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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of atrial natriuretic peptide (ANP) on urinary protein excretion were examined in patients with renal parenchymal diseases (RPD, n = 18) and those with diabetes mellitus (DM, n = 12). Before and 30 min after intravenous injection of ANP (50 micrograms), urine samples were collected. ANP injection increased urinary volume and urinary sodium excretion in both groups. In RPD, urinary protein excretion (UprV) increased by 87% (1.5 +/- 0.7 [SEM] to 2.8 +/- 1.1 mg/min, p less than 0.05). ANP also increased UprV in patients with diabetic nephropathy [N(+); 1.7 +/- 0.8 to 5.0 +/- 2.5 mg/min, p less than 0.05] and those without nephropathy [N(-); 0.10 +/- 0.02 to 0.22 +/- 0.07 mg/min, p less than 0.05]. Since ANP increased creatinin clearance in both groups (+9.4 +/- 2.5 ml/min in RPD and +24.1 +/- 3.5 ml/min in DM, p less than 0.01 for both), urinary protein to creatinine excretion ratios (UprV/UcrV) were determined, which should be a parameter of glomerular protein permeability. The UprV/UcrV ratio increased by 48% (p less than 0.01) and 24% (p less than 0.05) in RPD and in DM, respectively. ANP did not change urinary composition of albumin and globulin. In RPD, increases in UprV by ANP were positively related to the basal serum creatinin levels (r = 0.57, p less than 0.01). In DM group, ANP-induced increases in the UprV/UcrV ratio were higher in the N(+) subgroup than in the N(-) subgroup (+0.8 +/- 0.4 vs +0.09 +/- 0.04, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effects of atrial natriuretic peptide on urinary protein excretion in patients with renal parenchymal disease and those with diabetic mellitus]. 214 Oct 91

Arterial pressure is within 'normal' limits in most diabetic patients with or without microalbuminuria and elevated in 70% of patients with overt diabetic nephropathy. An abnormal increase in the level of urinary excretion is a strong predictor of the subsequent development of overt diabetic nephropathy and ultimately renal insufficiency. Correction of hypertension is associated with a reduction in the rate of decline of the glomerular filtration rate in overt diabetic nephropathy. In patients with microalbuminuria, short-term studies have shown that angiotensin converting enzyme (ACE) inhibitors, in contrast with calcium antagonists, decrease urinary albumin excretion. Additional studies assessing the long-term effect of antihypertensive agents on the evolution of early diabetic nephropathy are needed. The superiority of ACE inhibitors over other antihypertensive agents in the treatment of overt or early diabetic nephropathy remains to be demonstrated. In addition to arterial pressure control, it is possible that optimal glycaemic control in addition to the modification of protein intake, dietary sodium and serum lipid profile may alter the course of diabetic nephropathy.
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PMID:Diabetic nephropathy in normotensive patients. 218 54

Hypertension and diabetes mellitus are chronic medical conditions that frequently coexist. In the United States, it is estimated that 10 million persons suffer from diabetes mellitus, 60 million from hypertension, and 3 million from the combination of the two. There may be a causal relationship between hypertension and diabetes. Obesity may be a precipitating factor for both hypertension and non-insulin-dependent diabetes mellitus. Those with insulin-dependent diabetes mellitus generally become hypertensive only with the onset of nephropathy. Glucose tolerance, insulin resistance, and hyperinsulinemia frequently occur with essential hypertension and may be aggravated by hypertension therapy, especially with diuretics and beta-blockers. Hyperinsulinemia may be an important common factor promoting sodium retention, sympathetic nervous system stimulation, and inhibition of the sodium pump. The Working Group on Hypertension in Diabetes has outlined a flexible modified version of the stepped-care approach to the treatment of hypertension in diabetes. Management is complex because diabetes is associated with autonomic neuropathy, sexual dysfunction, hyperlipidemia, and fluid and electrolyte disorders. All these problems can be exacerbated by antihypertensive treatment. Nonpharmacologic measures, which address weight reduction and sodium restriction, are logical, but aggressive antihypertensive medication is invariably necessary. Diuretics and/or beta-blockers were the mainstay of treatment until the introduction of angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers. These newer agents have no deleterious effects on carbohydrate metabolism and are generally better tolerated. Antihypertensive therapy may slow the rate of deterioration in diabetic nephropathy. This was first shown with diuretics, beta-blockers, and hydralazine and more recently with ACE inhibitors, which provide effective blood pressure control and a significant drop in albuminuria without affecting the glomerular filtration rate adversely. ACE inhibition may also lead to increased insulin sensitivity and glucose disposal rate. Long-term trials are needed to assess the effects of these new agents on the treatment of hypertension in the diabetic population.
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PMID:Diabetes mellitus and hypertension. 222 Jul 97

