Cases reported "Uremia"

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1/25. Prerenal azotemia in a diabetic patient with hyporeninemic hypoaldosteronism and autonomic neuropathy.

    patients with hyporeninemic hypoaldosteronism show mild to moderate renal insufficiency, with a creatinine clearance of 20-75 ml/min, and asymptomatic hyperkalemia. A low degree of sodium wasting and mild hyperchloremic metabolic acidosis are also usually present. However, severe sodium wasting and volume depletion are not typically seen unless the patient is placed on severe sodium restriction or has some other cause of extrarenal sodium loss. In fact, acute renal failure has not been reported in such patients. We describe a diabetic patient with hyporeninemic hypoaldosteronism and autonomic neuropathy who developed recurrent episodes of acute renal failure due to prerenal azotemia during acute exacerbations of diarrhoea. In our case, despite significant hypovolemia, the renin-aldosterone axis was markedly suppressed, implying that sympathetic tone played a decisive role in renin regulation.
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ranking = 1
keywords = diabetic
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2/25. Chronic thrombotic microangiopathy associated with antineoplastic therapy with minimal hematologic effects.

    OBJECTIVE: To describe 6 patients who developed progressive renal failure and renal thrombotic microangiopathy (TM) not accompanied by the characteristic hematologic disturbances of TM syndromes. patients AND methods: Portions of renal biopsy specimens from each patient were examined by light and electron microscopy for histopathologic evidence of TM. Antecedent clinical events, laboratory evidence of hemolysis and thrombocytopenia, and clinical outcome were documented. medical records were reviewed and clinical data, including laboratory values, treatment, and outcome, were recorded. RESULTS: In each case, a slowly progressive uremia evolved after radiation and/or chemotherapy without laboratory evidence of acute hemolysis or thrombocytopenia. Renal biopsy specimens in all cases showed TM and tubulointerstitial scarring, suggesting both acute and chronic renal injury. Two of the 6 patients underwent plasma exchange therapy without improvement of renal function. Three patients treated with angiotensin-converting enzyme inhibitors for coexisting systemic hypertension remained stable or had mild improvement in renal function. CONCLUSIONS: A small subset of patients treated for malignancy developed slowly evolving uremia associated with renal TM without marked hematologic abnormalities. In the absence of thrombocytopenia and other typical laboratory findings, the diagnosis of renal TM may be overlooked.
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ranking = 0.18328611956422
keywords = microangiopathy
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3/25. The syndrome of acute bilateral basal ganglia lesions in diabetic uremic patients.

    Acute extrapyramidal movement disorders have rarely been reported in uremic patients. We had previously presented three cases of acute movement disorders with bilateral basal ganglia lesions in uremia, and had proposed that it is not a rare condition. The objective of this study is to establish a more accurate clinical profile of this rarely described clinical syndrome, and to call attention to its common occurrence. We prospectively studied six patients we encountered from March 1996 to June 2001. We also reviewed the clinical records of a large population of uremic patients and identified six more cases. The clinical manifestations, laboratory findings, neuroimages, and clinical outcomes of these 12 patients were analyzed. When possible, each patient was followed up to the present time. Twelve patients had acute onset of movement disorders and bilateral basal ganglia lesions. All of the patients were diabetic. They had acute-onset Parkinsonism or dyskinesias, together with various symptoms such as consciousness disturbance, dysarthria, dysphagia, or ataxia. The main laboratory test results of abnormalities consisted of elevated blood urea nitrogen, creatinine, and metabolic acidosis. They had uniform neuroimaging findings of symmetrical bilateral basal ganglion changes. These changes regressed or disappeared during follow-up. The clinical prognoses were diverse. We believe that this group of patients represents a well-demarcated clinical syndrome, which is not uncommon but has previously been rarely addressed. The underlying mechanism of such lesions may be associated with metabolic, as well as vascular factors.
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ranking = 1
keywords = diabetic
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4/25. Treating azotemia-induced anemia with erythropoietin improves diabetic eye disease.

