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One of the longest-running controversies in medicine concerns the aims of diabetes treatment. The question debated for 80 years has been whether the clinician should just relieve symptoms, or try to achieve the much more difficult objective of near-physiological normality as measured by an absence of glycosuria and/or normal blood sugar levels. At the beginning of World War One, most clinicians and physiologists thought the severity of diabetes was inversely proportional to the number of functioning islets of Langerhans. Hyperglycaemia, it was hypothesized, stressed the surviving islets and led to a downward spiral of increasing glandular fatigue and hyperglycaemia. The aim of undernutrition was to rest the damaged tissue in the hope of promoting a return of functional efficiency and possibly regeneration. Most experts stressed that rest of the islets could only be achieved by abolishing glycosuria and restoring normal blood sugar levels. The first clinical use of insulin in 1922 led to astonishing improvements in the health and strength of patients with diabetes and the concept of pancreatic rest seemed to be confirmed when some regained such carbohydrate tolerance that after weeks or months they could reduce the dose of insulin without developing glycosuria. Initially there were expectations that insulin would allow the islets of Langerhans to recover completely, so that diabetes was cured. Most physicians insisted that the best chance of preserving what pancreatic function remained was biochemical normality. It was also contended that patients who had normal blood sugar levels were more healthy than those without and had fewer 'complications'. The complications in question were mainly infective, since specific diabetic tissue damage was not recognized until the late 1930s. The toll of microvascular complications (retinopathy and nephropathy) in those whose lives had been saved by insulin did not become apparent until the late 1930s and early 1940s, when it generated an often acrimonious debate about whether they were due to the metabolic disorder or an associated phenomenon. Liberalization of diet in patients taking insulin began in 1926 and by 1930 it was clear that patients who were prescribed 200 g of carbohydrate per day felt better and more energetic than those on the old regimens of 50 g or less per day. Even these more liberal diets were measured but, in the early 1930s some paediatricians, feeling that a strict measured diet was psychologically damaging, experimented with 'free' or unmeasured diets.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The quest for normoglycaemia: a historical perspective. 795 85

The quality of life after a successful combined kidney-pancreas transplantation was studied in 17 diabetic patients with end-stage renal disease (ESRD) and in 11 patients who experienced a failure of one or both grafts. The control group comprised 23 patients who received a kidney transplantation only. The aspects of quality of life chosen for study were: physical, psychological and social wellbeing, daily activities, level of functioning and global quality of life evaluation. Additionally, future expectations, the perceived burden of treatment, and main reason for undergoing organ replacement therapy were evaluated. In only one aspect of quality of life did patients with a successful combined transplantation score significantly better than patients with a kidney transplantation, i.e., mobility in daily functioning and activities (p = 0.03). Patients with a failure of one or both grafts reported significantly more fatigue (p = 0.02), less energy (p = 0.04), and more social isolation (p = 0.05) than patients who had well-functioning grafts. The mean duration of hospitalization following combined transplantation is twice that for kidney transplantation only 10 vs 5 weeks. Although the combined transplantation group found the first 3 months after transplantation more burdensome (p = 0.04) and more often wondered whether it had been worth all the trouble (p = 0.05), they indicated the same willingness as the group with a kidney transplant only to undergo another transplantation under similar circumstances. Although the recipients of a kidney transplant had not been offered the choice of a combined transplantation, their reasons for transplantation did not, in essence, differ from those of recipients of a combined transplantation. In both groups the main motivation to opt for organ replacement therapy was the burden of dialysis, to stop the progressive deterioration of their health, and to experience a better quality of life.
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PMID:Quality of life after combined kidney-pancreas or kidney transplantation in diabetic patients with end-stage renal disease. 806 62

Patients with anemia caused by end-stage renal disease experience significant fatigue and decreased tolerance for activity. Epoetin alfa corrects anemia in virtually all of these patients, thereby providing several cardiovascular benefits, but some patients may develop increased blood pressure. Nephrology nurses should maximize the benefits of correcting anemia, while ensuring that blood pressure is optimally controlled, thus preserving cardiovascular function.
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PMID:Case study of the anemic patient: epoetin alfa--focus on blood pressure. 808 Mar 16

