CCBs that provide sustained reductions in proteinuria do so, in part, by improving glomerular size permselectivity.     

Hypertensive heart disease and the diabetic patient

Patients with diabetes mellitus are particularly vulnerable to cardiovascular disease. Although structural and functional myocardial complications are present in patients with diabetes alone, they are particularly severe in patients with both diabetes and hypertension. Considerable evidence--both in experimental animal models and in humans--points to hypertension as of critical importance in the pathogenesis of severe diabetic heart disease. In diabetic hypertensive cardiomyopathy, coronary artery disease as well as structural and functional abnormalities are more pronounced than would be expected from either process alone. The myocardial damage is attributed mainly to hypertension, whereas the myocellular dysfunction is attributed mainly to diabetes. Together, the consequences to the myocardium are devastating. Strict control of the hypertension and diabetes may have an ameliorative effect on the subsequent development of diabetic heart disease.     

Renal protection and angiotensin converting enzyme inhibition in microalbuminuric type I and type II diabetic patients

BACKGROUND: Many studies have emphasized the role of antihypertensive drugs and in particular angiotension converting enzyme (ACE) inhibitors in the retardation of diabetic nephropathy. Although these studies have focused predominantly on patients with overt proteinuria, more recently a number of investigators have explored the role of ACE inhibitors in both type I and type II diabetic patients with an earlier phase of diabetic renal disease known as microalbuminuria. These agents are now being considered as renoprotective agents not only in hypertensive patients but also in those with 'normal' blood pressure. Initially, studies in type I diabetic patients showed that ACE inhibition was effective in retarding the increase in albuminuria which was observed in placebo treated groups. More recently, several multi-centre placebo controlled studies have been performed suggesting that prolonged treatment not only reduced albuminuria but also preserved renal function. The role of ACE inhibition in microalbuminuric type II diabetic patients is less well characterised although several studies have recently described beneficial effects of ACE inhibition on albuminuria and possibly on renal function. REVIEW: Although ACE inhibitors have been clearly shown to reduce urinary albumin excretion in diabetic patients, the issue as to whether they confer a specific benefit over other classes of antihypertensive agents remains controversial. Several meta-analyses have suggested that ACE inhibitors are more potent at decreasing albuminuria or proteinuria than other antihypertensive agents, for a given reduction in blood pressure. The Melbourne Diabetic Nephropathy Study Group has instituted a study which is placebo-controlled and is confined to normotensive type I and type II diabetic patients. The ACE inhibitor perindopril has been compared not only with placebo but also with the dihydropyridine calcium channel blocker, nifedipine. Preliminary analysis reveals that after 12 and 24 months of treatment, perindopril is more effective in reducing albuminuria than placebo or nifedipine. CONCLUSION: ACE inhibitors are a promising class of antihypertensive agents in diabetic patients with microalbuminuria. These drugs should be considered as first line agents in such patients, even in the absence of systemic hypertension.     

Impact of salt intake on blood pressure and proteinuria in diabetes: importance of the renin-angiotensin system

Patients with hypertension and diabetes are frequently salt-sensitive. Consequently, increasing dietary salt intake results in a rise in systemic arterial pressure and an increase in proteinuria, as well as a progressive risk for developing renal injury. A difference in the renal hemodynamic response to salt appears, at least in part, to determine how the salt intake affects blood pressure. Greater dietary salt intake in salt-sensitive patients results in a blunted rise in renal plasma flow and an increase in body weight. Greater dietary salt consumption also results in a rise in glomerular filtration fraction and increasing proteinuria. Pharmacologic antagonism of the renin-angiotensin system helps restore the blunted renal plasma flow response to high salt intake and correlates with the fall in mean arterial pressure. Consequently, the pressor response to increasing dietary salt consumption in patients with diabetes and hypertension may be related to insufficient renal vasodilation, perhaps due to inadequate suppression of the renin-angiotensin system. Moreover, inadequate suppression of the renin-angiotensin system within the kidney results in an increase in efferent glomerular arteriolar tone and a rise in glomerular capillary pressure, increased proteinuria and a greater risk for renal injury. Many of the coexisting cardiovascular risk factors associated with salt sensitivity may be explainable in part by the overactivity of the renin-angiotensin system.     

