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

Duplex Doppler ultrasonography may explore renal perfusion in frequent diseases such as renal obstruction, reno-vascular hypertension, acute or chronic renal failure or diabetic renal complications by measuring Pourcelot's resistive index (RI) of renal parenchyma arteries for each kidney. A statistical and prospective study was performed on 574 patients. In healthy patients, the RI values, equal for each kidney were included in 0.45 and 0.7 (mean RI = 0.59). For other values, there was a renal pathology. Patients with idiopathic hypertension (mean RI = 0.59) or non obstructive dilatation (mean RI = 0.61) did not have an RI significantly different from healthy patients. In cases of renal obstruction, there was a significant increase in the RI for the pathological kidney (mean RI of 0.73). The sensitivity and the specificity was 100% for acute obstructions examined during the first 48 hours. In contrast, in case of renal artery stenosis greater than 70% there was a significant decrease in the RI for pathological kidney. So the RI increased significantly in both kidneys: when there was renal failure with active disease within the tubulo-interstitial compartment (mean RI of 0.77); in all cases of diabetic nephropathy (mean RI of 0.74) where the RI increased early before laboratory signs. Duplex Doppler ultrasonography may be an original method for renal explorations by providing not only morphological data but also physiological data with the perfusion study.
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PMID:[Duplex Doppler ultrasonography of intra-renal arteries. Normal and pathological aspects]. 177 87

Diabetic nephropathy is the most frequent cause of chronic renal insufficiency in adults. Its early stage, characterized by increased albuminuria, develops in susceptible subjects already manifestation of diabetes. This stage can be treated by inhibitors of the angiotensin-converting enzyme which reduce the pathologically elevated intraglomerular pressure even in normotonic subjects. Enalapril was administered for a period of 12 weeks to eight children and adolescents with a normal blood pressure and albuminuria of 30-300 mg/24 hours during repeated assessments. During treatment there was not only a significant decline of albuminuria (from 104.6 +/- 42.7 mg/24 hours to 47.2 +/- 15.4, p = 0.003) but also a drop of the pathological glomerular hyperfiltration (from 3.38 +/- 1.87 ml/s to 1.48 +/- 0.54 ml/s within six weeks - p = 0.02 and to 2.05 +/- 0.80 ml/s resp. within 12 weeks, n.s.). The favourable effect persisted also for some time after discontinuation of treatment. Treatment was relatively well tolerated by the patients. The problem remains whether it is possible to retard or prevent in this way the development of further stages of diabetic nephropathy, include chronic renal failure.
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PMID:[The effect of enalapril on the development of diabetic nephropathy in children and adolescents]. 189 36

Angiotensin converting enzyme (ACE) inhibitors are well established in the treatment of hypertension and cardiac failure. Experimental studies in rats have suggested that these agents may protect renal function in chronic nephropathy by a mechanism other than simply lowering the systemic blood pressure. In human studies of incipient diabetic nephropathy, worsening of microalbuminuria was prevented during 3 years of ACE inhibition. ACE inhibitors reduce arterial blood pressure in chronic nephropathy, and may cause a fall in glomerular filtration rate. In diabetic nephropathy, proteinuria was reduced by 2 months' treatment with enalapril to less than half of the values obtained in a control group treated with metoprolol. Nonrandomised trials have suggested that ACE inhibitors may slow the deterioration of renal function, but no comparisons with other antihypertensive agents in prospective studies have been published to date. In chronic renal failure, ACE inhibitors may worsen anaemia and hyperkalaemia. Renovascular hypertension can be treated with ACE inhibitors, but the treatment may lead to a compromised renal function. The dosage of these drugs should be reduced in renal failure and therapy should be started cautiously in this setting, with close monitoring of blood pressure, renal function and plasma potassium.
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PMID:Angiotensin converting enzyme (ACE) inhibitors and renal function. A review of the current status. 193 Jul 42

Although experiments in the rat suggest that glomerular hemodynamic alterations following a reduction of renal mass may be implicated in the progression of chronic renal failure, we argue that the deleterious effects of similar adaptations in human renal disease are unproven. In the otherwise normal solitary kidney the supranormal glomerular filtration rate (GFR) remains stable over the longterm, and in early diabetic nephropathy which is also accompanied by hyperfiltration, renal deterioration cannot be dissociated from a rise in systemic blood pressure. In patients with miscellaneous renal diseases and a depressed basal GFR there is indirect evidence that hyperfiltration might occur in some of the remnant glomeruli. However, at present there is little conclusive evidence to indicate that therapies which might normalize glomerular hemodynamics, e.g., dietary protein restriction, have any effect on progression of renal disease, or that angiotensin converting-enzyme inhibitors, which lower glomerular capillary pressure, have any advantage over other antihypertensive agents which are equally efficacious in lowering systemic blood pressure.
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PMID:Do glomerular hemodynamic adaptations influence the progression of human renal disease? 202 46

Haemostatic activation was measured in patients with either non-diabetic chronic renal failure (CRF) or diabetic nephropathy. We have investigated the relationship between these haemostatic markers and the rate of progression of renal failure. When compared with age- and sex-matched healthy controls, both patient groups showed significantly elevated plasma concentrations of D dimer, von Willebrand factor antigen (vWFAg), and C-reactive protein (CRP) (all P less than 0.001), as well as an increase in spontaneous platelet aggregation (P less than 0.01). Plasma concentration of platelet factor 4 was slightly but not significantly increased. Serum thromboxane was subnormal (P less than 0.01). Multiple regression analysis showed that in non-diabetic CRF proteinuria and serum TxB2 were independently related to the rate of progression of renal failure; in diabetic nephropathy proteinuria and vWFAg were independently related to the rate of progression. In both groups the relationship was stronger with proteinuria (standardised regression coefficients 0.56 and 0.45 respectively) than with serum TxB2 (0.29) or with vWFAg (0.37). We have found haemostatic activation in both non-diabetic and diabetic progressive renal failure. Proteinuria, and also in this study serum TxB2 and vWFAg, appear to be determining factors in the progression of renal failure, and their measurement may have prognostic value.
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PMID:Haemostatic activation and proteinuria as factors in the progression of chronic renal failure. 205 12

