Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with chronic renal failure, three kinds of treatments can slow the progression of renal insufficiency: optimal control of blood pressure; use of converting enzyme inhibitors; low-protein diet. The MDRD study strongly suggests that blood pressure should not be higher than 130/85 mmHg in patients with chronic renal failure, and than 125/75 mmHg in patients with chronic renal failure and proteinuria above 1 g/d. Converting enzyme inhibitors have been shown to be beneficial to patients with IDDM and either microalbuminuria or overt diabetic nephropathy and to patients with chronic renal failure and proteinuria above 1 g/d. A diet containing less than 1 g/kg/d of proteins should be prescribed to patients with chronic renal failure, and this protein content should be lowered to 0.75 g/kg/d (or to 0.60 g/kg/j in some cases) when creatinine clearance falls below 25 mL/min.
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PMID:[How to slow the progression of chronic renal insufficiency]. 1135 1

Hepatocyte nuclear factor-1alpha (HNF-1alpha) mutations are the most common cause of maturity-onset diabetes of the young. HNF-1alpha homozygous knockout mice exhibit a renal Fanconi syndrome with glucosuria and generalized aminoaciduria in addition to diabetes. We investigated glucosuria and aminoaciduria in patients with HNF-1alpha mutations. Sixteen amino acids were measured in urine samples from patients with HNF-1alpha mutations, age-matched nondiabetic control subjects, and age-matched type 1 diabetic patients, type 2 diabetic patients, and patients with diabetes and chronic renal failure. The HNF-1alpha patients had glucosuria at lower glycemic control (as shown by HbA1c) than type 1 and type 2 diabetic patients, consistent with a lower renal glucose threshold. The HNF-1alpha patients had a generalized aminoaciduria with elevated levels of 14 of 16 amino acids and an increased mean Z score for all amino acids compared with control subjects (0.66 vs. 0.00; P < 0.0005). Generalized aminoaciduria was also present in type 1 diabetic (Z score, 0.80; P < 0.0001), type 2 diabetic (Z score, 0.71; P < 0.0002), and chronic renal failure (Z score, 0.65; P < 0.01) patients. Aminoaciduria was not associated with microalbuminuria or proteinuria but was associated with glucosuria (1.00 glucosuria vs. 0.19 no glucosuria; P = 0.002). In type 1 diabetic patients, urine samples taken on the same day showed significantly more aminoaciduria when glucosuria was present compared with when it was absent (P < 0.01). In conclusion, HNF-1alpha mutation carriers have a mutation-specific defect of proximal tubular glucose transport, resulting in increased glucosuria. In contrast, the generalized aminoaciduria seen in patients with HNF-1alpha mutations is a general feature of patients with diabetes and glucosuria. Glucose may depolarize and dissipate the electrical gradient of the sodium-dependent amino acid transporters in the proximal renal tubule, causing a reduction in amino acid resorption.
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PMID:The generalized aminoaciduria seen in patients with hepatocyte nuclear factor-1alpha mutations is a feature of all patients with diabetes and is associated with glucosuria. 1152 70

The incidence of hypertension is increased in individuals with diabetes mellitus. This is especially true in patients with type 2 diabetes. In these patients high blood pressure is common at the time of diagnosis of diabetes, but the development of diabetes is often preceded by a period during which hyperinsulinemia and insulin resistance is already present. Diabetes represents by itself a major risk of cardiovascular morbidity and mortality. This risk is considerably enhanced by the co-existence of hypertension. One of the main complications of type 2 diabetes is nephropathy, which manifests initially by microalbuminuria, then by clinical proteinuria, leading to a progressive chronic renal failure and end-stage renal disease. Microalbuminuria is considered today as an indicator of renal endothelial dysfunction as well as an independent predictor of the cardiovascular risk. During recent years a number of studies have shown that tight blood pressure control is essential in diabetic patients in order to provide maximal protection against cardiovascular events and the deterioration of renal function. Of note, there is recent evidence indicating that blockade of the renin-angiotensin system with angiotensin II antagonists has marked nephroprotective effects in patients with hypertension and type 2 diabetes, both at early and late stages of renal disease.
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PMID:Diabetes and hypertension. 1182 35

Diabetes mellitus is one of the major causes of chronic renal failure. Typical findings of diabetic nephropathy are early hyperfiltration followed by microalbuminuria and overt proteinuria, resulting in a progressive decrease in glomerular filtration rate. Rapidly progressive glomerulonephritis has rarely been reported in patients with diabetes mellitus. Here, we describe a patient with MPO-ANCA-associated vasculitis, presenting with pulmonary-renal syndrome. Immunosuppressive treatment, including pulse methyl-prednisolone and cyclophosphamide, was administered and the disease was resolved.
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PMID:MPO-ANCA-associated pulmonary-renal vasculitis in a patient with diabetes mellitus. 1249 92

