Cases reported "Albuminuria"

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1/14. erythropoietin-dependent anaemia: a possible complication of diabetic neuropathy.

    We report the case of a 52-year-old woman with long-term type 1 diabetes mellitus, complicated with proliferative retinopathy, autonomic neuropathy and microalbuminuria and moderate renal failure. A normochromic, normocytic are generative anaemia had been diagnosed for three years. Clinical and biological investigations for the aetiology of anaemia remained normal or negative. Anaemia was associated with a concentration of erythropoietin (EPO) in the normal range, but inappropriately low regarding anaemia. Treatment with recombinant EPO induced a rapid increase in haemoglobin level and improved the patient's quality of life. The role of diabetic neuropathy in the genesis of anaemia, in conjunction with a modest renal impairment is discussed.
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2/14. Can glomerular mRNAs in human type 1 diabetes be used to predict transition from normoalbuminuria to microalbuminuria?

    BACKGROUND: mRNAs of pathogenetic importance in the development of diabetic nephropathy were measured in subjects with type 1 diabetes to determine whether these might be used to predict progression from normoalbuminuria to microalbuminuria. We proposed that conversion from normoalbuminuria to microalbuminuria would be most likely in subjects whose connective tissue growth factor (CTGF) and collagen mRNAs were above the 95% confidence interval (CI) for live renal donors and within the 95% CI for subjects with abnormal albuminuria. methods: Glomerular CTGF, collagen alpha2(IV), and control glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNAs were measured in microdissected glomeruli from living renal donors (n = 10), and subjects with normoalbuminuria (n = 12), microalbuminuria (n = 5), and overt proteinuria (n = 6). RESULTS: After 44 /- 2 months of follow-up, one subject converted from normoalbuminuria to microalbuminuria. Although the data are limited, progression from normoalbuminuria to microalbuminuria occurred in the only normoalbuminuric subject whose mRNA levels were above the live renal donors' 95% CI for CTGF and collagen alpha2(IV) and within the 95% CI of subjects with abnormal albuminuria. No clinical or histopathologic finding distinguished the progressor from the nonprogressors at the time of biopsy. CONCLUSION: This case report provides proof-of-principle that a panel of glomerular mRNA markers chosen because of their pathogenetic relevance may be useful adjuncts to albuminuria and histology in predicting clinical stability or clinical progression in diabetic nephropathy.
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3/14. Diabetic muscle infarction associated with multiple autoimmune disorders, iga deficiency and a catastrophically poor glycaemic control: a case report.

    We report a case of diabetic muscle infarction in a 22-yr-old woman, with an 11-yr history of poorly controlled Type 1 diabetes complicated by laser-treated pre-proliferative retinopathy, macroalbuminuria and severe autonomic neuropathy, also affected by iga deficiency, autoimmune hypothyroidism, coeliac disease and polygenic familiar hypercolesterolaemia. She was admitted to our Hospital for pain to the left thigh hindering her from walking. The pain had appeared without trauma about 2 months before admission, and worsened progressively in spite of anti-inflammatory drugs. Clinical picture (localised tender mass without skin signs of inflammation in an afebrile patient) and laboratory data (erythrocyte sedimentation rate 113 mm in 1 hr, fibrinogen 635 mg/dl) suggested the diagnosis of diabetic muscle infarction. magnetic resonance imaging (MRI) confirmed this hypothesis showing a hyperintense area in T2-weighted sequences at adductor muscle group with enhancement after intravenous contrast. Symptoms subsided over the following 4 weeks after bed rest, analgesics, aspirin and a good glycaemic control. The 3-month follow-up MRI showed total recovery. At hospital admission, the patient presented a very poor glycaemic control (HbA1c 15.5%). After discharge, she started--in order to avoid the weight gain associated with intensive insulin therapy--a daily intense isometric training, undergoing frequent hypoglycaemic episodes. In a few months, in spite of repeated laser treatment, retinopathy progressed to the proliferative stage with bilateral vitreous haemorrhages and visual acuity decreased dramatically notwithstanding vitrectomy. This case confirms the association of diabetic muscle infarction with poorly controlled long-standing diabetes with microvascular complications, suggests the possible role of autoimmunity, and underlines the risk of repeated hypoglycaemic episodes and isometric exercise in the progression of pre-proliferative retinopathy.
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4/14. diabetes mellitus and the kidney in adolescents.