Stratifying patients at risk of diabetic complications: an integrated look at clinical, socioeconomic, and care-related factors. SID-AMD Italian Study Group for the Implementation of the St. Vincent Declaration

OBJECTIVE: The aim of this study was to identify subgroups of patients for whom the interactions among clinical, socioeconomic, and care-related factors determine a substantial increase in the risk of developing long-term diabetic complications. RESEARCH DESIGN AND METHODS: We performed a case-control study aimed at identifying and quantifying the risk factors for the development of major diabetic complications (eye, renal, and lower limb complications) in type 1 and type 2 diabetic patients. A total of 886 patients with renal, eye, or lower limb complications and 1,888 control subjects were enrolled in 35 diabetes outpatient clinics and 49 general practitioners' offices in 17 out of the 20 Italian regions. The main results were obtained using recursive partitioning and amalgamation (RECPAM), a technique that attempts to integrate the advantages of main effect logistic regression and tree-growing. RESULTS: The application of RECPAM led to the detection of important interactions involving clinical, socioeconomic, and care-related characteristics and allowed the identification of internally homogeneous subgroups characterized by a marked difference in the risk of developing major complications. In type 1 diabetic patients, the interaction between hypertension and smoking habits led to a dramatic increase in the complication risk, while in type 2 diabetic subjects, a poor compliance with visit scheduling was the most important predictor of complications. Furthermore, a marked difference in the risk profile was associated with patient characteristics (age, years of education, occupation). CONCLUSIONS: In the definition of the risk profile for each individual patient, socioeconomic status and level of education need to be taken under serious consideration, since they can determine a complication risk not dissimilar from hard clinical variables, such as hypertension and diabetes duration. Specific educational interventions, targeted to the socially disadvantaged strata of the population, need to be designed and implemented.     

Diabetic nephropathy. Its relationship to hypertension and means of pharmacological intervention

Hypertension and diabetes mellitus are common chronic conditions which frequently coexist. Diabetic nephropathy is a major cause of elevated blood pressure in patients with insulin-dependent diabetes mellitus (IDDM). Diabetic nephropathy, arterial sclerosis, obesity and association of essential hypertension can be the causes of hypertension in patients with non-insulin-dependent diabetes mellitus (NIDDM). Ambulatory blood pressure monitoring has revealed that the nocturnal fall of blood pressure is blunted in patients with diabetic nephropathy. A blunted diurnal blood pressure variation is seen in microalbuminuric diabetic patients and even in some normoalbuminuric patients. Accumulating data suggest that normalisation of blood pressure in hypertensive IDDM patients is most important to minimise the loss of kidney function. Angiotensin converting enzyme (ACE) inhibitors have been reported to be effective in postponing the development of nephropathy and in slowing its progression. Whether only ACE inhibitors have such beneficial renal effects on diabetic nephropathy is under discussion. While many studies have suggested that insulin resistance and hyperinsulinaemia are related to an elevated blood pressure in hypertensive patients, there does not seem to be enough evidence to prove that insulin per se can raise blood pressure in humans. Neither an insulin infusion within a physiological range nor sustained hyperinsulinaemia and insulin resistance (e.g. patients with insulinoma, cystic ovary syndrome) have been associated with an elevated blood pressure. Insulin resistance in some hypertensive patients may be a consequence of a decreased blood flow due to an increased peripheral resistance. Preliminary evidence suggests that low birth weight or impaired fetal growth is related to hypertension and NIDDM. Familial clustering of diabetic nephropathy suggests the contribution of genetic susceptibility and/or environmental inheritance. The frequent association of nephropathy with hypertension has led to research on the genes related to hypertension (ACE, angiotensinogen). Nevertheless, to date no reliable and clinically useful genetic marker has been found. Attempts to correct the metabolic abnormalities derived from diabetes are a new topic in the treatment of diabetic nephropathy. The effects of HMG CoA reductase inhibitors (antihypercholesterolaemic drugs), aldose reductase inhibitors (inhibitors of the polyol pathway) and glycation inhibitors (inhibitors of formation of advanced glycosylation end-products) on diabetic nephropathy have been evaluated in animal studies and in some clinical trials. Thus far, results with HMG CoA reductase and aldose reductase inhibitors have been somewhat conflicting. The potential therapeutic role of glycation inhibition in the treatment of diabetes deserves further study.     