Clinical feature and creatinine metabolism were studied in 86 diabetic patients who had newly initiated dialysis treatment. In 32.5% of the patients, serum creatinine was below 8.0 mg/dl at the initiation of dialysis treatment. Gastrointestinal symptoms, general malaise, pulmonary edema and uremic encephalopathy were the causes which required dialysis treatment in those patients, and the frequency of pulmonary edema was significantly higher than in patients whose serum creatinine was above 8.0 mg/dl at the initiation of dialysis (p less than 0.05). There were no significant differences in serum urea nitrogen, potassium, sodium, albumin levels and hematocrit between low serum creatinine group (3.0-7.9 mg/dl) and high serum creatinine group (8.0-11.9 mg/dl) at the initiation of dialysis. Serum creatinine levels were highly correlated with creatinine generation rate (r = 0.788, p greater than 0.01). There was a significant correlation between creatinine generation rate and muscle volume (r = 0.863, p less than 0.001). Muscle volume of diabetic dialyzed patients was 29.5 +/- 7.0 cm3/cm in males and 26.9 +/- 5.0 cm3/cm in females, and those values were lower than those of non-diabetic dialyzed patients (p greater than 0.005). Frequency of the patients whose creatinine generation rate was below 1500 mg/day was 81.3% in diabetic hemodialyzed patients and this was significantly higher than in non-diabetic hemodialyzed patients (p less than 0.005). In conclusion, in patients with diabetic nephropathy who have to initiate dialysis treatment, uremic symptoms have progressed though serum creatinine levels are relatively low. This low serum creatinine levels in patients with diabetic end-stage renal disease are resulted from their low muscle volume.
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PMID:[Characteristics of the patients with diabetic nephropathy with relatively low serum creatinine at the initiation of dialysis]. 226 24

Increased sodium-lithium countertransport in erythrocytes is found in patients with insulin-dependent diabetes mellitus (IDDM) and nephropathy. To determine whether such an increase precedes the onset of nephropathy and, if so, whether it is associated with changes in renal function, we measured erythrocyte sodium-lithium countertransport in 52 patients with IDDM but not nephropathy or hypertension and in 32 control subjects. Seventeen of the 52 patients with IDDM (33 percent) had sodium-lithium countertransport activity that exceeded the maximal activity in the control subjects (0.39 mmol of lithium per hour per liter of cells). Eighteen of the 52 patients with IDDM were studied in more detail. The 7 patients with raised sodium-lithium countertransport values had glomerular filtration rates (median, 159 ml per minute per 1.73 m2 of body-surface area; range, 134 to 197) that were significantly higher (P less than 0.01) than those in the remaining 11 patients with IDDM and normal sodium-lithium countertransport (median, 126 ml per minute per 1.73 m2; range, 110 to 176) or in the 10 control subjects (median, 128 ml per minute per 1.73 m2; range, 93 to 151). In the seven patients with elevated sodium-lithium countertransport, the filtration fraction (median, 0.27; range, 0.22 to 0.37) was also greater (P less than 0.01) than that in control subjects (median, 0.22; range, 0.18 to 0.28). There were no differences in renal function between the patients with IDDM and normal sodium-lithium countertransport and the control subjects. We conclude that sodium-lithium countertransport is increased in patients with IDDM before the onset of nephropathy and is associated with hyperfiltration. Thus, elevated sodium-lithium countertransport activity may be an early marker of diabetic nephropathy.
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PMID:Increase in glomerular filtration rate in patients with insulin-dependent diabetes and elevated erythrocyte sodium-lithium countertransport. 230 Jan 21

The authors studied the effect of diabetes mellitus on the renal prostanoid (PN) system in rats with spontaneous hypertension. Marked changes of renal PN excretion, biosynthesis, and metabolism were revealed. The absence of signs of diabetic nephropathy in rats with hereditary determined hypertension may be attributed to increased production of prostaglandin E and prostacyclin. These PN augment the renal blood flow, prevent sodium retention in the organism, and inhibit the progress of arterial hypertension which is one of the signs characteristic of diabetic nephropathy.
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PMID:[The effect of diabetes mellitus on the renal prostanoid system and on the arterial pressure level in spontaneously hypertensive rats]. 238 40

