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

A high incidence of renal lesions is observed in patients with insulin-dependent diabetes. In the early stages of the disease glomerular capillary hemodynamics is altered with, in particular, glomerular hyperfiltration related to several factors: enhanced glomerular capillary flow rate, capillary hypertension and increased filtration area. These hemodynamic changes could affect development of the glomerular microangiopathy: the final outcome of this is the glomerulosclerosis associated with a progressively worsening and ineluctable chronic renal insufficiency. Hypertension, frequent in the early stages, is practically constant when the neuropathy stage has been reached; it is well established that hypertension accelerates the development of glomerular lesions and the progression of the renal impairment. Experimental and clinical studies have clearly demonstrated that antihypertensive treatment slows down the degradation of renal function. All antihypertensive drugs appear to be effective, but converting enzyme inhibitors, by their effects on renal hemodynamics, could play a particular role in the prophylactic treatment of diabetic nephropathy. Determination of urinary excretion of albumin (microalbuminuria), the global evidence of the onset of a nephropathy is useful for the follow up of the renal disease, allows follow up of the renal lesion and evaluation of the efficacy of treatment.
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PMID:[Arterial hypertension and diabetic nephropathy]. 149 60

In theory, transplantation of the islets of Langerhans is the method of choice for the treatment of insulin-dependent diabetes. In actual fact, medical teams who have been working on this subject for about two decades have met with the problem of islet isolation, and for the time being this treatment cannot be considered effective. Pancreas transplantation gives satisfactory results in diabetics with renal impairment when it is coupled with kidney transplantation. However, it cannot yet be applied to all diabetics as its results are mediocre when performed alone, and it requires chronic immunosuppression. Pancreas transplantation not only increases the quality of life but also has the advantage of acting on degenerative complications: it may improve diabetic nephropathy, retinopathy and neuropathy. The results obtained are getting better year after year, and they are now close to those observed with other organ transplantations.
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PMID:[Islets of Langerhans grafts and pancreas transplantation]. 149 35

Angiotensin II plays an important role in the kidney by regulating renal flow, glomerular filtration rate, mesangial cell function, and sodium reabsorption. Blockade of the renin-angiotensin system has powerful effects on kidney function. Studies in animal models of renal failure suggest that converting enzyme inhibitors slow down the inevitable progression of the renal failure. This could be in part due to their effect on reducing glomerular pressure or by reducing glomerular hypertrophy. In patients with malignant hypertension, diabetic nephropathy, and other causes of renal failure, preliminary evidence suggests that lowering the blood pressure with angiotensin-converting enzyme (ACE) inhibitors may possibly carry some other benefits compared with other blood pressure lowering regimens. However, single drug therapy is rarely sufficient to control blood pressure in these patients. Further properly controlled randomized trials should give a clear indication of whether any particular class of drug has any advantage in slowing down the progressive renal impairment for a given lowering of blood pressure. In patients with renovascular hypertension ACE inhibitors are effective drugs in lowering blood pressure. However, in certain settings they may cause a reversible decline in renal function.
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PMID:Blood pressure, angiotensin-converting enzyme (ACE) inhibitors, and the kidney. 158 Feb 76

End-stage renal disease attributed to hypertension has increased annually for the last decade and will probably worsen through the year 2000. Patients with diabetic nephropathy and patients with hypertensive renal disease account for most new cases annually. Evidence reveals that all levels of untreated hypertension are associated with potentially declining renal function. Data from the Hypertension Detection and Follow-up Program and other studies show that antihypertensive treatment can prevent progressive renal failure. An ablation model demonstrates glomerular hyperfiltration as a possible mechanism for progressive renal failure. Human data on the renal effects of antihypertensive agents are limited and inconsistent. Despite the limitations, the Working Group on Hypertension and Chronic Renal Failure concludes that controlled hypertension to less than 140/90 mm Hg reduces the incidence of end-stage renal disease. Patients with established renal impairment may benefit from individualized treatment to 130/85 mm Hg or less.
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PMID:National High Blood Pressure Education Program Working Group report on hypertension and chronic renal failure. 206 78

Hypertension contributes to the inexorable decline of renal function in patients with chronic renal impairment. Studies on the long-term use of converting enzyme inhibitors and calcium antagonists in the treatment of hypertension in patients with chronic renal failure are hereby reviewed. The data demonstrate that converting enzyme inhibitors are effective antihypertensives in diabetic nephropathy and other forms of chronic renal failure. Furthermore, the results suggest that long-term treatment with captopril may slow the progression of renal impairment in diabetic nephropathy, whereas the data are inconclusive for non-diabetic nephropathies. A reduction of proteinuria or albuminuria was also observed in most trials during long-term converting enzyme inhibition. Treatment with calcium antagonists also led to effective blood pressure control in hypertensive patients with renal disease. However, the very limited data in humans suggest no consistent beneficial effect on kidney function or proteinuria. More controlled studies are necessary to determine the relative efficacy and safety of converting enzyme inhibitors and calcium antagonists in comparison with "standard antihypertensives" in long-term antihypertensive treatment of patients with various forms of chronic renal failure.
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PMID:Converting enzyme inhibitors and calcium antagonists in the long-term treatment of hypertension in chronic renal failure. 219 80

