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

During long-term treatment of arterial hypertension with calcium antagonists of the dihydropyridine type activation of the sympathetic nervous system and subsequently also of the renin-angiotensin-aldosterone system persists, while the haemodynamic reaction to vasodilatation, manifested by an elevated pulse rate and minute volume from the initial stage of therapy, recedes. In type II diabetics the basal and stimulated response of the renin-angiotensin-aldosterone system is reduced. The administration of calcium antagonists of the dihydropyridine type does not stimulate significantly the renin-angiotensin-aldosterone system as the starting function of the sympathetic nervous system is impaired within the framework of vegetative neuropathy. In almost 20% NIDDM plasma renin activity and aldosterone do not respond to furosemide administration and the vertical posture. In others the response is found but takes place at reduced levels. Hyporeninaemic hypoaldosteronism is thus manifested not so much by a drop of plasma renin and aldosterone beneath the lower range of reference values as by a reduced response to stimulation. Functional hyporeninaemic hypoaldosteronism is another, frequent late complication of diabetes. In advanced forms a further block of the renin-angiotensin-aldosterone system by ACE inhibitors can then produce, even in the absence of diabetic nephropathy, in the stage of chronic renal failure dangerous hyperkaliaemia which may threaten the patient. Dynamic examination of the sympathetic nerve and the renin-angiotensin-aldosterone system makes it possible to predict this condition. In practice it is necessary in diabetics with arterial hypertension after starting with ACE inhibitors during the first days to monitor repeatedly plasma potassium and creatinine. ACE inhibitors and calcium antagonists are otherwise for diabetics drugs of first choice which can arrest the progression of nephropathy, effectively reduced the blood pressure without causing deterioration of insulin resistance and hyperlipoproteinaemia and lead even to regression of hypertrophy of the vascular wall and left ventricle.
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PMID:[The effect of long-term treatment of arterial hypertension with Ca antagonists on the renin-angiotensin-aldosterone system in diabetics. Hyporeninemic hypoaldosteronism]. 857 95

Disturbances of prolactin secretion occur both in the chronic renal failure and in diabetes mellitus. The study aimed to investigate if the diabetic nephropathy as a cause of chronic renal failure disturbs prolactin secretion. The study was conducted in 5 groups of patients: group I-12 patients with IDDM without diabetic nephropathy; group II-12 patients with IDDM with diabetic nephropathy treated conservatively; group III-16 patients with chronic renal failure of non-diabetic origin; group IV-12 patients with IDDM with end stage renal failure in the course of diabetic nephropathy treated with haemodialysis; group V-16 patients with end stage renal failure of non diabetic origin treated with haemodialysis. 12 healthy subjects served as the control group. In all investigated groups as well as in the control group the TRH test was performed. The mean serum prolactin concentration was estimated in the investigated groups just before the intravenous TRH injection and then after 15, 30, 45, 60 and 120 minutes. The mean area over the basic value (AOBV) of prolactin was also assessed. The patients with IDDM without diabetic nephropathy did not differ from healthy subjects both in the basic and TRH induced prolactin secretion. Basic and TRH induced prolactin secretion in patients with diabetic nephropathy both conservatively treated and treated with haemodialysis were lower than in patients with the same stage of chronic renal failure of non-diabetic origin.
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PMID:[Prolactin secretion in diabetic nephropathy of patients with diabetes mellitus type I (IDDM)]. 867 6

It is now well-established in experimental models in rodents that increased glomerular pressure results in the development of focal and segmental glomerulosclerosis, proteinuria and progressive renal functional deterioration. In humans, direct measurement of glomerular capillary pressure is impossible. However, it is widely accepted that glomerular hypertension is present in different clinical situations, like diabetic nephropathy, chronic renal failure associated with glomerulonephritides, some forms of essential hypertension and cadaveric kidney transplantation. Many studies were performed on the effects of protein-restricted died and/or angiotensin converting enzyme inhibition on the rate of progression of renal failure in these renal diseases. Although controversial, the overall results suggest that these therapeutic strategies may reduce the rate of progression, particularly in diabetic nephropathy.
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PMID:[Intraglomerular hypertension. Physiopathology and therapeutic implications]. 868 50

