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

Late complications such as retinopathy and neuropathy contribute substantially to the morbidity of patients with diabetes mellitus but have only moderate effect on their life expectancy. However, once diabetic nephropathy occurs, life expectancy of patients with diabetes mellitus is shortened considerably. This review discusses briefly several possible pathogenetic mechanisms involved in the development of diabetic nephropathy. Changes in renal hemodynamics as the initiating and contributing factor to the development of diabetic nephropathy are discussed in more detail. Finally, the article reviews possible therapeutic measures to prevent the development of diabetic nephropathy, or to slow down its progression.
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PMID:Diabetic nephropathy in insulin-dependent diabetic patients: renal hemodynamics and derived treatment strategies. 252 42

In vitro platelet aggregometry with epinephrine, adenosine-diphosphate, collagen and arachidonic acid was performed in 201 patients with diabetes, and in 106 healthy subjects. Those patients who were free of nephropathy showed hyperaggregability to collagen and arachidonic acid, and also to epinephrine and adenosine diphosphate, when neuropathy occurred. Patients with nephropathy, both with and without azotaemia, had diminished platelet responses to each of the four aggregating agents as compared to age- and sex-matched controls. Aggregability was not dependent on type of diabetes. It is concluded that diabetic nephropathy is characterized by decreased in vitro reactivity of platelets. Further researches are necessary to explain in vitro hypoaggregability besides the numerous evidence of in vivo hyperfunction of platelets in diabetes.
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PMID:[Differences in platelet aggregation in various microangiopathic complications of diabetes mellitus]. 264 41

Plasma inactive renin concentration (IRC) was determined in 92 diabetic patients with or without chronic diabetic complications, 23 non-diabetic patients with renal failure and 36 normal subjects. IRC of the diabetics was higher than that of normal persons. With the Pearson's correlation analysis, IRC of the diabetics correlated with duration of diabetes, degrees of chronic complications (nephropathy, retinopathy and neuropathy), but not with age of patient, HbA1c or mean blood pressure. The stepwise logistic analysis revealed the relation of neuropathy to mean blood pressure, serum creatinine concentration and duration of diabetes, retinopathy to mean blood pressure, duration of diabetes and serum beta 2-microglobulin and nephropathy to IRC and urinary NAG/Cr ratio. In addition, IRC was dependent on nephropathy but not on retinopathy or neuropathy. IRC in diabetics was high even in diabetics without albuminuria (group I) and significantly increased in diabetics with albuminuria but without increased serum creatinine level (group II) and more marked high levels were observed in diabetics with increased serum creatinine concentrations (group III). However, IRC of the non-diabetic patients with renal failure was not elevated, therefore, the increased IRC in nephropathy is likely to be specific to diabetic nephropathy. The correlation of other factors to increased IRC level seem to be due to nephropathy concomitant to these factors. Therefore, the increased level of IRC in diabetics is intimately connected to renal change in diabetes but whether it is the cause or result of nephropathy remains to be elucidated. It is concluded that the determination of IRC in diabetic patients was an effective means of assessment or forecast of nephropathy.
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PMID:[A study on inactive renin in the plasma of patients with diabetes mellitus]. 267 Jul 25

Both diabetic nephropathy and retinopathy result from microangiopathic processes although there is controversy as to whether this is true for neuropathy. Increased platelet aggregation has been reported in diabetics with nephropathy and retinopathy. The presence of increased platelet aggregation in diabetics with neuropathy could be due to the other coincident microvascular complications. We have, therefore, studied in vitro platelet aggregation in 10 diabetics with chronic symptomatic neuropathy but no other complications, 10 with neuropathy and severe retinopathy, 17 with retinopathy alone, and 23 diabetics with no complications. Increased platelet aggregation to adenosine diphosphate (ADP) and adrenaline was seen in diabetics with neuropathy alone (peak responses 85.0 +/- 5.5% and 82.9 +/- 6.2%, respectively) when compared with uncomplicated diabetics (peak response 74.9 +/- 10.1%, p less than 0.005, and 74.3 +/- 12.5%, p less than 0.01, respectively). The increased platelet aggregation in the patients with neuropathy alone was similar to that found in the diabetics with severe retinopathy. We conclude that increased platelet aggregation is associated with established microangiopathy and is also present in otherwise uncomplicated patients with neuropathy, and this may have pathogenic and therapeutic implications.
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PMID:Abnormal platelet aggregation in chronic symptomatic diabetic peripheral neuropathy. 295 Nov 76

