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Query: UMLS:C0011854 (type 1 diabetes)
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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

Between March 1988 and June 1994, 35 popliteal to distal artery vein bypasses were done in 32 diabetic patients. There were 16 males and 16 females with an average age of 60 years. Eighteen patients (56%) had insulin dependent diabetes mellitus. Medical risk factors included coronary artery disease (CAD) in 15 (47%), hypertension in 15 (47%), chronic renal failure (CRF) in 9 (28%), and cigarette smoking in 10 (31%). Indications for revascularization were: non-healing ulcerations in 18 (51%), gangrene in 15 (43%), and rest pain in 2 (6%). The distal anastomosis was to the posterior tibial artery in 9, anterior tibial artery in 8, dorsalis pedis artery in 10 and peroneal artery in 8 cases. All the bypasses were done with autogenous saphenous veins (in-situ 11, reversed 17, and free non-reversed 7). The limbs were graded into three groups based on the preoperative angiographic evaluation of their pedal arch: patent arch (Grade "0"), partial occlusion of the arch (grade "1.5") and little or no arch visualized (Grade "3"). Eight limbs had Grade "0", 16 had Grade "1.5" and 11 had Grade "3" pedal circulation. Bypass follow up was done by clinical exam and color duplex surveillance (CDS) for a mean duration of 24 months. CDS identified 4 failing bypasses which were surgically revised and have subsequently remained patent. There were 3 bypass occlusions which resulted in a major amputation in 2 patients. Three additional major amputations were performed for persisting infection despite a patent bypass. By life table analysis the cumulative primary & secondary patency and limb salvage rates for this group of diabetic patients were 75% at 2 years, 89% at 3 years and 82% at 3 years respectively (S.E. < 10%). The 3 bypass occlusions, which occurred at 1 week, 5 weeks, and 20 months, were in patients with both CRF and Grade "3" foot circulation (significantly different outcome compared to the rest of the group, by chi 2 test, p < 0.05). Good results can be achieved in the majority of diabetic patients undergoing short popliteal-distal bypasses. However, the combination of chronic renal failure and very limited foot circulation (Grade "3") has a significant adverse outcome.
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PMID:Revascularization of the ischemic diabetic foot using popliteal artery inflow. 880 38

The aim of the study was to answer the questions: 1) does the prolactin secretion in the TRH test (0.4 mg i.v.) differ in haemodialyzed patients with diabetes nephropathy in the end stage renal failure in comparison to haemodialyzed chronic renal failure patients with non-diabetic nephropathy and healthy subjects; 2) does the opiate receptors blockade with naloxone (2 mg i.v.) modify the prolactin secretion during the TRH test in those patients. 39 subjects were studied. The patients were divided into three groups: group I: 12 haemodialyzed patients with IDDM and diabetic nephropathy in the end stage renal failure, group II: 15 haemodialyzed chronic renal patients with non-diabetic nephropathy and the control group: 12 healthy persons. The basic prolactin secretion and area over basic value (AOBV) of the prolactin were estimated. Prolactin concentration was measured by LIA. 1) The basic prolactin secretion was significantly higher in the patients with chronic renal failure. 2) The basic prolactin secretion in IDDM patients with diabetic nephropathy in the end stage renal failure treated with haemodialysis was significantly lower than in haemodialyzed patients with chronic renal failure of non-diabetic etiology. 3) TRH and TRH with naloxone caused significant increase of prolactin secretion in all investigated groups, but the increase is significantly lower in chronic renal failure patients than in healthy subjects. 4) Naloxone decreases significantly the prolactin secretion during TRH test only in haemodialyzed patients with chronic renal failure of non-diabetic etiology.
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PMID:[Effects of opiate receptor blockade with naloxone on prolactin (PRL) secretion in patients with diabetes type I (IDDM) with chronic renal failure treated with hemodialysis (HD)]. 912 1

