Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin converting enzyme (ACE) inhibitors are well established in the treatment of hypertension and cardiac failure. Experimental studies in rats have suggested that these agents may protect renal function in chronic nephropathy by a mechanism other than simply lowering the systemic blood pressure. In human studies of incipient diabetic nephropathy, worsening of microalbuminuria was prevented during 3 years of ACE inhibition. ACE inhibitors reduce arterial blood pressure in chronic nephropathy, and may cause a fall in glomerular filtration rate. In diabetic nephropathy, proteinuria was reduced by 2 months' treatment with enalapril to less than half of the values obtained in a control group treated with metoprolol. Nonrandomised trials have suggested that ACE inhibitors may slow the deterioration of renal function, but no comparisons with other antihypertensive agents in prospective studies have been published to date. In chronic renal failure, ACE inhibitors may worsen anaemia and hyperkalaemia. Renovascular hypertension can be treated with ACE inhibitors, but the treatment may lead to a compromised renal function. The dosage of these drugs should be reduced in renal failure and therapy should be started cautiously in this setting, with close monitoring of blood pressure, renal function and plasma potassium.
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PMID:Angiotensin converting enzyme (ACE) inhibitors and renal function. A review of the current status. 193 Jul 42

The methods for proteinuria detection and assay are reviewed, insisting on the main factors which influence the sensitivity and specificity of the techniques currently used in clinical practice. The up-to-date classifications of proteinurias and the follow-up methods are critically discussed, with special emphasis on the intermittent proteinurias and their diagnostic and prognostic significance, as well as on the diagnostic value of microalbuminuria.
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PMID:Advances in the study of proteinurias. II. Quantitative and qualitative evaluation of urinary proteins. 194 9

Type I glycogen storage disease (GSD-I) is due to the deficiency of glucose-6-phosphatase activity in the liver, kidney and intestine. Although kidney enlargement occurs in GSD-I, renal disease has not been considered a major problem until recently. In older patients (more than 20 years of age) whose GSD-I disease has been ineffectively treated, virtually all have disturbed renal function, manifested by persistent proteinuria; many also have hypertension, renal stones, altered creatinine clearance or a progressive renal insufficiency. Glomerular hyperfiltration is seen in the early stage of the renal dysfunction and can occur before proteinuria. In younger GSD-I patients, the hyperfiltration is usually the only renal abnormality found; and, in some patients, microalbuminuria develops before clinical proteinuria. The predominant underlying renal pathology is focal segmental glomerulosclerosis. Renal stones and/or nephrocalcinosis are also common findings. Amyloidosis and Fanconi-like syndrome can occur, but rarely. The risk factors for developing the glomerulosclerosis in GSD-I include hyperfiltration, hypertension, hyperlipidemia and hyperuricemia. Dietary therapy with cornstarch and/or nasogastric infusion of glucose, aimed at maintaining normoglycemia, corrects metabolic abnormalities and improves the proximal renal tubular function. Long-term trial will be needed to assess whether the dietary therapy may prevent the evolution or the progression of the renal disease.
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PMID:Type I glycogen storage disease: kidney involvement, pathogenesis and its treatment. 202 44

Amyloidosis of the kidney is the most threatening complication in familial Mediterranean fever (FMF), and colchicine has been shown to reduce its occurrence. In the preclinical stage of kidney amyloidosis, no proteinuria is observed by the standard Albustix method. However, whether these patients have normal or increased urinary albumin excretion is not known. The purpose of this study was to evaluate albumin excretion in FMF patients treated with colchicine and to compare these values to those of a normal control group. Twenty-two subjects with FMF were compared with 16 normal subjects matched with regard to age and body surface area. The two groups did not differ with regard to female/male ratio and arterial pressure. Urine samples were collected overnight while patients were recumbent and in the daytime while they were ambulant. After measuring albumin concentration (Ua) by radio-immunoassay and creatinine concentration through the standard method, the urinary albumin excretion rate (UaV) and urinary albumin creatinine ratio (Ua/c) were calculated. In the FMF group, three patients had microalbuminuria--defined as an albumin excretion rate higher than 20 micrograms/min. Two of them had this condition only in the early morning collection. These three patients were characterized by a longer duration of symptoms (18 vs. 9 years). No patient in the control group had microalbuminuria. The mean UaV in the FMF group did not differ significantly from that of the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urinary albumin excretion in patients with familial Mediterranean fever: a pilot study. 203 23

