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Query: UMLS:C0730345 (
microalbuminuria
)
4,018
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
This perspective deals with prediction of overt diabetic nephropathy in patients with insulin-dependent diabetes mellitus (IDDM). The role of elevated urinary albumin excretion rate (
microalbuminuria
) in predicting diabetic nephropathy has been emphasized by new follow-up studies. Development of severe kidney impairment was seen in a large percentage of patients with
microalbuminuria
, but with more intensive care for diabetic patients, this percentage may be falling. Herein, I analyzed alternatives to
microalbuminuria
in predicting kidney disease in diabetes. 1) Parental predisposition to hypertension is not seen in all studies and therefore may not be a decisive factor, and it cannot be used in prediction of nephropathy. 2) Prediabetic blood pressure may predict nephropathy in certain non-insulin-dependent diabetic patients, but elevated blood pressure seems to develop after early
microalbuminuria
and is likely to be an aggravating factor in established
microalbuminuria
in IDDM patients. 3) At the clinical diagnosis of IDDM, diabetic nephropathy cannot be predicted. 4) Glycemic control is poor in normoalbuminuric patients with later development of
microalbuminuria
, and multiple glycosylated hemoglobin measurements are therefore important. 5) In diabetes, glomerular hyperfiltration is associated with late nephropathy, but it alone cannot be the decisive factor, because hyperfiltration in nondiabetic individuals does not produce kidney disease, according to new long-term follow-up studies. 6) Studies of glomerular structure and ultrastructure have not yet documented predictive values for overt nephropathy, but further studies are in progress. 7) Isolated blood pressure elevation without microabuminuria (probably representing essential hypertension in diabetes) has not been predictive. 8) It is clear that elevation of serum
creatinine
is a very late and insensitive parameter, occurring only with pronounced proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Prediction of clinical diabetic nephropathy in IDDM patients. Alternatives to microalbuminuria? 219 82
Plasma prorenin is abnormally high, whereas renin is normal or even low, in many patients with long-standing diabetes mellitus complicated by microvascular disease. Nephropathy or autonomic neuropathy has been put forward as a cause. We found that in 223 consecutive diabetics prorenin correlated positively with serum
creatinine
, the presence of macroalbuminuria (greater than 250 mg/L), and the presence of diabetic retinopathy, particularly the proliferative type. This correlation did not depend on the presence of neuropathy or whether the patient was receiving insulin. It was also independent of sex, age, duration of diabetes, blood pressure, and blood levels of glucose and hemoglobin-A1c. The association between elevated prorenin and retinopathy remained significant after adjustment for
creatinine
and the presence of macroalbuminuria. Of the whole group of diabetics 94 consecutive patients were assessed for the presence of
microalbuminuria
(30-300 mg/24 h). Independently of the presence of micro- or macroalbuminuria, the mean level of prorenin was not above normal in the patients without retinopathy and was 2-3 times normal in those with proliferative retinopathy. Thus, retinopathy appears to be a more important determinant of abnormally high prorenin than nephropathy. In addition, the renal vein to artery ratio of prorenin in 7 diabetics with both advanced nephropathy and proliferative retinopathy was not elevated, despite the high peripheral venous prorenin level and the impaired renal perfusion. Thus, the abnormally high prorenin level in these patients could not be explained by abnormal secretion by the kidneys. Finally, prorenin was not high in 16 nondiabetics with loss of sympathetic activity due to chronic autonomic neuropathy, which indicates that in the absence of diabetes, this type of autonomic failure is not sufficient to cause the high prorenin levels seen in diabetics. Our findings are evidence that abnormally high plasma prorenin levels in diabetics are not an immediate consequence of altered glucose metabolism. This abnormality is related to the development of microvascular disease in the eye and kidney and is at least in part due to decreased clearance of prorenin from the circulation, increased production from extrarenal sources, or both.
...