We characterized urinary excretion of C3 fragments among patients with systemic lupus erythematosus (SLE) as a possible indicator of renal involvement. 28 patients, representing a broad range of disease activity were admitted to our study. Urinary proteins were separated on 4-20% gradient SDS-PAGE gels, under reducing conditions, and transblotted to nitrocellulose. Western blots were developed with a polyvalent goat-anti-human C3d antiserum, and an alkaline phosphatase-conjugated rabbit anti-goat IgG. Three patterns were obtained: 1) no bands detected; 2) bands suggesting the presence of intact C3; and 3) samples with additional low molecular (< 4 x 10(4)) bands. The 12 patients with no C3 bands had minimal disease activity (e.g. fatigue, arthralgia, arthritis, rash, oral ulcers). The seven patients with intact C3 patterns also had minimally active disease. Their primary clinical findings included fatigue, pleurisy, renal disease which had been treated, hemolytic anemia, and arthritis. Patients with low molecular weight C3 fragments in their urine formed two sub-sets, based upon their presenting features. The first group had severe disease and contained all patients with active lupus nephritis (n = 4), while the second consisted of non-renal patients with primary clinical findings of moderate disease activity (e.g. thrombocytopenia, pneumonitis, arthritis). Our results suggest urinary excretion of low molecular weight C3 fragments correlates with active renal disease, but is a variable finding among SLE patients with non-renal manifestations of disease activity.
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PMID:Complement C3 fragments in urine: detection in systemic lupus erythematosus patients by western blotting. 819 18

Amantadine has found use primarily as an antiviral agent and in the symptomatic treatment of parkinsonism. However, the use of amantadine for the subjective alleviation of fatigue in multiple sclerosis and in the treatment of agitated aggressive behavior in the traumatic brain injured patient has also been described. Side effects of amantadine are primarily related to the central nervous system and include hallucinations, confusion, and nightmares. Toxic manifestations include acute psychosis, coma, cardiovascular toxicity, and death. Amantadine toxicity is a particular problem in patients with renal insufficiency because 90% of an oral dose is excreted unchanged in the urine. We present a case of amantadine-induced coma in a patient with multiple sclerosis and end-stage renal disease. Moreover, this degree of amantadine toxicity was profoundly apparent at a drug level usually not associated with such a severe presentation.
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PMID:Amantadine-induced coma. 821 67

Recent studies of obstructive sleep apnea and its comorbidity with other systemic diseases have stimulated interest in the relationship of apnea to renal disease and hypertension. Polysomnographic sleep studies in patients on dialysis who complain of day-time fatigue or sleepiness reveal significant apnea in up to 73% of those studied. Abnormalities in respiratory controller mechanisms from chronic hypocarbia, metabolic acidosis, and uremic toxins have been blamed for the occurrence of apnea in this setting. Proteinuria and sometimes nephrotic syndrome have been recognized in morbidly obese patients with sleep apnea syndrome. Renal biopsies of such patients have shown glomerulomegaly and focal segmental sclerosis. It is postulated that these lesions may result from increased glomerular filtration and blood flow. Elevated urine output, sodium and chloride excretion, and atrial natriuretic peptide have been well demonstrated in obstructive apnea patients and correct to control levels with treatment of the apnea. Both acute (with each apnea) and chronic daytime blood pressure elevation are frequently observed in sleep apnea patients, and occult sleep apnea is postulated as one possible cause of "primary" hypertension in middle-aged men. In younger patients, such hypertension seems to be more reversible with the elimination of apnea. In older patients, however, the cure of systemic hypertension cannot be guaranteed with the elimination of the apnea, and asymptomatic apnea patients tend not to tolerate the bother and discomfort of apnea treatment with nasal continuous positive airway pressure. Therefore, aside from a careful history regarding sleep symptomatology, polysomnographic studies of clinic populations with primary hypertension to search for apnea as a cause cannot be recommended.
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PMID:Obstructive sleep apnea and the kidney. 830 38

Severe renal disease in the setting of Epstein-Barr virus (EBV) infection is exceedingly rare. We report here the case of a 22-year-old man with acute EBV infection associated with severe interstitial nephritis. The patient developed chronic fatigue and chronic renal failure with a serological profile typical of primary EBV infection. Clinical improvement with anti-EBNA seroconversion occurred after acyclovir therapy. Our patient illustrates that chronic fatigue with major organ dysfunction and a serological profile of primary infection can be seen in chronic EBV infection. In such a case, acyclovir may prove beneficial.
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PMID:Epstein-Barr virus infection associated with interstitial nephritis and chronic fatigue. 879 88

Primary hemochromatosis is characterized by a specific pattern of clinical manifestations. It includes liver disease with hepatomegaly, glucose intolerance, e.g. diabetes, hyperpigmentation oft the skin, impotence/ amenorrhea, arthropathy, cardiomyopathy and fatigue. Laboratory investigation reveals significantly elevated serum ferritin and transferrin saturation with iron. The diagnosis is confirmed by liver biopsy and quantitative determination of elevated liver iron content. Wilson's disease represents a copper storage disease. Prominent clinical features are hepatomegaly and splenomegaly. Neurological alterations and detection of Kayser-Fleischer corneal rings are typical. In the acute initial phase the often young patients present with Coombs-negative hemolysis. Psychiatric alterations, cardiomyopathy, arthropathy, nephropathy, as well as thrombocytopenia and leucopenia are other clinical features. Laboratory parameters of Wilson's disease include low serum ceruloplasmin and serum copper. There is an elevated urinary copper excretion and elevated serum free copper concentration. The diagnosis is confirmed by liver biopsy with quantitative determination of an elevated liver copper content.
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PMID:[Current diagnosis: hereditary metabolic diseases of the liver (primary hemochromatosis, Wilson disease)]. 898 78