We investigated myocardial troponin T (TnT) level as a marker for myocardial injury at various stages of diabetic nephropathy, including end-stage renal failure. One hundred and four diabetic patients were included in this study. These patients were divided into 5 groups as follows: Group I, composed of 41 patients without nephropathy who served as controls; Group II, composed of 15 patients with micro-albuminuria; Group III, composed of 15 patients with macroalbuminuria; Group IV, composed of 8 patients with renal failure who were not receiving hemodialysis; and Group V, composed of 25 patients who were receiving hemodialysis for renal failure. The following markers of myocardial injury were measured in these patients: myocardial TnT, creatine kinase (CK), myoglobin (Mb), and myosin light chain-1 (MCL-1). Our results showed that as the disease state of diabetic nephropathy advanced to renal failure, myocardial TnT levels became elevated. Group V showed significantly higher myocardial TnT levels than either Group I, Group II or Group III. Group IV showed significantly higher myocardial TnT levels than either Group II or Group III. The rate of ischemic changes on electrocardiograms also tended to increase with advance to renal failure in these patients. However, there was no correlation between myocardial TnT levels and serum Cr levels, used as an index for renal function. Myocardial TnT levels had a higher specificity for cardiac muscle than other markers for myocardial injury and are not significantly influenced by renal function. Myocardial TnT may be useful as a marker of myocardial injury for patients with chronic renal failure.
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PMID:Myocardial troponin T levels in patients with diabetic nephropathy. 872 35

We inquired whether the type of diabetic glomerulosclerosis, diffuse or nodular, is of value as an alternative to microalbuminuria in predicting later progression of renal disease. To answer this question, we conducted a retrospective cohort study in eleven Japanese non-insulin-dependent diabetes mellitus patients with normo- to microalbuminuria. Nodular diabetic glomerulosclerosis was found in six patients, and diffuse diabetic glomerulosclerosis in five patients. The mean follow-up period was 41.5 months (range 12-65). Three patients developed persistent proteinuria and one developed chronic renal failure. Mean level of serum creatinine in all patients was elevated from 0.97 +/- 0.23 mg/dl (SD) to 1.10 +/- 0.37 mg/dl (P = 0.098). The rate of increase in serum creatinine was 0.068 +/- 0.115 mg/dl/year in nodular diabetic glomerulosclerosis, and 0.023 +/- 0.069 mg/dl/year in a diffuse one. No difference was found between these two types of diabetic glomerulosclerosis (P = 0.445). We conclude that in normo- to microalbuminuria diabetic nephropathy the type of diabetic glomerulosclerosis, diffuse or nodular, is not necessarily an alternative to microalbuminuria in predicting its later progression in Japanese non-insulin-dependent diabetes mellitus patients.
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PMID:Are glomerular lesions alternatives to microalbuminuria in predicting later progression of diabetic nephropathy? 879 27

The aim of this study was to determine the clinical significance of serum and urinary insulin-like growth factor I (IGF-I) in renal disease and diabetes mellitus. In renal portion, we measured their concentrations in patients with chronic renal disease (serum creatinine < 2.0 mg/dl) (CRD. n = 22) and those with chronic renal failure (serum creatinine > or = 2.0 mg/dl) (CRF, n = 26) and compared with normal healthy controls (C. n = 20). Serum concentrations growth hormone (GH) and IGF-I did not differ among these groups. Urinary IGF-I level was significantly increased in CRF (4.0 +/- 0.5 ng/mg creatinine) compared with CRD (2.8 +/- 0.6 ng/mg creatinine) and C (1.8 +/- 1.0 ng/mg) creatinine). Urinary IGF-I did not correlate with either serum GH or serum IGF-I. Urinary IGF-I, but not serum IGF-I, demonstrated a significant negative correlation with creatinine clearance. In diabetic portion, 29 patients with noninsulin dependent diabetes mellitus (NIDDM), whose serum creatinine were within normal range, and age-matched 12 subjects were enrolled. Serum IGF-I in NIDDM (130 +/- 11 ng/ml) was significantly lower than that in controls (201 +/- 11 pg/ml). In contrast, urinary IGF-I level in NIDDM (1.93 +/- 0.31 ng/mg creatinine) did not differ from that in controls (2.00 +/- 0.31 ng/mg creatinine). In NIDDM, urinary IGF-I had poor correlation with both serum IGF-I and albuminuria. The data in renal patients suggest the possible participation of renal IGF-I in the progression of renal disease, while in NIDDM with normal serum creatinine the role of renal IGF-I may be less in the early diabetic nephropathy.
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PMID:Serum and urinary levels of insulin-like growth factor I in patients with chronic renal disease and diabetes mellitus: its clinical implication. 879 28

