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

Diminished renal glomerular mesangial phagocytic function has been found in rats with streptozotocin induced diabetes. Similar impairment was produced by high dose cortisone and growth hormone, whereas oestrogen had a stimulant effect. The findings could be relevant to the understanding of human diabetic nephropathy.
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PMID:Mesangial cell dysfunction detected by accumulation of aggregated protein in rats with streptozotocin induced diabetes. 6 Jan 45

In 1953, Poulsen described the remarkable case of a woman with type I diabetes mellitus who experienced resolution of her retinopathy following postpartum pituitary necrosis. Since that time, many investigators have pursued the hypothesis that anterior pituitary hormones, particularly growth hormone, play a role in the pathogenesis of the microvascular complications of diabetes mellitus. While most observers have demonstrated the importance of growth hormone in the initiation and progression of diabetic retinopathy, the role of growth hormone in the development of diabetic nephropathy has been more difficult to document. In this case report, we describe a woman with long-standing type I diabetes mellitus complicated by retinopathy and nephropathy whose complications stabilized as she developed growth hormone deficiency.
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PMID:Hypopituitarism stabilizes the renal and retinal complications of diabetes mellitus. 148 75

Mice transgenic for growth hormone (GH) develop progressive glomerulosclerosis. The compositions of kidney extracellular matrix (ECM) and ECM mRNA were examined. The glomerulosclerotic areas in GH mice contained types I and IV collagen, laminin, and basement membrane heparan sulfate proteoglycan (HSPG), which increased with age. The type IV collagen, laminin B2, and HSPG mRNA levels in GH mice, measured by a solution hybridization RNase protection assay, were increased over normal littermates. These findings suggest that the accumulation of ECM components in the glomeruli of GH mice is regulated at the transcriptional level and that glomerulosclerosis is, in part, due to the excess production of ECM rather than simply a reduction in its turnover. The glomerular lesions in GH mice resemble diabetic nephropathy and may allow further dissection of the molecular basis of certain forms of glomerulosclerosis.
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PMID:Glomerulosclerosis in mice transgenic for growth hormone. Increased mesangial extracellular matrix is correlated with kidney mRNA levels. 202 27

Disturbed function of the axis hypothalamus-growth hormone-somatomeding C (IGF-1) plays an important role in the development of diabetic angiopathy. Patients with insuline dependent diabetes show increased secretion on GH but secretion of IGF-1 may be normal, decreased or increased. These disturbances are especially distinct in the prepubescent period when susceptibility to develop complications is bigger. Increased secretion of GH and IGF-1 plays an essential role in the development of retinopathy and diabetic nephropathy. The paper explains the role of GH in controlling glycaemia and in the development of vascular complications during diabetes.
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PMID:[The role of growth hormone in the development of complications in insulin-dependent diabetes]. 206 73

Glomerular hyperfiltration is a characteristic feature of insulin-dependent diabetes. We examined the relative roles of renal size, as well as glycemic parameters (HbA1c, glycosylated albumin, plasma glucose) in addition to growth hormone, somatomedin C, beta-hydroxybutyrate, alanine, and glycerol in determining the glomerular filtration rate (GFR). Sixty-two insulin-dependent patients with normal urinary albumin excretion rates (AER less than 15 micrograms/min), who were less than 50 years of age, were included in the study. Data were subjected to multiple regression analysis with GFR as a dependent variable. Renal volume was the primary statistical determinant of hyperfiltration, but HbA1c also significantly correlated with GFR. No correlation was found with glycosylated albumin or blood glucose, but RPF correlated strongly with GFR, and borderline correlation was found between renal volume and HbA1c. Renal hyperfiltration, defined as a GFR greater than 150 ml/min, was found in approximately 50% of patients with HbA1c values greater than 9.5%. Other studies suggest that such patients have a much higher risk of developing clinically evident diabetic nephropathy over the ensuing years. Renal volume appears to be the major determinant of GFR, but long-term metabolic control, as evidenced by the level of HbA1c, also contributes, partly independent of renal volume. Short-term metabolic control, as evaluated by blood glucose and serum-fructosamine, did not correlate with GFR. We suggest that exact determination of GFR and renal volume should be included in long-term prospective controlled intervention trials in patients with insulin-dependent diabetes mellitus (IDDM).
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PMID:Renal and glycemic determinants of glomerular hyperfiltration in normoalbuminuric diabetics. 215 Dec 27