To clarify the demographic and clinicolaboratory features of postdialysis fatigue (PDF), we enrolled 85 patients on maintenance hemodialysis in a cross-sectional study using validated questionnaires and chart review. Forty-three patients complained of fatigue after dialysis. On formal testing using the Kidney Disease Questionnaire, the PDF group had statistically greater severity of fatigue and somatic complaints than the group of patients without subjective fatigue (P = 0.03 and 0.04, respectively). On a scale measuring intensity of fatigue (1 = least to 5 = worst), the PDF group average was 3.4 +/- 1.2. PDF subjects reported that 80% +/- 25% of dialysis treatments were followed by fatigue symptoms. In 28 (65%) of patients, the symptoms started with the first dialysis treatment. They reported needing an average of 4.8 hours of rest or sleep to overcome the fatigue symptoms (range, 0 to 24 hours). There were no significant differences between patients with and without PDF in the following parameters: age; sex; type of renal disease; presence of diabetes mellitus, heart disease (congestive, ischemic), or chronic obstructive lung disease; blood pressure response to dialysis; type or adequacy of dialysis regimen; hematocrit; electrolytes; blood urea nitrogen; creatinine; cholesterol; albumin; parathyroid hormone; ejection fraction; and use of antihistamines, benzodiazepines, and narcotics. In the fatigue group, there was significantly greater use of antihypertensive medications known to have fatigue as a side effect (P = 0.007). Depression was more common in the fatigue group by Beck Depression score (11.6 +/- 8.0 v 7.8 +/- 6.3; P = 0.02). We conclude that (1) postdialysis fatigue is a common, often incapacitating symptom in patients on chronic extracorporeal dialysis; (2) no routinely measured parameter of clinical or dialytic function appears to predict postdialysis fatigue; and (3) depression is highly associated with postdialysis fatigue, but the cause-effect relationship is unclear.
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PMID:Postdialysis fatigue. 915 12

Symptomatic hypotension during hemodialysis is a disabling complication in end-stage renal disease (ESRD) patients, especially in certain groups of patients who are at higher risk for this problem. Autonomic dysfunction is thought to play a significant role. We evaluated the efficacy of midodrine, an oral agent with selective alpha-adrenergic agonist activity used in the treatment of neurogenic orthostatic hypotension, on 10 hemodialysis patients with persistent intradialytic hypotension. The patients were given a dose of midodrine (mean dose, 5.5 mg; range, 5 to 10 mg) 30 minutes before each hemodialysis session. We compared blood pressure, pulse, body weight, and laboratory values for 10 consecutive dialysis sessions off and on midodrine therapy. There was a statistically significant improvement in lowest intradialytic systolic blood pressure (from 96.6 to 114.7 mm Hg; P < 0.001), lowest intradialytic diastolic blood pressure (from 53.2 to 59.0 mm Hg; P = 0.002), lowest intradialytic mean arterial pressure (from 67.7 to 77.6 mm Hg; P < 0.001), posthemodialysis systolic blood pressure (from 116.5 to 127.1 mm Hg; P < 0.001), posthemodialysis diastolic blood pressure (from 66.6 to 69.7 mm Hg; P = 0.040), and posthemodialysis mean arterial pressure (from 83.2 to 88.8 mm Hg; P = 0.001) after patients were placed on midodrine. There also was a small but statistically significant decrease in intradialytic pulse rate (from 86.3 to 81 beats/min; P = 0.021) and posthemodialysis pulse rate (from 87.4 to 81.7 beats/min; P = 0.024) after initiation of midodrine therapy. There was no significant difference in any of the prehemodialysis blood pressure measurements or pulse rate off or on midodrine therapy. The improvements in intradialytic and posthemodialysis blood pressure were associated with a uniform subjective improvement in symptoms associated with dialysis hypotension, such as cramps, fatigue, dizziness, and weakness. Other than scalp paresthesia in one patient, no adverse effects were noted. Our results suggest that the administration of a single dose of midodrine before hemodialysis is an effective therapy for intradialytic hypotension. A prospective trial with adequate patient numbers and long-term follow-up would be useful to evaluate this drug's efficacy and safety profile in patients with ESRD.
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PMID:Intradialytic hypotension: is midodrine beneficial in symptomatic hemodialysis patients? 939 20


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