Patients with insulin-dependent diabetes mellitus (IDDM) have a significantly increased risk of macrovascular disease, particularly if they have persistent proteinuria. To determine whether altered levels of apolipoprotein(a) [apo(a)], the plasminogenlike glycoprotein of the potentially atherogenic lipoprotein(a); contribute to the increased risk of atherosclerosis, apo(a) levels were measured in 107 patients with IDDM and compared with nondiabetic control subjects and male elective coronary artery graft patients. Apo(a) levels were increased in diabetic patients with microalbuminuria (geometric mean 245 U/L, 95% confidence interval [CI] 142-427, n = 30) and albuminuria (mean 196 U/L, 95% CI 97-397, n = 18) with levels comparable to patients with coronary artery disease (mean 193 U/L, 95% CI 126-298, n = 40), which were higher than in the control group (mean 107 U/L, 95% CI 85-134, n = 140; P = 0.016). Apo(a) levels in diabetic patients without microalbuminuria (mean 86 U/L, 95% CI 63-116, n = 59) were comparable with the control population and less than in those with microalbuminuria (P less than 0.001) and albuminuria (P = 0.014). The elevated apo(a) levels found in patients with IDDM and increased urinary albumin loss may contribute to their heightened risk of macrovascular disease.
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PMID:Increased plasma apolipoprotein(a) levels in IDDM patients with microalbuminuria. 204 Mar 96

For the early diagnosis of diabetic nephropathy, it is best to use the albumin excretion rate (AER). However, it is a complicated test to perform in the outpatient setting, and it is sometimes affected by inaccurate urine collection. Therefore, we have used the albumin/creatinine ratio, which is measured simply with randomly collected urine, for evaluation of microalbuminuria and found it to be of equal diagnostic value to the AER. The AER, albumin/creatinine ratio, and creatinine excretion rate were measured in 86 patients with NIDDN who were negative for proteinuria. Urine was obtained after bed rest and in the outpatients department (without rest). 1) The reproducibility of time-restricted urine sampling was investigated using the rate of creatinine excretion. The mean coefficient of variation was found to be 42%, and inaccurate urine sampling appeared to cause variation in the AER. 2) The AER and albumin/creatinine ratio obtained in the outpatient setting were higher than those after bed rest, and urine collection at the time of outpatient examination was considered to be more useful than that after bed rest. To check variations in urine collection at the time of outpatient examination, the albumin/creatinine ratio in random urine samples was superior on the basis of the correlation coefficients to urine obtained after bed rest. 3) The urinary creatinine excretion rate showed a significant sex difference (males: 0.823 +/- 0.152 mg/g. creat., females: 0.577 +/- 0.194 mg/g. creat) (p less than 0.001), but there was no significant difference for BMI and age. The relationship between each level of microalbuminuria and the creatinine excretion rate did not change significantly. 4) The following formula was used to calculate the albumin/creatinine ratio corresponding to the AER. Albumin/creatinine ratio formula; (see text) An AER of 30 micrograms/min thus corresponds to an albumin/creatinine ratio of 36 mg/g. creat. for males and 51 mg/g. creat. for females. 5) The percentage of positive results for microalbuminuria in patients with NIDDM showed that the albumin/creatinine ratio and the AER were equal as diagnostic criteria, when the sex difference was taken into consideration. Thus, the albumin/creatinine ratio is equal to the AER for evaluation of microalbuminuria, and it is a simple and convenient test to use in daily clinical practice.
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PMID:[Clinical evaluation of the albumin/creatinine ratio in outpatients with diabetes]. 206 14

