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

The epidemiology, pathogenesis, significance and management of hypertension in diabetic subjects are discussed. In Type 1 diabetes the presence of diastolic hypertension is closely related to the presence of diabetic nephropathy, from the stage of persistent proteinuria onwards. There may also be some elevation of systolic pressure. The apparent increased prevalence of hypertension in Type 2 diabetes is largely explicable, directly or indirectly, by obesity but there may be an excess of systolic hypertension among elderly patients. Hypertension in the diabetic population is associated with an increased incidence of both microvascular and macrovascular complications, but whether the high blood pressure is causal is not clear. The possible roles of sodium and insulin, the renin-angiotensin system, catecholamines and physical factors are explored. All current antihypertensive agents have additional limitations and disadvantages when used in diabetic patients: diuretics and beta-blockers are probably the initial drugs of choice. Only in the case of diabetic nephropathy is there yet reasonable evidence of antihypertensive treatment reducing the rate of progression of the disease.
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PMID:Diabetes and arterial hypertension. 613 Oct 4

PRA, active renin, and inactive renin (IR; activated by dialysis to pH 3.3 and 7.4) were measured in the plasma of 53 patients with diabetes mellitus and 32 normal volunteers (group 1). Proteinuria was present in 21 diabetics (group 3; nephropathy) and absent in 32 diabetics (group 2). The mean PRA was lower in group 3 than in groups 1 and 2. PRA less than 0.2 ng/ml . h occurred more frequently and at a younger age in uncomplicated diabetics than in normal controls. Despite very low PRA, plasma aldosterone was normal in most of the diabetics. IR was significantly higher than normal in the uncomplicated diabetics and was greatly increased in diabetics with nephropathy. Since the kidneys are a principal source of IR, and since patients with diabetic nephropathy have consistently elevated plasma IR, it is possible that increased plasma IR in patients without proteinuria or reduced renal function might be an early sign of renal involvement. However, as other explanations of increased plasma IR exist, the hypothesis must be tested by longitudinal studies of diabetic patients.
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PMID:Increased inactive renin in diabetes mellitus without evidence of nephropathy. 633 80

We examined the inactive to active renin ratio in the renin granules of the cadaver kidneys and the plasma in patients with diabetic nephropathy. The inactive renin in the break-through fraction when the plasma or the renin from the renin granules was put into a pepstatin column was determined. The inactive renin in this fraction was activated by trypsin. Concerning plasma, the inactive to active renin ratio was 90 in the patients and 9 in the normal subjects. On the other hand, this ratio was 0.29 in the patients' kidneys and 0.28 in the control kidneys. These results suggest that the increase of the inactive to active renin ratio in plasma of diabetic nephropathy does not result from the change of the renin storage in the kidneys.
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PMID:The inactive to active renin ratio in the kidneys and the plasma in diabetic nephropathy. 633 70

The effects of 6 weeks of treatment with captopril on the renal hemodynamics of 16 patients with treatment-resistant renal hypertension (six had diabetic nephropathy, seven had other renal parenchymatous disease, and three had renovascular disease) were studied. Significant changes in glomerular filtration rate, filtration fraction, plasma renin activity, urinary aldosterone, and mean blood pressure were noted in the patients with renal parenchymatous disease, but not in those with diabetic nephropathy. Renal blood flow remained unchanged in all patients. Captopril was well tolerated.
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PMID:Effect of captopril on renal hemodynamics in the treatment of resistant renal hypertension. 635 31

Low basal and stimulated plasma renin activity (PRA) levels have been reported in patients with diabetic nephropathy (DN). We have measured PRA before and after stimulation with captopril in 28 patients with DN and in 25 control patients. Renal function impairment was similar in both groups. Most patients were treated with furosemide. In 19 patients with DN the PRA-response to dihydralazine was also studied. PRA before and after captopril were higher in the DN than in the control group (p less than 0.001). PRA increased from 4.6 +/- 3.6 to 6.3 +/- 5.3 in the DN, and from 1.8 +/- 2.7 to 2.7 +/- 3.4 in the control patients. The increases in PRA, caused by decreased angiotensin II feed-back inhibition, were comparable. PRA did not increase after dihydralazine despite a pronounced blood-pressure reduction. The difference in response to these stimuli indicate selective lesions involving both the sympathetic innervation and the renal baroreceptor function in DN. Overhydration is a plausible explanation to the low PRA earlier reported in DN. The results thus indicate that a preserved renin secretion capacity is present in DN. Differences in PRA between the both groups can only partly be explained by other factors than DN. Our findings indicate a role for the reninangiotensin-system in hypertension in DN.
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PMID:Renin secretion in advanced diabetic nephropathy. 638 85

Plasma of normal pregnant women and plasma of some patients with diabetic nephropathy contain increased quantities of an inactive form of renin compared with normal plasma. In order to evaluate the significance of the increased levels of inactive renin in these conditions, we isolated and compared inactive renin from several plasma sources and from human kidney. Renal inactive renin and inactive renin from normal plasma and plasma of patients with diabetic nephropathy and plasma of pregnant women displayed reversible acid activation and similar binding characteristics to cibacron-blue. Using cibacron-blue affinity chromatography, we obtained a totally inactive renin preparation from renal cortex and from plasma of subjects from each of the clinical states. Gel filtration of these preparations and detection of inactive renin using a modified acid activation technique indicated that human inactive renin exists in at least two forms with the following apparent molecular weights: 56,300 +/- 1,500 and 49,200 +/- 1,000 for renal inactive renin, 58,000 and 49,000 for inactive renin in normal plasma, 58,500 and 52,000 for inactive renin in diabetic plasma, 57,000 and 49,000 for inactive renin in pregnancy plasma. These studies suggest that: 1) the kidney is a major source of circulating inactive renin in man, 2) inactive renin from normal, diabetic and pregnancy plasma is similar, and 3) human inactive renin is heterogeneous.
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PMID:Characterization studies of inactive renin from human kidney and from several plasma sources. 675 78