Diabetes and hypertension: the bad companions

DIABETES AND HYPERTENSION: Diabetes mellitus and hypertension are interrelated diseases that strongly predispose people to atherosclerotic cardiovascular disease. Hypertension is about twice as frequent in individuals with diabetes as in those without. The prevalence of coexisting hypertension and diabetes appears to be increasing in industrialized nations because populations are aging, and both hypertension and non-insulin-dependent diabetes mellitus (NIDDM) increase with age. An estimated 35-75% of diabetic cardiovascular and renal complications can be attributed to hypertension. ESSENTIAL HYPERTENSION: Essential hypertension accounts for the majority of hypertension in individuals with diabetes, particularly those with NIDDM, who constitute over 90% of those with a dual diagnosis of diabetes and hypertension. Diabetic nephropathy, which occurs after 15 years of diabetes in one-third of those with insulin-dependent diabetes and 20% of those with NIDDM, is an important contributing factor to the development of hypertension in the diabetic. New investigations should focus increasingly on identifying appropriate antihypertensive agents that not only lower blood pressure but also reduce cardiovascular risk and retard the rate of progression of diabetic renal disease.     

A comparison of ultrastructural changes on endomyocardial biopsy specimens obtained from patients with diabetes mellitus with and without hypertension

The pathogenesis of diabetic cardiomyopathy is unknown. The synergistic, or enhanced, effect of hypertension on pathological changes in the heart of diabetic patients has been highly suspected. The purpose of this study was to evaluate the myocardial changes related to diabetes mellitus with and without hypertension, using biopsy specimens. We examined the ultrastructural changes in biopsy specimens of the endomyocardium obtained from 25 patients. They were divided into four groups: controls without hypertension or diabetes mellitus (n = 6), and patient with hypertension (n = 3), diabetes mellitus (n = 8), and diabetes with hypertension (n = 8). The diabetic patients showed nearly normal or mildly depressed systolic left ventricular function. Ultrastructural pictures were analyzed for thickening of the capillary basement membrane, presence of toluidine blue-positive materials (i.e., materials showing metachromasia) in the myocytes, size of myocytes, and interstitial fibrosis. The thickening of the capillary basement membrane, the accumulation of toluidine blue-positive materials, and interstitial fibrosis were all significantly greater in the patients with diabetes mellitus compared to the control subjects. The myocytes tended to be small (cell atrophy) in the diabetes group. Although these pathological changes in the heart were characteristic of diabetic patients, irrespective of the presence or absence of hypertension, the presence of hypertension increased the pathological changes of myocardial cells as well as abnormality in the capillary vessels in patients with diabetes mellitus. Alterations in the myocardial cells and capillaries, caused by diabetes mellitus, may lead to myocardial cell injury and interstitial fibrosis and, ultimately, to ventricular systolic and diastolic dysfunction, especially when the diabetes is accompanied by hypertension.     

Nephropathy of type II diabetes: evidence for hereditary factors?

Family studies point to an important genetic element in the genesis of diabetic nephropathy, but it is not known whether renal abnormalities are present prior to the onset of diabetes. To address this issue we examined all consecutive patients suffering from type II diabetes with a duration of more than 10 years who attended a diabetes outpatient clinic. Ninety-four patients had nephropathy, 307 did not. All offspring who were phenotypically normal (no hypertension, normal oral glucose tolerance, non-smoking) and agreed to participate were examined, 26 from nephropathic and 30 from non-nephropathic diabetic parents. They were compared with 30 offspring matched for age, gender and BMI from non-diabetic parents as controls. We measured urinary albumin excretion under baseline conditions and at several time points after ingestion of 300 g cooked beef and submaximal treadmill exercise, respectively. In addition, casual blood pressure, ambulatory blood pressure, urinary albumin and urinary alpha-1-microglobulin were measured. Primary renal disease was excluded by clinical examination. Under baseline conditions, median urinary albumin excretion rate (AER; microgram/min) was significantly (P < 0.005) higher in offspring of nephropathic type II diabetic patients (7.8; range 1.04 to 19.5) than in the offspring of non-nephropathic type II diabetic patients (4.8; 0.36 to 17.5) and controls (4.4; 0.16 to 18.4). Submaximal treadmill exercise caused a greater proportional increase of AER in offspring of nephropathic type II diabetics (median 16-fold) than in offspring of non-nephropathic diabetic patients (6.3-fold) or controls (4.8-fold). In offspring of nephropathic diabetic patients casual and particularly ambulatory systolic blood pressures were significantly higher, but AER was not correlated with blood pressure. In summary, higher values, albeit within the normal range, for baseline and postexercise albuminuria were noted in phenotypically normal offspring of parents with type II diabetes and nephropathy. The observation suggests that changes in transglomerular albumin traffic are demonstrable prior to the onset of diabetes and diabetic nephropathy in subjects with a potential genetic predisposition to these conditions.     