An elevation in intracellular calcium ([Ca2+]i) in rats with chronic renal failure and elevated blood levels of PTH is associated with down-regulation of the mRNA of many proteins. Similarly, in phosphate depleted animals that have normal renal function and low blood levels of PTH, [Ca2+]i is elevated and the mRNA of PTH-PTHrP receptor is down-regulated. The effect of elevation in [Ca2+]i on molecular machinery of many proteins may represent a generalized phenomenon. Diabetes mellitus may also be associated with a rise in [Ca2+]i and therefore down-regulation of the mRNA of proteins may also occur. The present study examined the effect of streptozotocin-induced diabetes mellitus in rats on the [Ca2+]i of the renal proximal tubular cells and on their mRNAs of the PTH-PTHrP, V1a and AT1 receptors. The basal levels of [Ca2+]i of these cells increased significantly (P < 0.01) after one day of diabetes and remained elevated thereafter. There was a significant (r = 0.67, P < 0.01) direct correlation between the [Ca2+]i of the cells and blood levels of glucose up to 350 mg/dl, and the value of [Ca2+]i plateaued with higher concentrations of glucose. Three days of amlodipine therapy prevented and reversed the elevated levels of [Ca2+]i despite marked hyperglycemia. The mRNA of all three receptors in the kidney were down-regulated and this defect was prevented by amlodipine which normalized the [Ca2+]i of the cells. The results show that: (1) the hyperglycemia of IDDM in rats causes a significant elevation in the basal levels of [Ca2+]i of the renal proximal tubular cells and down-regulation of their mRNA of PTH-PTHrP, V1a and AT1 receptors; (2) normalization of the [Ca2+]i of these cells by treatment of the diabetic rats with amlodipine prevented the elevation of [Ca2+]i and the down-regulation of the mRNA of these receptors; (3) these effects occurred in the presence of normal renal function and normal blood of PTH and phosphorus.
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PMID:Elevation of [Ca2+]i of renal proximal tubular cells and down-regulation of mRNA of PTH-PTHrP, V1a and AT1 receptors in kidney of diabetic rats. 918 88

Diabetic nephropathy is one of the main causes of chronic renal failure in developed countries. The genesis and development of diabetic nephropathy is associated in both types of diabetes with a more rapid progression of other secondary complications and an increased mortality, in particular cardiovascular mortality. The main causes of development of diabetic nephropathy are prolonged hyperglycaemia along with a so far not elucidated inborn disposition. The course of diabetic nephropathy is characterized more clearly in type 1 diabetes. The clinically manifest stage is already irreversible and in the course of years it develops into chronic renal failure. Preventive and curative measures include maintenance of optimal metabolic control, systematic control of blood pressure, in particular by ACE-inhibitors, and a reduction of protein intake. Systematic multidisciplinary collaboration in care for patients with diabetic nephropathy helps to prevent the progression of other secondary complications such as diabetic foot and diabetic retinopathy. At present in the Czech Republic dialysis methods substituting renal function are available to practically all patients with diabetic nephropathy. As regards survival time and quality of life the optimal method of renal function replacement for patients in the terminal stage of diabetic nephropathy is transplantation.
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PMID:[Care of patients with diabetic nephropathy]. 947 80

Thirty-two patients with diabetes mellitus (22 IDDM and 10 NIDDM, 21 males and 11 females, age 44+/-11.8 years) were followed for 5.2+/-3.8 years after the onset of chronic renal failure, with the aim of evaluating the effect of low protein diets on the rate of decline of the residual renal function. During the 1.8+/-1.6 year follow-up period on free or uncontrolled low protein diet the mean rate of decline of creatinine clearance was 0.9+/-0.6 ml/min/month, significantly greater than that observed during 3.7+/-3.1 years on low or very low protein diets. The reduction of protein intake was followed by a significant decrease in daily urinary protein loss. A better glycaemic control was obtained on the low protein diet, and the daily insulin requirement decreased. The anthropometry, as well as the serum concentrations of rapid turnover proteins, did not change, in spite of the low or very low protein dietary supply for a long duration. The values of mean arterial pressure were quite similar during the follow-up period on free or uncontrolled low protein diet and during the study period on the low protein diet. A good compliance with reduced dietary intake (as demonstrated by the measurement of the daily urea excretion) was obtained in a large number of patients. In conclusion, our study confirms the protective effect on the residual renal function of low protein diets in IDDM and NIDDM patients with chronic renal failure due to diabetic nephropathy, in the absence of any sign of protein malnutrition.
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PMID:Dietary treatment of diabetic nephropathy with chronic renal failure. 987 Apr 26