Cardiovascular and Renal function were examined in two populations of long-term insulin-dependent diabetics, those with microalbuminuria, a sign of early, subclinical nephropathy and those with clinically manifest diabetic nephropathy. In addition, clinical variables of possible importance for the occurrence and prognosis of diabetic nephropathy were analyzed. Microalbuminuria - a mean of three over-night urinary albumin excretion rates greater than 20 micrograms/min - was found in 16% of Albustix-negative, normotensive, insulin-dependent diabetics. The microalbuminurics had higher supine blood pressures than normoalbuminurics. The albumin excretion rate in microalbuminurics correlated to blood pressure at rest but not to glycosylated haemoglobin. The cardiovascular responses to five different test manoeuvres revealed more evident signs of autonomic nerve dysfunction in microalbuminurics than in normoalbuminurics. The circulatory reactions during mental stress however, were almost identical in the two subgroups. Despite similar glomerular filtration rate and renal plasma flow the albumin excretion during mental stress increased in microalbuminurics, but remained unchanged in normoalbuminurics. It is postulated that a disturbance of glomerular basement membrane permeability is a pre-requisite for the elevated albumin excretion seen in microalbuminurics. Inability to regulate glomerular haemodynamics, due to autonomic nerve dysfunction, may also be a contributing factor. Such dysfunction perhaps even explains why microalbuminurics have higher blood pressures at rest compared with normoalbuminurics. In manifest diabetic nephropathy the rate of renal functional decline correlated to arterial blood pressure, while glycemic control showed no such relation. Patients with rapidly progressive nephropathy showed higher values of growth hormone than slow progressors. In patients with diabetic renal failure, cardiac catheterization revealed reduced stroke work and elevated left ventricular end-distolic pressure during exercise. Autonomic nerve dysfunction and arterial hypertension possibly contributed to the impaired cardiac performance. The existence of a specific diabetic cardiopathy must even be considered. There was a male predominance both in subclinical and manifest diabetic nephropathy. Age at onset of diabetes was lower in micro- as compared to normoalbuminurics. Duration of diabetes had no prognostic implication in subclinical or manifest nephropathy. The mortality rate was high in patients with manifest nephropathy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies of cardiovascular and renal function in subclinical and manifest diabetic nephropathy. 316 65

Susceptibility to diabetic nephropathy may be related to a predisposition to arterial hypertension. We have studied the activity of sodium-lithium countertransport in red cells, a marker of risk for essential hypertension, in white European adults with insulin-dependent diabetes and diabetic nephropathy, a matched group of patients with diabetes without renal disease, and nondiabetic patients with renal disease. Measures of metabolic control and concentrations of plasma free insulin and growth hormone were similar in the two diabetic groups. The degree of impairment in renal function was similar in the diabetic and nondiabetic patients with renal disease. Body-mass index and plasma potassium concentrations were similar in all three groups. Diastolic blood pressure was elevated to a similar degree in the two groups with renal disease, as compared with that in the diabetic patients without renal disease. The rates of sodium-lithium countertransport in red cells were significantly higher in the diabetic patients with renal disease (mean +/- SD, 0.55 +/- 0.19 mmol of lithium per liter of red cells per hour) than in the diabetic patients without renal disease (0.33 +/- 0.16; P less than 0.005) and in the nondiabetic patients with renal disease (0.31 +/- 0.14; P less than 0.001). Predisposition to hypertension, as indicated by elevated sodium-lithium countertransport activity in red cells, may serve as a marker for the risk of renal disease in patients with insulin-dependent diabetes.
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PMID:Increased sodium-lithium countertransport activity in red cells of patients with insulin-dependent diabetes and nephropathy. 333 2

