Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With a double-antibody radioimmunoassay performed on unconcentrated cerebrospinal fluid, eight of 14 patients in an acute phase of multiple sclerosis had levels of 3.4 to 15.4 ng per milliliter of the P1 fragment (residues 43-88) of myelin encephalitogenic protein. Encephalitogenic protein-P1 was found only in the acute phase and was present in six of seven persons in the first week of an exacerbation and absent in 29 multiple sclerosis patients who were stable or had a gradually progressive course. Six of 117 controls had detectable cerebrospinal fluid encephalitogenic protein-P1. Only in two of these, one with a recent cerebral infarction and one with diabetic nephropathy who was in coma, were the levels in the range encountered in patients in the acute phase of multiple sclerosis. Although not entirely specific for multiple sclerosis, the presence of material in the cerebrospinal fluid of multiple sclerosis patients cross-reacting with encephalitogenic protein-P1 appears to be a characteristic of acute exacerbations.
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PMID:Myelin encephalitogenic protein fragments in cerebrospinal fluid of persons with multiple sclerosis. 7 67

A personal series of 6780 patients with diabetes mellitus is reported. Of these 1410 were thought to have insulin-dependent (Type 1) diabetes and 4926 non-insulin-dependent (Type 2) diabetes. Among the former, 128 patients were only diagnosed when in severe ketoacidosis or coma. In 116 patients the diabetes was diagnosed in pregnancy. Chronic alcoholism was an aetiological factor in 75 patients; in 52 it led to the diagnosis being made, and it complicated treatment in 129 additional patients. In the patients with Type 2 diabetes whose treatment was stabilized 23.5% were having insulin injections, 44.5% tablets, and 32.0% diet only. Sight-threatening retinopathy developed in 21.3% of patients with Type 1 and 7.9% of those with Type 2 diabetes. The rate of developing sight-threatening retinopathy was 1.1% of patients per year. Blindness occurred in 0.28% of patients with Type 1 diabetes per year and 0.097% per year in Type 2 diabetes. If the mean survival of patients with retinopathy going blind is 7.5 years, this would mean 7500 people in the UK blind from diabetic retinopathy. There was a striking drop in the annual incidence of blindness after 1970 coinciding with the introduction of specific treatment for diabetic retinopathy. Juvenile cataract developed in 1.7% of patients who developed Type 1 diabetes before 30 years of age. Clinically important diabetic neuropathy developed in 17.4% of patients with Type 1 and 11.6% of those with Type 2 diabetes. The main features were paraesthesiae and numbness (49%), neuropathic ulceration (37%), pain (5%), autonomic symptoms (5%), and amyotrophy (4%). Oculomotor palsies and mononeuropathies were noted. Foot ulceration occurred in 81 patients with Type 1 and 279 of those with Type 2 diabetes. Charcot changes in the feet were noted in 21 patients. Major amputations were needed in 18 patients with Type 1 and 60 with Type 2 diabetes. Proteinuria believed to be due to diabetic nephropathy developed in 12.8% of patients with Type 1 and 4.7% of those with Type 2 diabetes. The prevalence of early renal failure was 4.6% and 1.4%, respectively. Coronary artery disease was noted in 9% of patients with Type 1 diabetes, and was more common in those who developed diabetes after 20 years of age. Myocardial infarction was as common in women as in men. In Type 2 diabetes coronary artery disease gave rise to symptoms in 19.1%, and myocardial infarction was more common in men.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diabetes in the United Kingdom: a personal series. 182 47