PMID:High plasma prorenin in diabetes mellitus and its correlation with some complications. 220 21
Renal functional reserve capacity was evaluated in 19 normotensive type I diabetics without
microalbuminuria
. All patients had normal basal renal function as assessed by 24-hour
creatinine
clearances higher than 120 ml/min. PAH, inulin, and
creatinine
clearances were carried out every hour before, during, and after infusion of an amino acid (AA) solution. The same experiment was repeated after ACE inhibition with captopril (25 mg). Two groups of patients were found: Group A (responders) showed a significant rise in GFR after AA infusion (inulin clearances from 117 +/- 8 to 138 +/- 10 ml/min) (p less than 0.05), whereas in Group B (non-responders) no significant change in GFR was observed. Groups were comparable in age, duration of diabetes, metabolic control, and mean arterial blood pressure. Group B, however, had a significantly higher basal inulin clearance (167 +/- 17 ml/min) than Group A (117 +/- 8 ml/min). In Group A ACE inhibition completely blocked the AA-induced rise in GFR, while basal GFR in Group B was significantly reduced (167 +/- 17 to 148 +/- 8 ml/min) after captopril administration. In both groups renal plasma flow was enhanced by ACE inhibition. A rise in glucagon was observed in all patients during AA infusion. It is concluded that type I diabetics with normal basal renal function already have reduced (Group A) renal functional reserve capacity, which is completely abolished (Group B) when concomitant hyperfiltration occurs. ACE inhibition reduces hyperfiltration and is capable of blocking the AA-induced rise in GFR in these patients.
...
PMID:[Behavior of the renal functional reserve in type I diabetic patients: effect of ACE-inhibition]. 221
Left ventricular diastolic function was assessed by pulsed Doppler echocardiography in non-diabetic controls (n = 11) and in patients with type 1 diabetes without microvascular disease (n = 16; diabetic controls), with
microalbuminuria
(n = 9), or with early persistent proteinuria (n = 11). The peak filling velocities during the early and atrial phases of left ventricular diastole and their ratio (E:A ratio) were measured. All patients with diabetes had a normal serum concentration of
creatinine
and exercise electrocardiogram. The mean E:A ratio was significantly lower in those with proteinuria than in the diabetic controls because of an increase in peak atrial filling velocity; most patients with proteinuria had an abnormal E:A ratio of less than 1.0. Multiple regression analysis showed that systolic blood pressure was the major determinant of both the peak filling velocity during the atrial phase of diastole and also left ventricular mass. Blood pressures were significantly higher in the proteinuria group than in the diabetic controls. Glycaemic control and autonomic function did not influence diastolic filling. The slightly raised blood pressures at the earliest stages of diabetic nephropathy are sufficient to alter left ventricular diastolic compliance--this may reflect early hypertensive heart disease. These data do not preclude a specific heart muscle disease related to diabetes, but suggest that these slightly raised blood pressures contribute significantly to left ventricular dysfunction in these patients, in whom the risk of cardiovascular disease is already greatly increased.
...
PMID:Abnormal diastolic function in patients with type 1 diabetes and early nephropathy. 222 5
1969 subjects underwent albumin index [A.I., urine microalbumin (mg/liter)/
creatinine
(g/liter)] in early morning urine, 75 g oral glucose tolerance test (OGTT), determination of plasma lipids (total cholesterol, triglyceride and high density lipoprotein-cholesterol) and a resting electrocardiogram. There was no history of treatment for diabetes mellitus and hypertension. The relationship between
microalbuminuria
, and hyperglycemia or high blood pressure at non-diagnostic level was examined. Then, plasma lipid levels or changes in electrocardiogram were correlated with the degree of
microalbuminuria
. Subjects were divided into 4 groups according to 75 gOGTT and into 3 groups according to blood pressure based on WHO definition, and A.I. was divided into 4 categories (0-9.9, 10.0-19.9, 20.0-49.9, and 50.0-199.9 mg/gCr). Mildly or moderately enhanced
microalbuminuria
(A.I.) was found in subjects with hyperglycemia or high blood pressure at non-diagnostic level. In normotensive subjects, neither hyperglycemia in fasting nor after glucose challenge increased urine microalbumin above normal range, while in borderline hypertensives, diabetic glucose intolerance produced 2 and 3 fold increases respectively compared with normotensives. There was a linear increase in urine microalbumin in relation to the glucose intolerance in newly diagnosed hypertensives. No correlation could be found between
microalbuminuria
and plasma lipid levels, while the prevalence of electrocardiographic changes increased 3 folds in group with the heaviest
microalbuminuria
compared with the other 3 groups excreting less microalbumin.