The mechanism of lowered renin-aldosterone system was investigated in 17 patients with diabetic nephropathy (serum Cr less than 3 mg/100 ml) with concomitant control of the blood sugar level. The response of plasma renin activity (PRA) to upright stimulation was lower in the low renin group (group I) than in the normal to high renin group (group II) and in the control group. The PRA response to theophylline was delayed in group I. The percentage of the luminal area of the arteriole in the biopsy specimens was larger in group I and the control group than in group II. Plasma aldosterone concentration (PAC) was not increased by angiotensin II in group I. Low PRA in diabetic nephropathy with slightly to moderately impaired renal function may not be due to hyaline destruction of the arteriolar walls, but to other factors such as sympathetic nervous dysfunction. The adrenal responses of PAC to angiotensin II may also be impaired.
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PMID:Renin-angiotensin-aldosterone system in mild diabetic nephropathy. 675 74

Normal plasma contains inactive renin, which becomes active when plasma is dialyzed to pH 3.3 and to pH 7.5, or treated with pepsin or trypsin. Under optimal conditions, each of these procedures activated the same quantity of renin, which was not further increased by repeating or combining two procedures, thus suggesting that the same pool of inactive renin was activated by each procedure. When plasma was fractionated by gel filtration, dialysis activated very little renin in eluates. Trypsin activated renin, but under some conditions also destroyed renin. Pepsin fully activated the inactive renin in eluates without evidence of destruction of renin. The pepsin-activated renin of normal plasma eluted from Sephadex G-100 in a peak of apparent molecular weight (MW) 58,000 and from Sephacryl S-200 with apparent MW 53,000, like big renin in plasma of patients with diabetic nephropathy. Inactive renin was usually increased in amount in plasma of sodium-depleted normal men, but the elution volume did not change with sodium intake. When renin was fully activated in plasma incubated with pepsin or trypsin, the apparent MW of the main peak of big renin did not change appreciably. Inactive renin in plasma was usually increased after sodium depletion, but the elution volume did not change. Active renin of normal plasma had an apparent MW near 41,000 on both gels. Thus, we conclude that big renin is present in normal plasma in amounts at least equal to and usually greater than active renin (the ratio depending on sodium intake) and that pepsin activation readily demonstrates big renin in eluates from gel filtration.
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PMID:Inactive renin of high molecular weight (big renin) in normal human plasma. Activation by pepsin, trypsin, or dialysis to pH 3.3 and 7.5. 678 Apr 60

Congenital or acquired nephron number reduction and diabetes mellitus both induce hyperfiltration and intrarenal hypertension. These hemodynamic factors have been suggested to play an important role in the initiation and progression of diabetic and nondiabetic glomerulopathies. In a prevalence cohort of all 50 albuminuric (> or = 300 mg/24 hr), non-insulin-dependent diabetic mellitus (NIDDM) patients (aged < 66 years) attending a diabetic clinic during 1987, we identified four patients with acquired oligonephropathy who had developed diabetic nephropathy. Three patients only had a single functioning kidney (nephrectomy in two cases), and the remaining patient had unilateral severely reduced kidney function and elevated plasma renin concentration. These patients represent 8% of our NIDDM population with albuminuria, and are the only patients in our NIDDM population younger than 66 years (n = 363) known to have single kidneys. However, systematic renography screening was not performed. During the observation period, which ranged from 16 to 100 months, albuminuria increased from 2.3 g/24 hr (range, 1.2 to 3.4 g/24 hr) to 3.2 g/24 hr (range, 0.7 to 9.4 g/24 hr), glomerular filtration rate decreased to 6 mL/min/yr (range, 4 to 12 mL/min/yr), and blood pressure remained stable at 142/92 mm Hg. Three patients received antihypertensive medication. Two of the patients died after 16 and 26 months of observation, respectively, due to acute myocardial infarction and stroke. The results of our study of NIDDM patients support the concept that reduced nephron number predispose patients to the development of diabetic nephropathy.
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PMID:Acquired oligonephropathy and diabetic nephropathy. 750 63

Captopril renography was utilized to assess the presence of angiotensin II dependent renovascular dysfunction in (1) 28 patients with mild to moderate essential hypertension (EH) with unimpaired renal function, and (2) 25 hypertensive patients with diabetic nephropathy (HDN). These studies were classified according to the diagnostic criteria outlined by the Working Party on Diagnostic Criteria of Renovascular Hypertension with Captopril Renography and the mean parenchymal transit time (MPTT) was used as an index for detecting the presence of angiotensin II dependent renal haemodynamic change. Patients with EH showed non-significant or non-specific alterations in the MPTT. Four patients in the HDN group showed a significant prolongation of MPTT in the presence of renin-angiotensin-aldosterone activation due to renal artery stenosis, and the other patients in this group showed a significant decrease in MPTT after captopril, consistent with increased blood flow and improved tubular transport function in the presence of microangiopathy only. We conclude that addition of MPTT to the standard diagnostic criteria of captopril renography may be helpful in predicting the beneficial or detrimental impact of angiotensin II inhibition treatment in HDN and in limiting the test protocol in EH to one post-captopril study.
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PMID:Predictive value of captopril transit renography in essential hypertension and diabetic nephropathy. 760 34


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