Disorders of fluid and electrolyte metabolism in elderly diabetics were studied. High frequency of hyperkalemia (20.8%), hypomagnesemia (14.6%), hypocalcemia (13.7%), hyperphosphatemia (8.6%), hyponatremia (8.1%) and hyperchloremia (7.2%) was observed among 332 elderly diabetics. Furthermore, hyperkalemia, hyperphosphatemia, hyponatremia, hyperchloremia, hypercalcemia and hypermagnesemia were more frequent in diabetics with renal insufficiency (serum Cr greater than or equal to 1.5 mg/dl) than in diabetics with normal renal function (serum Cr less than or equal to 1.4 mg/dl). In addition, statistically significant negative correlation were observed between plasma glucose levels and serum levels of sodium and chloride in diabetics with normal renal function. These results clearly demonstrated that the most important causal factor of electrolyte disorders in elderly diabetics might be the renal dysfunction due to diabetic nephropathy and/or nephrosclerosis. Moreover, glucose intolerance is also one of the causal factors for hyponatremia and hypochloremia. Disorders of fluid and electrolyte metabolism were manifest in 31 diabetic patients with hyperosmolar non-ketotic coma. The frequency of patients with abnormally elevated serum levels of sodium, potassium and chloride, and patients with abnormally lowered serum levels of calcium was high in this morbid state. Water and sodium deficit, examined in 11 cases of hyperosmolar non-ketotic coma, was 4780 +/- 2100 ml (107 +/- 43 ml/kg body weight) and 290 +/- 170 mEq (6.8 +/- 4.2 mEq/kg body weight), respectively. However, no significant deficit of potassium was observed in the patients. Statistically significant positive correlations between water deficit and serum Cr levels and with serum effective osmolarity were observed. However, there were no significant correlations between water deficit and plasma glucose levels, serum sodium levels and serum osmolarity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Disorders of fluid and electrolyte metabolism in elderly diabetics]. 279 74

Urinary insulin excretion has been measured in diabetic children. In nine well controlled diabetics urinary insulin excretion (mean and 2SD) was significantly greater than that found in healthy controls (8.8; 4.4-17.5 versus 3.8; 2.3-6.4 microU/min/1.73 m2). In ten ketoacidotic diabetic children a 50 fold increase of the urinary insulin excretion has been observed (464.8; 158.2-1363 microU/min/1.73 m2). The hyperinsulinuria proved to be reversible: significantly decreased excretion rate (12.9; 9.7-12.3) could be measured 8-10 days after recovery from coma. The hyperinsulinuria during ketoacidosis indicates severe reversible tubular dysfunction. Recurrent ketoacidotic episodes might play a role in the development of diabetic nephropathy.
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PMID:Hyperinsulinuria in diabetic ketoacidosis. 308 82

In 1936, Kimmelstiel and Wilson described the nodular glomerulosclerosis in patients with diabetes mellitus on insulin treatment. The nodular glomerulosclerosis is referred to as diabetic nephropathy. Fifteen years earlier insulin was discovered. This discovery at the University of Toronto (Canada) in 1921-22 by Banting, Macleod, Best and Collip was one of the most dramatic events in the history of the treatment of the disease. The impact of insulin was so sensational because of the incredible effect it had on diabetic patients. Those who first watched starved, sometimes comatose, diabetics receive insulin and return to life witnessed one of the genuine miracles of modern medicine. The discovery has became the "elixir of life" for millions of human beings around the world. Insulin had not emerged out of a vacuum but was the culmination of years of work by dozens of scientists in many countries. The Canadian scientists were the first to succeed in isolating insulin. Their work, however, was accurately constructed to confirm the ideas of earlier researchers, such as Murray, Paulesco, Allen, Minkowski, Derwitt, Zuelzer. These men, in addition to Banting, Macleod, Best and Collip, knew they were making medical history but paradoxically, with their "elixir of life" they allowed some complications of diabetes to emerge. Diabetic nephropathy was one of them. The struggle of the "Toronto quartet" for credit was inspired by man's desire to have a place in history, to have a sort of immortality open to him, an aspiration that is certainly legitimate. But perhaps the Canadian group misjudged both their situation and posterity's point of view. They probably failed to consider the unintentional effect of insulin treatment: diabetic nephropathy as a consequence of adding years to a diabetic's life.
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PMID:[Historical Archives of Italian Nephrology. Diabetic nephropathy and insulin discovery: two parallel histories]. 1473 16