...
PMID:Microalbuminuria in subjects with no history of diabetes mellitus and hypertension: the relationship with hyperglycemia and high blood pressure at non-diagnostic level. 222 27
Abnormal rates of urinary albumin excretion have been shown to predict the development of nephropathy and may signal atherosclerotic disease in diabetic patients. This study demonstrated the feasibility of measuring
microalbuminuria
in diabetic patients from a large family practice population. Although only one half of the 473 diabetic patients offered free screening took advantage of the testing, those participating did not differ in terms of sex, race, type of diabetes, mean age, systolic blood pressure, and fasting blood glucose levels from those not electing to participate. Over 40% of those screened had abnormally elevated albumin excretion rates as defined as greater than 0.02 g of albumin per gram of
creatinine
. Those participating in the screening perceived the process as useful and were able to comply with directions for overnight urine collection. Results show that screening for
microalbuminuria
in diabetic patients cared for by family physicians is feasible, simple, and inexpensive. Interventions to slow or reverse the progression of abnormal
microalbuminuria
and future risk for nephropathy in those with diabetes are underway.
...
PMID:Screening diabetic patients for microalbuminuria. 223 Jun 75
We studied the effects of perindopril, an angiotensin converting enzyme (ACE) inhibitor administered during 12 months, on
creatinine
clearance, albuminuria and glycaemic control in diabetic subjects with mild to moderate hypertension. After 1 month placebo, 40 insulin-treated patients were divided into 3 groups based upon their urinary albumin excretion rate. Group 1 had a normoalbuminuria (less than 15 mg/24 h), group II had a
microalbuminuria
(15-150 mg/24 h) and group III had a macroproteinuria (greater than 150 mg/24 h and Albustix +). They were given perindopril 4 to 8 mg orally once daily, and received a stable diet. Diastolic blood pressure was normalized within the first 3 months in 80% of the patients. From these, 28 (14.7 and 7 from groups I, II and III respectively) were followed during a total active treatment period of 12 months. They were matched for age, duration of diabetes and hypertension, systolic and diastolic blood pressures, daily insulin dose, postprandial plasma C-peptide and quality of glycaemic control. Mean supine diastolic blood pressure was decreased by 15 and 18% at 1 and 12 months respectively. Heart rate was not significantly modified. At 3 months, plasma ACE activity was nearly totally inhibited while plasma renin activity was markedly increased. In patients of group II,
microalbuminuria
was reduced from 66 +/- 13 (mean +/- SEM after placebo) to 39 +/- 6 mg/24 h after 1 month perindopril and this effect was maintained at 12 months. In group I, albuminuria remained within the normal range. In group III, macroproteinuria was not consistently modified by perindopril.
Creatinine
clearance did not change and glycaemic control remained stable throughout the study in the 3 groups. No major side effects were observed. We conclude that perindopril normalizes blood pressure in a large majority of hypertensive diabetic patients without affecting the quality of diabetes control. It also induces a marked and sustained reduction of
microalbuminuria
in patients at risk of developing diabetic nephropathy.
...