    BACKGROUND: Coincidental with the pandemic growth of diabetes as the prime cause of end-stage renal disease (ESRD), blindness attributable to diabetic retinopathy has become a major concern for all those involved in the care of diabetic ESRD patients. Vision loss is linked to progression of proliferative retinopathy and macular edema. methods: Extracted from a study of azotemic anemic pre-ESRD patients treated with erythropoietin, a cohort of five diabetic subjects was reassessed in terms of stability of renal function, changes in blood rheology, and course of diabetic eye disease. RESULTS: All subjects reported subjective improvement in well-being, including enhanced effort tolerance following an increase in hematocrit from a baseline level of to 29.6 /- 2.0% to a level of 39.5 /- 2.4% after one year of treatment with erythropoietin (P = <0.0005). Neither hypertension nor deterioration of renal function was noted in any subject. Three patients with macular edema evinced substantive improvement-based stable vision and documented resolution noted in flourescein angiography. CONCLUSION: erythropoietin treatment of anemic azotemic diabetic patients is well tolerated. In a small observational retrospective study of three patients with macular edema, retention of vision and resolution of exudates was noted.
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ranking = 1.8
keywords = diabetic
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5/25. Acute bilateral basal ganglia lesions in patients with diabetic uremia: an FDG-PET study.

    PURPOSE: head CT and MRI show characteristic changes in the syndrome of acute bilateral basal ganglia lesions in patients with diabetic uremia. However, they do not provide further insight into the underlying pathophysiology. To further clarify the biologic mechanism of the syndrome, F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) was used in 2 patients. methods: PET studies were performed in 2 diabetic uremic patients with acute movement disorders. The cerebral glucose metabolic rates in these 2 patients were compared with 11 normal age-matched controls. The images were further analyzed with statistical parametric mapping to identify regions of significant metabolic abnormality. RESULTS: The cases showed markedly reduced glucose metabolism in the bilateral basal ganglia, especially in the bilateral putamens, where the glucose uptake was nearly absent. CONCLUSIONS: FDG-PET correlates better with the clinical conditions and provides more pathophysiological information than head CT or MRI scans in bilateral basal ganglia lesions in patients with diabetic uremia. We propose that acute exacerbation of a long-term glucose utilization failure in the basal ganglia cells produced these lesions.
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ranking = 1.4
keywords = diabetic
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6/25. Allograft diabetic nephropathy may progress to end-stage renal disease.

    Mesangial expansion and glomerular basement membrane thickening characteristic of diabetic nephropathy recur in diabetic recipients of renal allografts from non-diabetic donors but progression to renal failure is minimally documented. Three female renal allograft recipients (aged 40, 62 and 73 yr), who developed end-stage renal disease (ESRD) due to recurrent diabetic nephropathy (two patients) and de novo diabetes (one patient) are reported. Onset of proteinuria, uncontrolled hypertension, azotemia, renal allograft pathologic findings and the need for hemodialysis were analyzed. None of the kidney donors (one cadaver, two living related) had known diabetes or perturbed glucose metabolism pre-transplantation. The three patients presented had different varieties of diabetes; type 1, type 2 and new onset diabetes after transplantation (NODAT). In each subject, proteinuria was detected by dipstick at a mean of 8.3 yr (range 8-9) post-transplantation and increased to the nephrotic range (3.7-4.8 g/day) inducing hypoalbuminemia and azotemia. A histopathologic diagnosis of allograft diabetic nephropathy was made in a mean of 11.7 yr (range 10-14), based on glomerular basement membrane thickening, nodular and diffuse intercapillary glomerulosclerosis, arteriolosclerosis, and tubular atrophy with marked tubular basement membrane thickening characteristic of advanced diabetic nephropathy. All three patients manifested uremia and resumed hemodialysis. Two patients died from sepsis within 2 months and one patient died 2.5 yr later after resumption of maintenance hemodialysis. We infer that recurrent or de novo diabetic nephropathy in renal allografts follows a clinical decade-long course irrespective of diabetes. Reports of ESRD due to allograft diabetic nephropathy (ADN) have been limited because of shorter survival of diabetic transplant recipients and few kidney biopsies performed in patients with chronic allograft dysfunction. The occurrence of allograft diabetic nephropathy in some, but not all patients, however, suggests that individual genetic variability modulates disease expression.
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ranking = 2.8
keywords = diabetic
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7/25. Gabapentin in the treatment of uremic itch: an index case and a pilot evaluation.