This study evaluated paediatric nursing students' knowledge of diet therapy to establish whether it was sufficient to prepare them for practice. A questionnaire sampled 19 1st-year and nine 4th-year students' diet therapy knowledge in relation to chronic renal failure, cystic fibrosis, juvenile diabetes mellitus and liver disease. The knowledge of 1st and 4th-year students was compared and then evaluated against criteria, devised by the researcher to measure whether this knowledge level was sufficient for practice. The Mann-Whitney Utest showed a significant difference between the 1st and 4th-years' diet therapy knowledge. The mean score for overall diet therapy knowledge of 4th-year students was 46 per cent. The results suggest that knowledge of diet therapy is insufficient to prepare nursing students for practice and that this topic needs further emphasis in paediatric nurse education.
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PMID:Diet therapy--a forgotten art? 1122 22

In patients with chronic renal failure, three kinds of treatments can slow the progression of renal insufficiency: optimal control of blood pressure; use of converting enzyme inhibitors; low-protein diet. The MDRD study strongly suggests that blood pressure should not be higher than 130/85 mmHg in patients with chronic renal failure, and than 125/75 mmHg in patients with chronic renal failure and proteinuria above 1 g/d. Converting enzyme inhibitors have been shown to be beneficial to patients with IDDM and either microalbuminuria or overt diabetic nephropathy and to patients with chronic renal failure and proteinuria above 1 g/d. A diet containing less than 1 g/kg/d of proteins should be prescribed to patients with chronic renal failure, and this protein content should be lowered to 0.75 g/kg/d (or to 0.60 g/kg/j in some cases) when creatinine clearance falls below 25 mL/min.
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PMID:[How to slow the progression of chronic renal insufficiency]. 1135 1

Correlation studies have suggested that IGF-binding protein (IGFBP)-1 is a dynamic regulator of free IGF-I. To further study this, we developed a monoclonal immunofluorometric assay specific for the binary complex of IGF-I and IGFBP-1 in human serum. An IGFBP-1 antibody, which recognizes all phospho-forms of IGFBP-1, was used for coating. An europium-labeled IGF-I antibody served as tracer. Assay incubation was performed at conditions approaching those in vivo (i.e. pH 7.4, 37 C). The assay was highly specific: no signal was obtained unless both IGF-I and IGFBP-1 were present and neither IGFBP-2, -3, -4, nor IGF-II caused any cross-reaction. The linear standard curve covered 3 orders of magnitude, and within and in-between assay coefficients of variation were less than 5 and 15%, respectively. To study the dynamic relationship between free IGF-I and binary complex formation, seven healthy subjects were fasted for 72 h. Samples were collected every 3 h. During fasting, free IGF-I was reduced by two thirds (P < 0.0001). IGFBP-1 and the binary complex increased in parallel (P < 0.0001), and levels correlated positively in all subjects (0.89 < or = r < or = 0.98; P < 0.0001). Free IGF-I correlated inversely with IGFBP-1 (-0.81 < or = r < or = -0.48; 0.0001 < or = P < or = 0.05) and the binary complex (-0.79 < or = r < or = -0.41; 0.0001 < or = P < or = 0.05). To study overnight fasting levels, we compared healthy controls and patients with type 1 diabetes and chronic renal failure (n = 10), because these patients show profound alterations in their IGF-system. In both groups, the binary complex was increased about 2.5-fold (P < 0.0001), whereas IGFBP-1 was increased by 5- to 6-fold (P < 0.0001). Accordingly, free IGF-I was severely reduced (P < 0.0001). In conclusion, the assay enables us to study the role of IGFBP-1 as a dynamic regulator of free IGF-I. Our results clearly show that IGFBP-1 and free IGF-I are tightly associated peptides. Furthermore, it has now become possible to compare levels of IGF-I carried within the binary complex IGFBP-1:IGF-I in different (patho-) physiological conditions.
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PMID:Development and clinical evaluation of a novel immunoassay for the binary complex of IGF-I and IGF-binding protein-1 in human serum. 1178 56

A cumulative incidence of diabetic nephropathy of 30-35% has been documented after duration of diabetes of at lest 25 years in type 1 diabetes mellitus and 15-25% in type 2 diabetes mellitus. Diabetic Nephropathy has become the leading cause of chronic renal failure. Several strategies has been suggested to prevent renal disease in patients with diabetes mellitus. Two main treatment strategies for primary prevention of diabetic nephropathy are improved glycaemic control and lowering the blood pressure particularly with angiotensing-converting-enzyme inhibitors. Other therapeutics include, lipid-lowering therapy, dietary protein restriction, smoking cessation and aspirin therapy.
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PMID:[Diabetic nephropathy: strategies for prevention]. 1198 70


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