PMID:[Long-term decrease of microalbuminuria after one year of treatment with perindopril in hypertensive diabetic patients]. 228 20
To clarify the ultrastructural changes of renal proximal tubulus in initial nephropathy having
microalbuminuria
, we observed 80 biopsies of non-insulin-dependent diabetics by light and electron microscopically morphometric analysis. The patients were divided into four groups; group I; no proteinuria (p.u.) & normal serum
creatinine
(Cr.); less than 1.5 mg/dl, group II; p.u. less than or equal to 0.5 g/day & normal Cr., group III; p.u. greater than 0.5 g/day & normal Cr., group IV; Cr. greater than 1.5 mg/dl. Age-matched 20 normal patients and 40 patients with IgA-nephropathy (20 cases with Cr. less than or equal to 1.5 mg/dl, 20 cases with Cr. greater than 1.5 mg/dl) were used as controls. In diabetics in Group I and II, significant changes were as follow. 1) general mitochondrial enlargement in size in proximal tubular cells, and significantly related to the level of fasting blood glucose, 2) enlargement of proximal tubular cells and their nuclei in size, 3) thickening of the proximal tubular basement membrane, and in group I, it indicated to get worse in future, 4) no relationship between the mitochondrial enlargement and other parenchymal parameters such as glomerular sclerotic change, interstitial fibrosis, luminar narrowing of arterioles and prognosis. Glomerular nodular-lesion, glomerular sclerotic change, and cortical tubulointerstitial fibrosis only appeared in the advanced stages; Group III and IV. We concluded that mitochondrial enlargement could be caused by the initially urinary excretion of low molecular proteins and microalbumin in diabetics, probably due to disturbances of ATP synthesis, reduction of active transport, and finally decreased of reabsorption in the proximal tubulus.
...
PMID:[Mitochondrial enlargement of renal proximal tubulus as a cause of microalbuminuria in non-insulin dependent diabetics]. 228
To determine causal mechanism(s) of
microalbuminuria
seen in patients with noninsulin-dependent diabetes mellitus (NIDDM), multivariate analysis (principal component analysis) was applied, using patient's age, disease length, fasting blood sugar level (FBS), hemoglobin A1c (HbA1c %), and presence of hypertension as variables. Albumin concentration in the first morning urine was determined by the Latex Photometric Immunoassay (LPIA), and was expressed as albumin index (AI, albumin excretion per gram
creatinine
). Sixty five cases who had been continuously negative or equivocal (+/-) for urinary protein by an usual paper test method were analysed. The result indicated these patients could be separated into following three groups. Group A (12 cases) showed the highest AI value, was characterized by longer disease length (greater than 10 yrs), and was thought to be in transitional phase into clinical proteinuric stage. Group B (7 cases) was characterized by poor diabetic control and normalization of the
microalbuminuria
might be possible by strict control measures. In Group C (14 cases), patients were in relatively early stage of the disease, and were under good diabetic control, but presence of hypertension was thought to be a provocative factor.
...
PMID:[Principal component analysis for microalbuminuria in patients with noninsulin-dependent, maturity-onset diabetes mellitus]. 230 26
We studied the relationship of slight albuminuria (
microalbuminuria
) to serum lipid and lipoproteins in a representative group of middle-aged Type 2 (non-insulin-dependent) diabetic patients. A random sample of non-diabetic control subjects was also examined. Diabetic patients had both at diagnosis and after five years higher total, LDL- and VLDL-triglyceride levels and higher VLDL-cholesterol, but lower HDL-cholesterol levels than non-diabetic subjects. No consistent difference was found in LDL-cholesterol levels between diabetic and non-diabetic subjects. The prevalence of
microalbuminuria
(greater than 35 mg/24h) remained about the same in diabetic patients at both examinations (19-20%). The diabetic patients with persistent
microalbuminuria
were slightly hyperglycaemic and they tended to have lower
creatinine
clearance at the 5-year examination than those without persistent
microalbuminuria
. There were no differences in the blood pressure levels or the occurrence of hypertension between the diabetic groups with and without
microalbuminuria
. At the baseline examination, no differences were seen in serum lipids and lipoproteins between diabetic patients with and without
microalbuminuria
. In patients with persistent
microalbuminuria
, a statistically significant increase in VLDL-cholesterol (p less than 0.05) and VLDL- and LDL-triglyceride levels (p less than 0.05) and a decrease in HDL-cholesterol level (p less than 0.05) was seen at the 5-year follow-up. These changes could not be explained by age, sex, body mass index or HbA1. In conclusion, persistent
microalbuminuria
predicts and aggravates abnormalities in lipoprotein composition and a decrease in HDL-cholesterol in patients with Type 2 diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Microalbuminuria predicts the development of serum lipoprotein abnormalities favouring atherogenesis in newly diagnosed type 2 (non-insulin-dependent) diabetic patients. 234 36
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