During the last ten years, several studies proved the applicability of urinary albumin quantification in the early diagnosis of diabetic nephropathy. Owing to its high accuracy and its comparable low methodological effort, only the albumin determination was emphasised. Parallel studies of urinary protein patterns, however, using sodium dodecylsulfate-polyacrylamide gel-electrophoresis demonstrated the increased excretion of other high- and low-molecular mass proteins in different stages of diabetic nephropathy. Consequently an extension of the mere albumin assay including a macromolecular (e.g. transferrin) and a micromolecular (e.g. alpha-1-microglobulin) protein seems meaningful. According to this study, both methodological lines (combined quantitative and qualitative analysis, respectively) are useful tools in the early detection and the follow up of diabetic nephropathy.
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PMID:[Urinary proteins as indicators of diabetic nephropathy]. 246 Jun 66

We show our experience, results and complications with Intermittent Peritoneal Dialysis (IPD). We treated with this technique 28 patients with end stage renal disease (ESRD), between 1981-1988; (24 adults, 8 of them with diabetic nephropathy (6 non insulin dependent diabetic patients and 4 children) for 3 to 36 months. IPD was well tolerated. The extracellular volume control, haematocrit and plasma protein values, as well as, ac-base equilibrium nutritional status, ureic nitrogen and creatinine plasma levels, were fully satisfactory. There was statistical difference only in the Na+ (p less than 0.001), alkaline phosphatases (p less than 0.005), glucose (p less than 0.05) plasma values and glycosylated hemoglobin (p less than 0.05), between diabetics and non diabetics group. The peritonitis rate was 0.065 and 0.074 peritonitis/patients-month; respectively (NS) and were caused by Gram (-) bacteria. St Aureus and St Epidermides. The survival curves of patients and method, in both groups, were similar (NS). We conclude IPD is a good alternative of therapy for ESRD, also for diabetics patients, whom haven't got more infection rate than non diabetics patients.
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PMID:[Intermittent peritoneal dialysis: a 6 years' experience]. 251 81

The progression of diabetic nephropathy can be arrested by an improvement in diabetic control. High glucose concentrations increase the flux through the aldose reductase pathway, and it has been proposed that this may contribute to renal damage. Aldose reductase is present in both the glomerulus and the renal tubule. Biochemical changes associated with increased sorbitol production have been demonstrated in animal models, including myo-inositol depletion, reduced Na+-K+ ATPase activity, and activation of the pentose phosphate and glucuronate-xylose pathways. Selective inhibition of aldose reductase reverses these biochemical changes and prevents some of the structural and functional abnormalities in diabetic rats. The potential beneficial effects of aldose reductase inhibitors on diabetic kidney disease in man are at present being investigated.
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PMID:Aldose reductase in the etiology of diabetic complications: 2. Nephropathy. 252 43

Proximal tubular reabsorption of sodium and water was investigated in long-term insulin-dependent diabetic patients with normoalbuminuria (group I, n = 19), microalbuminuria (group II, n = 39), diabetic nephropathy (group III, n = 12) and in 13 healthy age-matched subjects. Glomerular filtration rate was measured with the single injection, 51Cr-EDTA technique. The fluid flow rate out of the proximal tubules was assessed by the renal lithium clearance. Although glomerular filtration rate was significantly elevated in the diabetic patients (Group I: 122 +/- 16, Group II: 121 +/- 18, Group III: 110 +/- 17, CONTROLS: 105 +/- 13 ml/min X 1.73 m2), lithium clearance was similar in the four groups (Group I: 19 +/- 6, Group II: 22 +/- 7, Group III: 19 +/- 5, CONTROLS: 23 +/- 4 ml/min X 1.73 m2). Both absolute and fractional proximal reabsorption of sodium and water was enhanced in diabetes. Indices of distal tubular function did not differ between controls and patients with insulin-dependent diabetes. Sodium clearance was about the same in the four groups. Our study suggests that the enhanced proximal reabsorption of sodium and water in insulin-dependent diabetic patients is still observed despite the presence of incipient or overt diabetic nephropathy.
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PMID:The increased proximal tubular reabsorption of sodium and water is maintained in long-term insulin-dependent diabetics with early nephropathy. 259 38


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