To update 2 National High Blood Pressure Education Program working group reports on hypertension and chronic renal failure and renovascular hypertension, a working group was appointed by the director of the National Heart, Lung, and Blood Institute. Literature was searched through MEDLINE and the National Heart, Lung, and Blood Institute information center library. Scientific evidence was given precedence over clinical anecdotal experience. The working group members produced initial draft documents that were circulated to additional experts on hypertension and renal disease. This reiterative process occurred for 18 draft documents. The final report was sent to the representatives of the 44 organizations on the Coordinating Committee for vote and unanimously approved September 1, 1995. The report recommended treatment of hypertension to the goal of 130/85 mm Hg with whatever therapy is necessary to prevent the development of hypertensive nephrosclerosis or the progression of established renal disease of diverse causes. It seems reasonable to recommend angiotensin-converting enzyme inhibitors as initial therapy for patients with diabetes and microalbuminuria or overt diabetic nephropathy with and without hypertension. Renovascular disease has emerged as a major cause of end-stage renal disease, especially in the elderly. Newer screening procedures for the noninvasive screening of renovascular disease include the captopril test, renal scintigraphy following captopril administration, duplex scanning, and magnetic resonance angiography.
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PMID:1995 update of the working group reports on chronic renal failure and renovascular hypertension. National High Blood Pressure Education Program Working Group. 882 47

Pituitary-adrenocortical axis is disturbed in patients with chronic renal failure. Such abnormalities have been described in diabetic patients, too. The studies were performed to answer the following questions: 1) Is there a difference in basal ACTH and cortisol plasma level between patients with diabetic nephropathy and normal subjects? 2) Does haemodialysis affect ACTH and cortisol plasma level in patients with diabetic nephropathy? 18 patients with diabetic nephropathy and 10 normal controls were the subjects of this study. Blood samples for ACTH and cortisol determination were collected from each patient with diabetic nephropathy four times: before haemodialysis from the arterial line of dialyzer (0a) after 60 minutes of haemodialysis from the arterial (60a) and the venous (60v) line of dialyzer and after 240 minutes of haemodialysis from the arterial line (240a). Blood samples from normal controls were collected at 6 a.m. to determine ACTH and cortisol level. All the diabetic patients were on chronic 4-hour-haemodialysis 3 times a week. An artificial kidney Fresenius 4008 E, polysulfone dialyzers F5 and acetate dialysing solution were used in the studies. Plasma samples were analyzed for cortisol and ACTH by RIA. The studies brought to following conclusions: 1) The basal ACTH plasma level is significantly higher in patients with diabetic nephropathy than in normal controls. There is no significant difference in cortisol plasma level between diabetic patients and the control group. 2) Haemodialysis effects significant decrease of ACTH in plasma of diabetic patients. There is no statistic significance in cortisol plasma level in diabetic patients during haemodialysis.
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PMID:[Effect of hemodialysis on the pituitary adrenocortical axis in patients with diabetic nephropathy]. 884 11

Diabetic nephropathy is the most frequent cause of chronic renal failure. The onset of microalbuminuria in patients with diabetes mellitus, which seems to be related to blood pressure and the control of glycemia, is predictive of the development of true proteinuria. This multicenter, single-blind, randomized study examined the effects of benazepril and nicardipine on overnight microalbuminuria in 57 normotensive and 46 hypertensive diabetic patients. At the end of a 3-month placebo run-in period, the patients were stratified on the basis of the presence or absence of arterial hypertension and, within each stratum, randomized to receive one daily tablet of 10 mg benazepril or one tablet of 20 mg nicardipine twice daily for 6 months. Renal hemodynamics was investigated in 25 patients. Both drugs decreased overnight microalbuminuria throughout the study period, but benazepril was more effective than nicardipine (p = 0.025); in the patients with hypertension, both drugs led to a similar marked reduction in systolic and diastolic blood pressure. This study shows that benazepril was more effective than nicardipine in reducing overnight microalbuminuria in patients with diabetes mellitus, independently of their antihypertensive properties.
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PMID:Effects of benazepril and nicardipine on microalbuminuria in normotensive and hypertensive patients with diabetes. 887 95

The study was undertaken to observe the co-relation between microangiopathic changes in diabetic retinopathy and microvascular changes in diabetic nephropathy. Included in the study were 64 patients with chronic renal failure who were on maintenance dialysis, 40 had hypertension alone, 21 hypertension and diabetes and 3 had diabetes alone. On examination of retina, of 40 hypertensive patients, 14 had positive findings, while in the hypertensive and diabetic group, 20 patients out of 21, had positive findings. Nine patients in the hypertensive group had delayed choroidal filling on fluorescein angiography which was not very accurately reflected on Funduscopy. In the diabetic and hypertensive group, 13 patients having proteinuria of more than 1 gm, also had exudates and haemorrhages in the fundus. It was concluded that a correlation exists between the arterial changes in the fundus of the eye and the glomeruli of the kidney.
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PMID:A co-relation of the eye and kidney-in diabetes mellitus and hypertension. 892 Jun 1


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