Proteinuria, other selected urinary abnormalities and hypertension among teenage secondary school students in Nairobi, Kenya

Four hundred and three teenage secondary school students (50.6% males) from two girls' and two boys' Nairobi City Schools, selected by stratified sampling, were screened to determine the prevalence of proteinuria, haematuria, nitrituria and hypertension. Nine students (2.2%) had significant proteinuria while 14 (3.5%) had microscopic haematuria. Two students had combined proteinuria and haematuria. There was no statistically significant difference in the prevalence of proteinuria and/or haematuria between the sexes. Other urinary abnormalities detected were leucocyturia in 14(3.5%) and nitrites in four (1%). Leucocyturia was commonner in females (p = 0.001). Cloudy urinary appearance was significantly associated with the presence of leucocyturia (p = 0.0028) and proteinuria (p = 0.0276). Neither personal history of recurrent sore throat and skin infections nor family history of hypertension, diabetes mellitus or kidney disease was significantly associated with proteinuria or haematuria. Blood pressure tended to increase with age. Mean systolic and diastolic blood pressures were significantly higher in boys than girls in the age group 15-18 years (P < 0.001). Of the 397 students whose blood pressures were measured, four (1%) were found to be hypertensive. Weight and body mass index were strong positive correlates of blood pressure. The prevalence of proteinuria, haematuria, other urinary abnormalities and hypertension ranges between 1% and 3.5% among teenage secondary school children. The majority are asymptomatic and have no significant associations. It is recommended that routine urinalysis and blood pressure measurements should be part of the school health service so as to identify asymptomatic students who require close monitoring and/or intervention.     

Modern principles of therapy of hypertension in diabetic patients]

Arterial hypertension is the most frequent cardiovascular complication of diabetes mellitus. Diabetes mellitus-type-1 occurs in about 30% of patients and it is connected to development of diabetic nephropathy, while type-2 occurs in as much as 70% of cases, having fast atherosclerosis as a base in its etiopathogenesis. The therapy of arterial hypertension in diabetic patients is specific and in some ways different depending on the type of diabetes mellitus as well as other complications characteristic for diabetes. Apart from drug therapy, it includes: body weight reduction in obese patients, restriction of sodium chloride, proteins and alcohol drinking, as well as other risk factors (smoking, for example). Drug therapy means application of different groups of antihypertensive agents (selective beta-blockers, diuretics, angiotensin-converting enzyme inhibitors, calcium channel antagonists and postsynaptic alpha-1 blockers). Some of them have adverse effects on metabolism of lipids, while some have other adverse effects which must be taken into account when determining therapy. However, angiotensin-converting enzyme inhibitors and calcium channel antagonists are the most preferred today as the most effective and with least adverse effects.     

Acute renal failure in patients with type 1 diabetes mellitus

Acute renal failure (ARF) is a serious condition which still carries a mortality of around 50%. People with diabetes may be at increased risk of developing ARF, either as a complication of diabetic ketoacidosis or hyperosmolar coma, increased incidence of cardiovascular disease, or due to increased susceptibility of the kidney to adverse effects in the presence of underlying diabetic renal disease. During the period 1956-1992, 1,661 cases of ARF have been treated at Leeds General Infirmary. Of these, we have identified 26 patients also having type 1 diabetes. ARF due to diabetic ketoacidosis is surprisingly uncommon (14 cases out of 23 patients whose notes were reviewed). All cases of ARF complicating ketoacidosis in the last decade have been associated with particularly severe illness requiring intensive care unit support, rather than otherwise 'uncomplicated' ketoacidosis. We discuss the conditions that may result in ARF in patients with diabetes and the particular difficulties that may be encountered in management.