Diabetic nephropathy in type I diabetic patients, as it is currently understood, progresses in a stepwise fashion from normoalbuminuria to microalbuminuria, then to overt proteinuria and progression to chronic renal failure, and ultimately to end-stage renal disease. The role of early blood pressure changes in relation to diabetic nephropathy is now better understood in light of recent data using ambulatory blood pressure monitoring as a means to monitor blood pressure changes noninvasively throughout the day. Cross-sectional studies with type I diabetic patients with microalbuminuria have shown that the normal nocturnal blood pressure often fails to fall normally during sleep. The question of which comes first, microalbuminuria or a rise in blood pressure in patients with type I diabetes, was recently addressed in a prospective study. An increase in systolic blood pressure during sleep precedes the development of microalbuminuria and may play a causative role in its development.
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PMID:Circadian changes in blood pressure and their relationships to the development of microalbuminuria in type 1 diabetic patients. 1264 61

The relationship between blood levels of N-carboxymethyl-lysine (CML) or pentosidine and the severity of microangiopathy was investigated in patients with type 2 diabetes. Blood CML and pentosidine levels were measured by ELISA in 97 type 2 diabetics (46 men and 51 women). CML and pentosidine levels were significantly higher in patients with chronic renal failure than in those with normoalbuminuria, microalbuminuria, or macroalbuminuria (all p < 0.05). Among the diabetics without nephropathy (n = 49), blood CML levels were significantly higher in the patients who had proliferative diabetic retinopathy than in those without retinopathy or those who had background retinopathy (both p < 0.01). In contrast, blood pentosidine levels showed no significant differences among the three retinopathy groups. These findings suggest that the blood level of CML is related to the severity of both nephropathy and retinopathy, while the pentosidine level is only related to the severity of nephropathy.
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PMID:Relationship between blood levels of N-carboxymethyl-lysine and pentosidine and the severity of microangiopathy in type 2 diabetes. 1564 71

Risk assessment for a number of workplace or environmental chemicals, especially heavy metals and industrial organic compounds, relies mostly on clinical and epidemiologic findings. The low incidence of chronic nephropathies raises methodological issues in carrying out and interpreting human data on the progression of early changes towards end-stage renal disease. To overcome such limitations of epidemiological studies, two main approaches have been explored: (i) human studies relying on biomarkers and (ii) experimental animal models. Animal experiments have been useful to characterize early changes, such as hyperfiltration, eventually leading to chronic renal failure. Animal studies provided insights into the mechanisms underlying microalbuminuria and microproteinuria. Such biomarkers of early changes, developed for use at the workplace, have then been used to monitor such chronic disorders and multifactorial diseases as diabetes and arterial hypertension. Another area where occupational medicine has provided evidence is the effectiveness of primary prevention over other possible approaches. Avoidance of exposure to heavy metals and volatile hydrocarbons and their derivatives, mainly in individuals with diagnosed renal disorders, remains the best approach towards a substantial reduction in the burden of renal diseases.
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PMID:Contribution of studies on renal effects of heavy metals and selected organic compounds to our understanding of the progression of chronic nephropathies towards renal failure. 1635 May 50

It has been suggested that the finding of acanthocyturia in patients with hematuria points to the presence of glomerulonephritis. However, little attention has been paid to the finding of acanthocyturia in diabetic patients with hematuria. Here we studied 93 consecutive diabetic patients and explored the prevalence of microscopic hematuria and acanthocyturia in association with normoalbuminuria (NO; urinary albumin excretion (UAE) of < 30 mg/g x creatinine), microalbuminuria (MI; UAE of 30-299mg/g x creatinine), macroalbuminuriaMA; UAE of > or = 300mg/g x creatinine), or chronic renal failure (CRF; serum creatinine levels of > or = 1.1mg/dl for male and > or = 0.9mg/dl for female). We defined microscopic hematuria as > or = 5 erythrocytes per high-power field and acanthocyturia as > or = 5% acanthocytes (erythrocytes of doughnut-like appearance with vesicle-shaped protrusions) among 100 erythrocytes in the centrifuged urinary sediment. Microscopic hematuria was found in 12 (24%) out of 49 patients with NO, in 9 (43%) out of 21 patients with MI, in 6 (75%) out of 8 patients with MA, and in 7 (47%) out of 15 patients with CRF. Patients with microscopic hematuria showed a significant increase in urinary albumin excretion as compared to those without (836 +/- 265 vs. 135 +/- 56, p < 0.01). Of patients with microscopic hematuria, acanthocyturia was observed only in 2 (22%) out of 9 patients with MI and in 2 (33%) out of 6 patients with MA. Two of 4 patients with acanthocyturia had elevated serum levels of IgA and chronic tonsillitis, which indicated the occurrence of IgA nephropathy in these patients. Thus, microscopic hematuria was common and associated with elevated UAE, while acanthocyturia was rare and observed only in patients with elevated UAE. We propose that more attention should be paid to the finding of acanthocyturia in diabetic patients with hematuria and albuminuria.
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PMID:[Hematuria and acanthocyturia in patients with diabetes]. 1637 48