Forty percent of patients with insulin-dependent diabetes will develop nephropathy during the course of their disease, thus being the most important single disorder leading to end-stage renal failure (ESRF). Intensive metabolic control delays onset of diabetic nephropathy, the first omen of which is appearance of subclinical albuminuria, also termed microalbuminuria. Moreover, it is now established that intensive treatment of hypertension reduces rate of decline in GFR and thus postpones ESRF. When uremia eventually sets in, a range of biochemical and endocrine abnormalities can be included among those characteristics of diabetes mellitus per se. These include elevated plasma levels of growth hormone, glucagon and free fatty acids, which may participate in the uremic insulin resistance superimposed on the preexisting diabetic carbohydrate intolerance. Hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) are two established modalities of renal replacement therapy in diabetes mellitus. Controlled clinical trials for comparison of CAPD versus HD treatment of diabetics are, however, still needed. The survival rate is approximately 80 and 65-95% in insulin-dependent diabetic patients at 1 year during treatment with HD and CAPD, respectively. However, it is general experience that diabetics on CAPD exhibit a glycemic control, superior to that attained during HD. It has not been proved that patient survival after cadaveric renal transplantation is better than on dialysis. The degree of vascular heart disease seems to be the major determinant for survival of kidney-transplanted diabetic patients.
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PMID:End-state renal failure in diabetic nephropathy: pathophysiology and treatment. 391 47

Somatostatin (SRIH) has recently been shown to be effective in reversing many of the early changes of diabetic nephropathy. It is unknown whether SRIH exerts its protective effects via its ability to suppress growth hormone (GH) or via other direct renal effects. Since changes in glomerular prostaglandin (PG) E2 production are thought to be an important part of the underlying pathophysiology of diabetic nephropathy, we sought to determine if SRIH altered glomerular PG E2 production in the rat. Whole glomeruli isolated from streptozotocin-diabetic rats and from controls were incubated with either saline, captopril, or varying concentrations of SRIH, and PG E2 production was determined by direct radioimmunoassay of media. Incubation with captopril (10(-4) M) resulted in equivalent increases in PG E2 production in glomeruli from both control and diabetic rats (140.8 +/- 12.8% and 150.2 +/- 18.9% respectively). Incubation with high concentrations of SRIH (10(-6) M) also resulted in significant increases in glomerular PG E2 production in both diabetic and control rats. However, at low SRIH concentrations (10(-10) M), glomerular PG E2 production was increased only in the diabetic rats (167.0 +/- 11.4% vs 95.3 +/- 9.2% in normals). We conclude that SRIH increases glomerular PG E2 production, and that glomeruli from diabetic rats appear to be more sensitive to lower concentrations of SRIH when compared to normal rats. It is possible that this effect on PG E2 production may underlie the favorable effects of SRIH on the glomerulus in diabetes.
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PMID:Effects of somatostatin and captopril on glomerular prostaglandin E2 production in normal and diabetic rats. 810 53

Urinary growth hormone (UGH) excretion was assessed in 44 adult subjects (10 control, 21 insulin dependent diabetics (Group I), 13 diabetics in poor glycaemic control (Group II)). UGH was markedly elevated in the diabetic population. The UGH excretion in (1) control subjects ranged from undetectable levels to 0.7 microU/h, mean 0.4, (2) Group I 73-422 microU/h, mean 250 and (3) Group II 10-5,283 microU/h, mean 705. There was a significant correlation between UGH excretion and albumin excretion rate (AER) (r = 0.38, P < 0.05) in the subjects studied although only 50% of patients had an AER of > 20 micrograms/min. A stronger correlation was observed between beta 2-microglobulin and UGH excretion (r = 0.7, P < 0.01). There was no significant change in the 6-h serum GH levels following treatment in the patients in Group II. However a 23-79% decline in UGH excretion was observed following improvement of glycaemic control, although UGH levels failed to revert to normal. We conclude that the major factor responsible for increased UGH excretion in DM appears to be reduced tubular reabsorption of the hormone. This test may therefore prove useful as an additional marker for screening for diabetic nephropathy and may help in the understanding of the contribution of renal tubular abnormalities to the nephropathic process.
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PMID:Urinary growth hormone measurements as a marker of renal tubular function in diabetes mellitus. 828 58


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