Reports of renal replacement therapy in diabetes usually refer to patients with insulin-dependent diabetes mellitus (IDDM) only, and little is known about renal failure in non-insulin-dependent diabetics (NIDDM). A high proportion, 46/141 (32%), of the diabetics treated at our unit since 1974 had NIDDM. They were older at treatment (56 +/- 9 years, mean +/- SD) compared to the IDDM patients (39 +/- 10 years, p less than 0.001), and had a shorter duration of diabetes (13 +/- 8 years versus 23 +/- 8 years, p less than 0.001). Asians and Afro-Caribbeans accounted for 48% of the NIDDM patients (22/46) compared to only 7% of those having IDDM (6/95, p less than 0.0001). Non-diabetic renal disease accounted for the renal failure in 32% (15/46) of the NIDDM patients but only in 10.5% (10/95) of the IDDMs (p less than 0.001). Despite these differences the prevalence of other diabetic complications (retinopathy, neuropathy, and cardiovascular disease) was similar. Patient survival after transplantation was poorer in NIDDM than IDDM (23% and 57%, respectively, at 2 years). Survival on dialysis was equally poor in NIDDM and IDDM. Thus, NIDDM patients treated for renal failure are more commonly non-European and more often have non-diabetic renal disease. Yet other diabetic complications occur to the same extent in both IDDM and NIDDM patients with diabetic nephropathy.
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PMID:Non-insulin-dependent diabetes and renal replacement therapy. 296 85

Kidney transplantation is now firmly established as the standard treatment for all diabetic patients with end-stage renal failure. In an analysis of all renal transplants at the University of Minnesota between June 1, 1980 and May 31, 1987, there were no differences in renal allograft functional survival rates for diabetic and nondiabetic recipients. At one year the survival rates were 84% (n = 151) and 86% (n = 260) for those treated with azathioprine, prednisone and ALG; 86% (n = 101) and 87% (n = 104) for those treated with cyclosporine-prednisone, and 92% (n = 165) and 89% (n = 191) for those treated with triple therapy (cyclosporine, azathioprine, and prednisone). Pancreas transplantation remains an investigational procedure for nonuremic diabetic patients but may be considered therapeutic in diabetic renal allograft recipients because such patients are obligated to immunosuppression and only the surgical risks of pancreas transplantation need to be considered, which are now acceptably low. Recipients of pancreas transplants performed simultaneous with the kidney have patient and pancreas graft survival rates of greater than 90% and +/- 60% at several institutions, including our own. The potential for benefit of pancreas transplantation, however, is greater in the nonuremic nonkidney transplant patient, and pancreas transplantations are being performed in such patients at a few institutions. An early beneficial effect of pancreas transplantation preexisting proliferative retinopathy has not been discerned, although long-term retinopathy has been stable in patients with functioning grafts. Preliminary studies have shown a beneficial effect on neuropathy and on microscopic lesions of diabetic nephropathy, but at the expense of cyclosporine toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal transplantation in diabetic patients is confirmed therapy while pancreas transplantation should be performed only in an investigational setting. 297 67