    Diabetic nephropathy continues to be a major complication of both types I and II diabetes; renal disease in the two types of diabetes exhibits no major differences with regard to initiation, progression, or treatment. The increasing prevalence of type II diabetes among adolescents means that understanding diabetic nephropathy and its prevention and treatment strategies is increasingly important for physicians caring for this population. The most important prevention and treatment modalities for diabetic nephropathy are improved glycemic control and aggressive blood pressure control, beginning as soon as possible after the diagnosis of diabetes.
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5/14. proteinuria developing after clinical islet transplantation resolves with sirolimus withdrawal and increased tacrolimus dosing.

    sirolimus is a potent immunosuppressant, which may permit the avoidance of nephrotoxic calcineurin inhibitors (CNI). However, cases of proteinuria associated with sirolimus have been reported following renal transplantation. Here, we report three cases of proteinuria (1, 2 and 7 g/day) developing during therapy with sirolimus plus low-dose tacrolimus following clinical islet transplantation (CIT) in type I diabetic subjects. The proteinuria resolved after discontinuation of sirolimus, substituted by mycophenolate mofetil (MMF) combined with an increased dose of tacrolimus. A renal biopsy in one case indicated only the presence of diabetic glomerulopathy. Five other CIT recipients developed microalbuminuria while on sirolimus which all resolved after switching to tacrolimus and MMF. The resolution of proteinuria from the native kidneys of CIT recipients after the discontinuation sirolimus suggests that, at least in some individuals, sirolimus itself may have adverse renal effects. sirolimus should be used cautiously with close monitoring for proteinuria or renal dysfunction.
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6/14. Diabetic glomerulosclerosis and chronic renal failure with absent-to-minimal microalbuminuria.

    We report the case of an elderly black woman with a 20-year history of insulin-independent diabetes mellitus (IDDM), chronic renal failure, hypertension, proliferative retinopathy, and classical histologic features of diabetic glomerulosclerosis on renal biopsy. Repeat determinations of urinary albumin excretion rates failed to disclose significant microalbuminuria. This presentation should remind the clinician that a small minority of patients with IDDM of long duration may have severe diabetic glomerulosclerosis and renal insufficiency without detectable microalbuminuria.
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7/14. antihypertensive agents in patients with diabetes: trade-off between renal and cardiovascular protection.

    PURPOSE: Management of hypertension in patients with diabetes should address both renal and cardiovascular protection. The use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin ii receptor blockers (ARBs) for control of hypertension in patients with diabetic nephropathy is widely advocated by various international guidelines. Use of any agent that provides tight control of blood pressure is indicated in patients with diabetes but without nephropathy. methods: In this article, the authors present a clinical case scenario and review current clinical evidence supporting the use of ACE inhibitors and ARBs in patients with diabetic nephropathy. In addition, the use of ACE and ARBs in patients with diabetes but without nephropathy will be discussed. RESULTS: Available trial evidence confirms the survival benefits of patients taking ACE inhibitors with diabetic nephropathy. However, the efficacy of ARB inhibitors on survival is unknown. In patients with diabetes without nephropathy, only ACE inhibitors have been found to reduce the risk of onset of microalbuminuria, while all agents affect survival provided a tight control of blood pressure is monitored. CONCLUSIONS: Dose of ACE inhibitors should be titrated appropriately to obtain proven benefits. In summary, current evidence supports the use of ACE inhibitors in patients with and without nephropathy because of renal and cardiovascular benefits.
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8/14. Effect of improved metabolic control on loss of kidney function in type 1 (insulin-dependent) diabetic patients: an update of the Steno studies.