Hypertension is common in chronic renal disease and is a risk factor for the faster progression of renal damage, and reduction of blood pressure (BP) is an efficient way of preventing or slowing the progression of this damage. International guidelines recommend lowering BP to 140/90 mm Hg or less in patients with uncomplicated hypertension, and to 130/80 mm Hg or less for patients with diabetic or chronic renal disease. The attainment of these goals needs to be aggressively pursued with multidrug antihypertensive regimens, if needed. The pathogenesis of hypertensive renal damage involves mediators from various extracellular systems, including the renin-angiotensin system (RAS). Proteinuria, which occurs as a consequence of elevated intraglomerular pressure, is also directly nephrotoxic. As well as protecting the kidneys by reducing BP, antihypertensive drugs can also have direct effects on intrarenal mechanisms of damage, such as increased glomerular pressure and proteinuria. Antihypertensive drugs that have direct effects on intrarenal mechanisms may, therefore, have nephroprotective effects additional to those resulting from reductions in arterial BP. Whereas BP-lowering effects are common to all antihypertensive drugs, intrarenal effects differ between classes and between individual drugs within certain classes. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) have beneficial effects on proteinuria and declining renal function that appear to be mediated by factors additional to their effects on BP. These RAS inhibitors are recommended as a first-line antihypertensive approach in patients with chronic kidney disease. The addition of diuretics and calcium channel antagonists to RAS inhibitor therapy is also considered to be a rational strategy to reduce BP and preserve renal function. Calcium channel antagonists are a highly heterogeneous class of compounds, and it appears that some agents are more suitable for use in patients with chronic renal disease than others. Manidipine is a third-generation dihydropyridine (DHP) calcium channel antagonist that blocks both L and T-type calcium channels. Unlike older-generation DHPs, which preferentially act on L-type channels, manidipine has been shown to have beneficial effects on intrarenal haemodynamics, proteinuria and other measures of renal functional decline in the first clinical trials involving hypertensive patients with chronic renal failure. Preliminary results from a trial in diabetic patients who had uncontrolled hypertension and microalbuminuria despite optimal therapy with an ACE inhibitor or an ARB suggest that manidipine may be an excellent antihypertensive drug in combination with RAS inhibitor treatment in order to normalise BP and albumin excretion in patients with diabetes.
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PMID:Renal protection in hypertensive patients: selection of antihypertensive therapy. 1639 60

Insulin resistance (IR) is associated with multiple risk factors for cardiovascular disease. Many studies have shown that IR is present in chronic renal failure (CRF), and recent evidence suggests that IR can also occur in the early stages of renal disease. Patients with diabetic nephropathy (DN) have an increase in cardiovascular mortality, and since IR may be a contributing factor, this emphasizes the importance of a detailed understanding of the mechanisms linking IR and renal dysfunction at different stages of DN. IR can be detected early on in DN, e.g. at the stage of microalbuminuria (MA) and this could indicate a common genetic trait for IR and DN. As DN progresses further, IR is aggravated and it may, in addition to other factors, possibly accelerate the decline in renal function toward end-stage renal disease (ESRD). Several potentially modifiable mechanisms including circulating hormones, neuroendocrine pathways and chronic inflammation, are said to contribute to the worsening of IR. In ESRD, uremic toxins are of major importance. In this review article, we address the association between different stages of DN and IR and attempt to summarize major findings on potential mechanisms linking DN and IR. We conclude that IR is a consequence, and potentially also a cause of DN. In addition, there are probably genetic and environmental background factors that predispose to both IR and DN.
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PMID:Insulin resistance in diabetic nephropathy--cause or consequence? 1670 44


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