Echocardiography was used to study the prevalence and severity of left ventricular hypertrophy in patients with established diabetic nephropathy (persistent proteinuria for at least 2 y plus severe retinopathy). Fifteen patients had mild renal impairment (serum creatinine less than 150 mumol l-1), 14 patients had moderate renal impairment (serum creatinine 150-400 mumol l-1), and 20 patients had severe renal impairment (serum creatinine greater than 400 mumol l-1). Thirty-six of the 49 (73%) were on anti-hypertensive treatment, despite which mean blood pressure was 161 +/- 25/89 +/- 9 (+/- SD) mmHg. Left ventricular hypertrophy was demonstrated in 42 of the 49 patients (85%), and increased in severity with increasing renal impairment. Interventricular septal + left ventricular posterior wall thickness was 25 +/- 3 mm in those with mild renal impairment, 28 +/- 6 mm in those with moderate renal impairment and 30 +/- 4 mm in those with severe renal impairment. The most severe left ventricular hypertrophy was seen in the Afro-Caribbean patients. Left ventricular hypertrophy was present even in those with marginally raised blood pressure and was related to age and serum creatinine but not to present blood pressure or duration of proteinuria.
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PMID:Cardiac hypertrophy in diabetic nephropathy: an echocardiographic study. 297 44

The progression of renal failure was analyzed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosuppressive treatment. The reciprocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephropathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p less than 0.01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration. For those with linear progression of renal failure there was a significant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure. Calcium phosphate product correlated poorly with the rate of deterioration. We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure. Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephritis.
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PMID:Renal pathology and proteinuria determine progression in untreated mild/moderate chronic renal failure. 320 6

From August 1974 to January 1985, 53 patients (26 men; seven Maoris) mean age 45 (SD 15) years, with diabetes mellitus for a mean of 12 (SD nine) years had a renal biopsy and were followed. Indications for biopsy were nephrotic syndrome, proteinuria, renal impairment (five) and hematuria (one). Mean plasma creatinine concentration was 0.22 (SD 0.18) mmol/L and protein excretion 3.4 (SD 2.5) g/24 h. Diabetic nephropathy was demonstrated in 39 patients and significantly associated with retinopathy and insulin dependent diabetes mellitus (IDDM). Of the 39 patients followed for 25.7 (SD 22.8) months, 18 had died (nine myocardial infarction, six uremia, two sepsis, one stroke) and nine had begun dialysis. The five-year cumulative renal survival was 28%. The presence of the nephrotic syndrome and the plasma creatinine concentration at presentation were the best predictors of survival. Diabetics with IDDM of 20 years duration, retinopathy and heavy proteinuria, who survive the other complications of their disease, are likely to have diabetic nephropathy requiring renal replacement therapy.
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PMID:Renal disease in diabetics--which patients have diabetic nephropathy and what is their outcome? 324 62

Protein restriction has been used in the treatment of renal disease and may also be beneficial in the management of diabetic nephropathy. We evaluated the effects of moderate protein restriction (0.6 g/kg ideal body weight per day) for a 3-mo period on renal function in seven diabetic patients. Moderate protein restriction led to a decrease of approximately 50% in the albumin excretion rate in patients with overt proteinuria or microalbuminuria. This decrease occurred in some patients without a decrease in glomerular filtration rate, renal plasma flow, or plasma albumin concentration and may reflect subtle changes in filtration properties or permeability of glomeruli. In this pilot study moderate protein restriction has marked effects on albumin excretion irrespective of the initial degree of renal impairment. It is therefore suitable for longer-term study of its effects on the progression of renal disease in both patients with overt and incipient diabetic nephropathy.
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PMID:Proteinuria and renal function in diabetic patients fed a diet moderately restricted in protein. 340 3

A sensitive single measure of diminishing renal function is of importance in attempts to modify the progression of diabetic nephropathy. In 12 insulin-dependent diabetics with proteinuria plasma concentrations of beta 2-microglobulin were found to correlate more closely than plasma creatinine concentrations or creatinine clearance with glomerular function as measured by clearance of 52Cr-EDTA. The plasma beta 2-microglobulin concentration was raised in all patients with diminished glomerular filtration rate (below 80 ml/min/1.73 m2). By contrast, in two of these patients plasma creatinine concentration was normal. Plasma beta 2-microglobulin concentrations were stable throughout the day and not affected by food intake, unlike plasma creatinine concentrations, which rose in the afternoon and evening and after a meat meal. Plasma beta 2-microglobulin concentrations were the same in venous and capillary blood, the capillary blood being readily self-collected. Concentrations of beta 2-microglobulin were stable for up to 24 hours when whole blood was stored at 4 degrees C; adding aprotinin inhibited loss of beta 2-microglobulin for up to seven days. The results of this study suggest, therefore, that measuring beta 2-microglobulin concentrations is a simple and accurate method of detecting minor degrees of renal impairment and monitoring the effects of treatment.
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PMID:Beta 2-microglobulinaemia: a sensitive index of diminishing renal function in diabetics. 616 71


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