To determine whether pancreas transplantation is capable of preventing diabetic somatic neuropathy, metabolic studies and electron microscopic morphometry of the sciatic nerve were performed monthly for 2 years in four groups of highly inbred rats: (1) NC-28 nondiabetic controls; (2) DC-82 untreated alloxan-diabetic controls; (3) WPT-122 diabetic rats that received a syngeneic whole-pancreas transplant; and (4) IT-90 diabetic rats that received intraportal injections of 1500 to 2000 syngeneic pancreatic islets. Five diabetic nerve lesions were quantitated by a "blind" protocol: intra-axonal glycogen deposits, axons with glycogen deposits, demyelinated axons, intact axoglial junctions in paranodal terminal myelin loops, and basal lamina thickness of vasa nervorum. Untreated diabetic control animals had significant and progressive increases in all five nerve lesions compared to nondiabetic controls (p less than 0.01). Whole pancreas transplants produced precise metabolic control of diabetes and prevented development and progression of all five diabetic nerve lesions throughout the 2-year study period. Pancreatic islet transplantation produced strict metabolic control and prevented diabetic neuropathy for the first 6 months, but then diabetes recurred and nerve lesions that were similar in severity to those in untreated diabetic rats developed. The finding that whole pancreas transplantation prevents diabetic somatic neuropathy adds to and extends our previous studies showing that whole-pancreas transplants prevent diabetic nephropathy.
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PMID:Effect of pancreas transplantation on diabetic somatic neuropathy. 313 31

In vitro platelet aggregometry was performed in 201 patients with diabetes mellitus, and in 106 controls. The complication-free and retinopathic patients showed hyperaggregability to collagen and arachidonic acid, and also to epinephrine and adenosine diphosphate when neuropathy occurred. Patients with nephropathy, both with and without azotemia, had diminished in vitro platelet responses to each of the four stimuli as compared to age- and sex-matched controls. These characteristics were independent of the type of diabetes. It is concluded that diabetic nephropathy is characterized by reduced platelet in vitro reactivity. Further research is necessary to explain in vitro hypoaggregability in contrast to the numerous proofs of in vivo hyperfunction of platelets in diabetes.
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PMID:Platelet hyper- and hypoaggregability in different microangiopathic complications of diabetes mellitus. 340 79

Diabetic nephropathy develops in about 45% of insulin dependent diabetics of whom two-thirds will develop renal failure, the rest dying from cardiovascular disease. Most of the excess mortality of insulin dependent diabetics occurs in those with proteinuria. Among non-insulin dependent diabetics nephropathy is also an important cause of increased mortality but this is mainly from cardiovascular disease. Once diabetic nephropathy is established it progresses relentlessly to end-stage renal failure over about seven years, but ranging from five to 20 years. The explanation for the different rates of progression in individual patients is not understood. Hypertension accompanies diabetic nephropathy and its treatment may retard the progression of renal failure. Other forms of intervention include glycaemic control which has not been shown to have any effect, and protein restriction for which no conclusions can be drawn at present. The diagnosis of diabetic nephropathy is straightforward in the presence of a typical history and clinical features. Non-diabetic renal disease is sometimes the cause of renal failure and may require specific treatment; prognosis for renal failure treatment may be better than for nephropathy patients with other diabetic complications. Other diabetic complications develop as diabetic nephropathy progresses, most notably cardiac and peripheral vascular disease. Proliferative retinopathy and neuropathy are considerable problems and their management needs attention both before and after renal failure treatment.
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PMID:Clinical diabetic nephropathy: natural history and complications. 353

Fasting plasma zinc levels were determined in 45 IDDM and in 40 NIDDM patients. Mean values were similar in both groups, but diabetic men showed a significantly higher plasma zinc (p less than 0.05) than diabetic women. In patients with diabetic nephropathy a lower zinc level was associated with decreased plasma albumin as compared to patients without complications (p less than 0.001). Neuropathy and macro-angiopathy were also associated with lower zincemia (p less than 0.05) but in the presence of normal albumin levels. In IDDM without nephropathy a significant positive correlation was found between plasma zinc and plasma glucose, albumin, branched chain amino acids and glutamine, while in NIDDM without nephropathy a significant positive correlation exists between plasma zinc and the amino acids glutamine, valine, histidine and lysine.
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PMID:Plasma zinc levels in diabetes mellitus: relation to plasma albumin and amino acids. 375 14


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