    BACKGROUND: The prevalence of renal itch in patients on dialysis is approximately 30%, but its treatment is often ineffective. We describe an index case of a hemodialysis (HD) patient suffering from painful diabetic neuropathy (PDN) treated with gabapentin; the first administration of the drug led to the complete remission of the concomitant uremic pruritus. Subsequently, we report the results of a pilot evaluation aimed at testing the effectiveness and safety of low gabapentin doses in HD patients with uremic pruritus. methods: Five consecutive HD patients unresponsive to antihistamines received 4-week gabapentin treatment at a starting dose of 100 mg after every thrice-weekly HD, which was subsequently adjusted based on clinical response. Puritus severity was evaluated by means of a visual analogue scale (VAS) before each HD session on days 0, 2, 4, 7, 14, 21, 28 and 35. safety was assessed using adverse event data. RESULTS: All patients experienced a rapid subjective improvement in pruritus, with the mean VAS score decreasing from 8.4-1.6 after the first drug administration. Three patients required a dose increase to 100 mg four times a week to obtain better itch control. Two patients experienced complete itch remission. CONCLUSION: Although a double-blind placebo-controlled clinical trial should be conducted to better elucidate the efficacy and toxicity of gabapentin in patients with uremic itch, our data suggest that gabapentin could be considered an effective and safe alternative treatment for uremic pruritus.
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ranking = 0.2
keywords = diabetic
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8/25. Acute reversible parkinsonism in a diabetic-uremic patient.

    Acute movement disorders with basal ganglia lesions have been recently described in diabetic-uremic patients of Asian descent. The process is often reversible, with a favourable clinical outcome. Metabolic (i.e. uremic toxins) and microangiopathic changes have been suggested to be involved in its pathophysiology, even though racial and/or genetic factors might play a role too. In this report, we present a Caucasian diabetic patient with a long-lasting mild uremia in which acute parkinsonism occurred after a steep and unexpected increase of the serum creatinine. The follow-up demonstrated a significant improvement of the neurological signs and symptoms, the creatinine level lowered close to the premorbid levels, and after several months the patient had fully recovered. Our case history suggests that this unusual clinical syndrome is most probably not restricted to Asian patients. Because its potentially favourable outcome, it should be regularly included in the differential diagnosis of acute movement disorders.
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ranking = 1.2
keywords = diabetic
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9/25. Severe proximal myopathy in advanced renal failure. diagnosis and management.

    Myopathies encountered in uremic patients may have different pathogenetic mechanisms and treatment. Secondary hyperparathyroidism may cause uremic myopathy responding to specific treatment. This study aimed at presenting a case illustrative of the clinical features, diagnosis and management of uremic parathyroid myopathy. A 66-year old man with renal failure from membranous nephropathy developed sensory signs of uremic neuropathy and progressive painless weakness of the pelvic girdle muscles bilaterally. Motor nerve conduction velocity was normal, electromyogram was consistent with a myopathic pattern, while muscle biopsy showed a pattern of atrophy more consistent with a neuropathic pattern. Serological tests for collagen vascular diseases and hyperthyroidism were negative, while serum muscle enzymes were not elevated and serum phosphate levels were not low. serum parathyroid hormone level was grossly elevated, while serum calcium was mildly elevated in a small fraction of the measurements, serum alkaline phosphatase showed a progressive rise and skeletal bone survey did not disclose osteopenia or signs of parathyroid bone disease. A course of calcitriol failed to improve the myopathy, which responded promptly and dramatically to parathyroidectomy. Uremic parathyroid myopathy, which has a characteristic clinical picture, must be differentiated from other neuropathic or myopathic conditions that require specific treatments. Progressive parathyroid myopathy is, by itself, an indication for parathyroidectomy, which is curative in this case.
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ranking = 0.010732980007042
keywords = vascular disease
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10/25. Clopidogrel-associated acute migratory arthritis following kidney-pancreas transplantation.

    Clopidogrel is a potent inhibitor of platelet aggregation and has been used as an alternative, or as an adjunct to aspirin in reducing the risk of thrombosis. A 34-year-old uremic type 1 male diabetic patient who underwent simultaneous kidney-pancreas transplantation was given clopidogrel as he was allergic to aspirin. He developed polyarthralgia one week later, followed in a few days by symmetrical migratory polyarthritis, which resolved completely on withdrawing the drug. The implications to clinical management in a transplant setting are discussed.
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ranking = 0.2
keywords = diabetic
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