Eighty-eight type I diabetics were subjected to neurological and myographic examination and tests were performed assessing the condition of the vegetative nervous system. Forty-four patients (50% of the group) suffered from diabetic nephropathy with different expression in the stage of chronic renal failure. The authors revealed significant positive correlation between the results of tests of vegetative neuropathy and all evaluated parameters of the neurological and electromyographic finding. In patients with a S-creatinine level above 125 mumol/l in both tests of vegetative neuropathy and in all examined parameters of peripheral nerves highly significantly lower values were recorded than in diabetic patients with normal renal function. In diabetics without renal insufficiency, however, the correlations between the findings on the autonomous and peripheral nervous system were also statistically significant.
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PMID:[The relation between peripheral and autonomic neuropathies in insulin-dependent diabetics]. 216 Mar 29

Medicare's End-Stage Renal Disease (ESRD) Program provides funding for life-saving renal replacement therapy for patients with irreversible chronic renal failure. Although more than 100,000 patients are currently alive due to dialysis and transplantation, mortality among ESRD patients is still much higher than in the general population. Gross mortality, calculated from aggregate statistics such as those available from the annual ESRD facility survey, is an extremely imprecise measure of mortality and can lead to misleading conclusions. Standard methods of survival calculation such as actuarial life-table analyses provide more accurate descriptions of variations and trends in mortality. The most important characteristic influencing mortality among ESRD patients on dialysis is the changing age and diagnostic distribution. The average age of dialysis patients has increased by over 5 years during the past decade. Patients whose renal failure is attributed to diabetic nephropathy currently account for 30% of all patients initiating renal replacement therapy each year and constitute the fastest growing group of ESRD patients. From 1982 to 1987, 1-year survival on dialysis was 72.7% for patients whose renal failure was attributed to diabetic nephropathy and 79.8% for all other patients. Survival decreases rapidly with advancing age at time of renal failure, from 95.1% among patients 15 to 24 years to 52.5% for patients over the age of 85 (for non-diabetics). Survival rates for whites are 5% to 6% lower than for other racial categories. There are no obvious trends in mortality among dialysis patients over the past decade. For patients whose renal failure is attributed to diabetic nephropathy, survival rates have remained constant despite overall aging in this group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mortality rates among dialysis patients in Medicare's End-Stage Renal Disease Program. 218 27

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

Ultrasonograms of 546 kidneys were obtained in 280 patients undergoing chronic dialysis. Dialysed kidneys could be detected in 529 of the 546 kidneys (96.9%) by ultrasonic examination. The ultrasonic diagnoses on dialysed kidneys were contracted kidney in 313 kidneys (59.2%) and acquired cystic disease of the kidney in 107 kidneys (20.2%). Ultrasonic measurement of the size of kidney (length and thickness) revealed that the kidneys in patients with chronic renal failure were much smaller than normal ones. But the kidneys in patients undergoing dialysis for more than 8 years gradually increased in size with incidence of acquired renal cysts. The kidneys in patients with diabetic nephropathy were greater in length and thickness than those with chronic glomerulonephritis. Sonographic features of dialysed kidneys were unclear renal imaging, unidentified central echoes, cortico-medulla + border and increased parenchymal echogenicity. Irregularity of the renal contour had a tendency to increase in number with incidence of cysts in long-term dialysis patients. The ultrasonograms of the kidneys with diabetic nephropathy showed fewer changes than normal ones. No major complication of the kidney was detected in the present study. However, two retroperitoneal hematomas and one renal cell carcinoma developed within two years after this examination. We believe that regular screening of the kidneys by ultrasonic examination is mandatory in patients on chronic dialysis for early diagnosis and treatment of these complications.
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PMID:[Ultrasonographic study on kidneys in patients with chronic renal failure. Part I. Ultrasonic measurement of renal size and analysis of renal ultrasonotomograms]. 223 8

Renal failure, once established by loss of a critical amount of functional renal mass, tends to be progressive. A large body of experimental evidence supports the hypothesis that glomerular capillary hypertension is important in the pathogenesis of progressive chronic renal failure of diverse types, including subtotal renal ablation and diabetic nephropathy. Converting enzyme inhibitors are effective in slowing or arresting the progression of glomerular injury in these experimental models, in association with normalization of both systemic and intrarenal pressures. Clinical studies of diabetic nephropathy and chronic renal failure of other etiologies support the concept that these same renal hemodynamic factors are important in human renal disease and that treatment with converting enzyme inhibitors may prove to be a useful therapeutic intervention. Whether the converting enzyme inhibitors have specific advantages over other antihypertensive agents due to beneficial renal hemodynamic effects, as suggested by experimental studies, is a question that awaits further investigation. Furthermore, the pathogenesis of hypertensive glomerular injury is complex and involves the participation of diverse biologic systems. We predict that a wide variety of therapeutic maneuvers, with disparate mechanisms of action, may be effective in arresting or preventing glomerular injury.
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PMID:Angiotensin converting enzyme inhibitors and progression of chronic renal failure. 225 70


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