Long-term protein intake may have pathogenic influence on development of late diabetic complications. A review of the latest results in insulin-dependent diabetic patients shows that short-term lowering of protein intake reduces the characteristic early glomerular hyperfiltration as well as microalbuminuria and proteinuria in diabetic nephropathy. A sustained beneficial effect on the progression rate of nephropathy may be achieved. Based on this evidence it is advisable to avoid the traditionally high protein intake in diabetes. We suggest a protein-controlled diet--with protein comprising 14 energy %--as a goal in uncomplicated diabetes. In patients with progressive albuminuria or proteinuria prescription of a low-protein diet with 10% protein should be considered as supplementation to antihypertensive treatment. At present we do not find sufficient evidence for suggesting an intake of 10% protein (corresponding approximately to recent recommendations on 0.8 g prot/kg body weight) also in uncomplicated diabetes. Both a 10 and 14% protein diet will differ somewhat from the diet of the background population and the present diet of many diabetic patients. Therefore the introduction of such diets requires a careful individualized diet therapy in which repetitive evaluation and estimation of compliance are performed. A reduction of protein intake to 10 energy % represents a profound diet intervention.
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PMID:Reducing protein in the diabetic diet. 207 71

The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain to be established. However, there is now evidence that renal disease clusters in families and that genetic factors are of central importance in determining liability. A predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Genetically controlled hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. This suggestion derives from the observation that the fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first sign of renal damage is the appearance of microalbuminuria and of a small elevation in arterial pressure, changes associated with significant mesangial expansion. Microalbuminuria is associated with abnormalities of lipoprotein profiles possibly as a consequence of insulin-resistance-induced hyperinsulinemia. It could be postulated that the environmental changes brought about by diabetes lead in susceptible individuals to increased systemic and intraglomerular pressure on the one hand and mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities would further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered of reduction in renal function, more hypertension, more proteinuria, more glomerular obsolence, more hyperlipidemia and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Mechanisms of diabetic renal and cardiovascular disease. 207 90

Clinically apparent proteinuria in essential hypertension is associated with increased cardiovascular and total mortality and is an independent risk factor for cardiovascular and cerebrovascular disease. Subclinical elevation of urinary albumin excretion is seen more frequently than clinical proteinuria in essential hypertension and the levels of microalbuminuria (excretions of 30 to 300 mg/24 h) correlate with blood pressure. The increased urinary albumin excretion in hypertension may be explained by several factors such as renal hemodynamic changes, permselectivity changes of the glomerular filter, and structural arteriolar and glomerular changes due to nephrosclerosis. It has been clearly demonstrated that microalbuminuria is a risk factor for the development of clinical proteinuria, renal failure and increased cardiovascular mortality in insulin-dependent diabetes mellitus. It is still not known whether microalbuminuria also predicts development of proteinuria and decline in renal function in hypertension but there is some evidence indicating that microalbuminuria may be a marker of increased cardiovascular risk in hypertensives.
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PMID:Microalbuminuria in essential hypertension. 208 Oct 17

Diabetic nephropathy continues to be a common complication and has an unfavorable prognosis. Metabolic and hemodynamic factors determine the natural history of the condition. Of importance for the prognosis is the detection of nephropathy at an early stage. Such early diagnosis is not possible through the detection of microalbuminuria (incipient nephropathy stage). At this stage, further progress can be reversed by optimizing the metabolic situation and initiating early treatment of increasing blood pressure. For this reason, all diabetics should be submitted to early screening for microalbuminuria. When proteinuria persists (clinically manifest nephropathy stage), renal function usually declines progressively. Vigorous treatment of hypertension, optimal metabolic management, and normalization of protein intake can slow down the rate of continued loss of renal function.
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PMID:[Diagnosis and therapy of diabetic nephropathy]. 208 27


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