Nonketotic hyperosmolar coma (NHC) is characterized by severe hyperglycemia; absence of, or only slight ketosis; nonketotic acidosis; severe dehydration; depressed sensorium or frank coma; and various neurologic signs. This condition is uncommon in type 1 diabetes. Because of little or no osmotic diuresis in patients with diabetic nephropathy, increases in plasma osmolality and therefore the likelihood of neurologic symptoms are limited. A 20-year-old male patient with type 1 diabetes with chronic kidney disease on conservative treatment (glomerular filtration rate [GFR], 18 mL/dk) presented with acute nonketotic hyperosmolar syndrome. The patient was admitted presenting with thirst, fatigue, and drowsiness. Blood biochemistry levels were urea 87 mg/dL, creatinine 5.09 mg/dL, glucose 830 mg/dL, glycosylated hemoglobin (HbA1c) 8%, C peptide <0.3 ng/mL, sodium 131 mmol/L, chloride 93 mmol/L, potassium 5.2 mmol/L, and calculated serum osmolality 385 mOsm/kg. The presumptive diagnosis on admission was nonketotic hyperosmolar syndrome precipitated by urinary infection. This is the first case report of hyperosmolar coma in a patient with type 1 diabetes with chronic kidney disease.
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PMID:Nonketotic hyperosmolar coma in a patient with type 1 diabetes-related diabetic nephropathy: case report. 1641 50

A patient on hemodialysis for end-stage renal disease secondary to diabetic nephropathy was admitted in a coma with Kussmaul breathing and hypertension (232/124 mmHg). She had extreme hyperglycemia (1884 mg/dL), acidosis (total CO(2) 4 mmol/L), hyperkalemia (7.2 mmol/L) with electrocardiographic abnormalities, and hypertonicity (330.7 mOsm/kg). Initial treatment with insulin drip resulted in a decrease in serum potassium to 5.3 mmol/L, but no significant change in mental status or other laboratory parameters. Hemodialysis of 1.75 hours resulted in rapid decline in serum glucose and tonicity and rapid improvement of the acidosis, but no change in mental status, which began to improve slowly after the hemodialysis was stopped, but with ongoing treatment with continuous insulin infusion. The rate of decline in tonicity during hemodialysis (14.5 mOsm/kg/h) was high, raising concerns about neurological complications. In this case, extreme hyperglycemia with ketoacidosis, hyperkalemia, and coma developing in a hemodialysis patient responded to insulin infusion. Monitoring of the clinical status and the pertinent laboratory values is required to assess the need for other therapeutic measures including volume and potassium replacement and emergency dialysis. The indications for and risks of emergency dialysis in this setting are not clearly defined.
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PMID:Extreme hyperglycemia with ketoacidosis and hyperkalemia in a patient on chronic hemodialysis. 1883 70

We report on a case of an elderly woman with chronic renal impairment, secondary to diabetic nephropathy, who developed a deep coma and seizure shortly after consumption of star fruit. She was managed in the intensive care unit, and her consciousness level improved dramatically after an 8-hour charcoal haemoperfusion and 30 hours of continuous haemofiltration. There were no long-term neurological or renal sequelae 9 months later. Early recognition of this condition, intensive dialytic therapy and supportive measures, as well as early initiation of charcoal haemoperfusion may improve the management of this potentially treatable condition.
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PMID:Star fruit intoxication successfully treated by charcoal haemoperfusion and intensive haemofiltration. 1934 44

Carbonic anhydrase inhibitors, such as acetazolamide, are widely used in the treatment of open-angle glaucoma. Severe metabolic acidosis is a rare complication of acetazolamide use, and life-threatening acidosis occurs most commonly in elderly patients, in patients with advanced renal failure, and in patients with diabetes. We describe an unusual case of an elderly patient with diabetic nephropathy and chronic renal failure who presented to the emergency department with severe metabolic acidosis and coma after exposure to high doses of acetazolamide in the postoperative period of ophthalmic surgery. As symptoms of acetazolamide intoxication and uremia are similar, high suspicion is required to detect excessive plasma drug concentrations and intoxication in patients presenting with concomitant uremia. Clinical symptoms are potentially reversible with prompt diagnosis and treatment, including supportive treatment, bicarbonate therapy, and renal replacement therapy. Hemodialysis is particularly helpful in the management of acetazolamide overdose as the medication is dialyzable.
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PMID:Acetazolamide Intoxication in an Elderly Patient with Diabetes and Chronic Renal Failure after Cataract Surgery. 3208 41