    We re-examined 69 of the 70 patients entering the two independent Steno Studies of effects of improved metabolic control on progression of late diabetic complications. They were analysed according to an intent to treat after follow-up for 8 years (Steno Study 1) and 5 years (Steno Study 2). The glycaemic control had improved in the insulin infusion group compared with the conventional treatment group (mean HbA1c) by 2.0 /- 0.6% vs 0.7 /- 1.2 in Steno Study 1 and by 1.8 /- 1.2% vs 0.4 /- 1.3 (p less than 0.01) in Steno Study 2. In the insulin infusion groups three patients had died during episodes of ketoacidosis. These were not caused by malfunction of the insulin infusion pumps. In the conventional treatment groups, three patients suffered five cardiovascular events causing two deaths. From the sixth month of Steno Study 1 the annual change of the glomerular filtration rate was -3.7 (-5.4 to -2.0) ml.min-1.1.73 m-2 vs -1.0 (-2.1 to -0.1) (conventional vs insulin infusion group, mean (95% confidence interval, p less than 0.01]. The change in urinary albumin excretion was associated with the glycaemic control (n = 69, r = 0.49, p less than 0.0002). No progression was observed among 32 patients with low range microalbuminuria (30 to 99 mg/24 h).(ABSTRACT TRUNCATED AT 250 WORDS)
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9/14. Microalbuminuria: a major risk factor in non-insulin-dependent diabetes. A 10-year follow-up study of 503 patients.

    The impact of microalbuminuria on mortality as well as other risk factors was investigated in a 10-year follow-up study of 503 predominantly non-insulin-dependent diabetic patients of whom 265 had died. Using Cox's regression analysis the prognostic influence of age, sex, age at diagnosis, known diabetes duration, blood pressure, fasting plasma glucose, relative weight, serum creatinine, retinopathy, and treatment was evaluated as well as morning urine albumin concentration (UAC) in four categories, i.e. UAC less than or equal to 15 micrograms/ml (normal), 15 micrograms/ml less than UAC less than or equal to 40 micrograms/ml, 40 micrograms/ml less than UAC less than or equal to 200 micrograms/ml and UAC greater than 200 micrograms/ml. Age, UAC, known duration, and serum creatinine were the only significant risk factors. After correction for the other three independent risk factors, the hazard ratios in the elevated UAC categories relative to the group with UAC less than or equal to 15 micrograms/ml were 1.53 (p = 0.007), 2.28 (p = 0.000002), and 1.82 (p = 0.02). The statistically significant correlations with UAC were: age (r = 0.09, p less than 0.05), duration (r = 0.14, p less than 0.01), systolic blood pressure (r = 0.12, p less than 0.01), serum creatinine (r = 0.33, p less than 0.001), and fasting plasma glucose (r = 0.12, p less than 0.01). Increased UAC was associated also with retinopathy (p = 0.01). Fifty-eight per cent of the deaths were caused by cardiovascular disease or stroke; only 3% died from uraemia. A reinvestigation including blood pressure, fasting plasma glucose, and UAC was made on 208 survivors.
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10/14. Diabetes-like renal glomerular disease in Fanconi-Bickel syndrome.

    The Fanconi-Bickel syndrome is a rare inherited disorder of metabolism characterized by hepatic glyconeogenesis, galactose intolerance, renal fanconi syndrome with nephromegaly, and glycogen accumulation in proximal renal tubular cells. An 8-year-old patient with this disease and severe rickets due to medically resistant hypophosphatemia was found to have the previously unrecognized complication of renal glomerular hyperfiltration, microalbuminuria, and diffuse glomerular mesangial expansion. Similar to patients with glucose-6-phosphatase deficiency, the glomerular disease in this patient resembles incipient diabetic nephropathy. The fanconi syndrome may be due to the defective transport of glucose at the proximal tubular basolateral membrane, which results in accumulation of glucose and secondarily glycogen within tubular cells. Since the metabolic defect, as evidenced by glycogen accumulation, selectively involves proximal renal tubular cells in the kidney of patients with Fanconi-Bickel syndrome and glucose-6-phosphatase deficiency, the abnormalities in renal glomerular hemodynamics and mesangial construct in these rare diseases are likely due to renal tubular factors, if the mechanism originates in the kidney. A delineation of these phenomena may further our understanding of the pathogenesis of diabetic nephropathy.
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