Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During a prospective screening for proteinuria in diabetic patients, isolated Bence-Jones proteinuria was detected in 2 cases. The first patient, a 52-year-old black female, was seen for evaluation of a slow but progressive weight loss which was attributed to poor adjustment of insulin therapy. The patient gained weight after an increase of the daily insulin administration. She had plasmocytosis in a bone marrow aspirate, but no other evidence of myelomatosis. The second patient, a 59-year-old black male who was seen for routine evaluation of his diabetes, had no clinical or laboratory evidence of myelomatosis. Although precise definition of these cases as "benign" or "idiopathic" Bence-Jones proteinuria is impossible without prolonged follow-up, at the time of presentation they appeared to fit this classification. This observation is one further example that isolated Bence-Jones proteinuria may be seen without any evidence of malignant B-cell dyscrasia.
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PMID:"Idiopathic" Bence-Jones proteinuria. 10 Oct 13

Two lysosomal glycohydrolases, beta-galactosidase and beta-N-hexosaminidase which have been associated with kidney disease were measured in the urine of 110 youngsters with juvenile diabetes mellitus. The mean enzyme excretions in the diabetic group were intermediate between those of normal youngsters and those with active renal disease. Three youngsters with known kidney disease had elevations comparable to others in the diabetic group but no direct correlation could be shown between enzyme elevations and proteinuria or Addis count abnormalities. Positive correlations were seen between enzyme levels and indices of metabolic balance including blood sugar, cholesterol and triglycerides but not with urine sugar or ketones. Duration and estimated stage and control of diabetes also correlated with the urinary enzymes. These preliminary studies are consistent with the possibility that the excretion of these enzymes reflects the ongoing renal damage which occurs in most juvenile diabetics.
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PMID:Urinary acidic glycohydrolases as an index of kidney damage in juvenile diabetes mellitus. 11 9

The female patient initially showed the acquired type of total lipoatrophy at about 8 years of age. At 12 years of age, the onset of diabetes mellitus was speculated from advanced pyodermia and dedentition. At 29 years of age, glucosuria was found, and she developed proteinuria, ascites, and pretibial edema. The physical examination revealed: hepatosplenomegaly, complete absence of subcutanous fat, cutaneous xanthomas, and emaciated facies with pronounced zygomatic arches. Diabetic retinopathy was revealed in the ophthalmological examination, and nephropathy was evident in renal biopsy specimens. She also had peripheral diabetic neuropathy. No adipose tissue was found in the mesenterium under peritoneoscopy. The hepatic biopsy specimen revealed advanced portal liver cirrhosis. Laboratory findings included: hyperlipidemia, elevation of BMR without evidence of hyperthyroidism, impaired renal function, and undetected anti-insulin antibodies and anti-insulin antibodies. Endocrinological examinations revealed normal value, except for an impaired hGH response in the arginine test. C-peptide immunoreactivity was high. Her condition was fairly well controlled by 140 units of insulin injection daily.
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PMID:Lipoatrophic diabetes. Report of a case. 15 92

The typical patient with diabetes mellitus seen at major hospitals in Papua New Guinea between 1974 and 1977 had florid symptoms, a very high blood glucose, was non-obese and non-ketotic and, frequently had neuropathy and proteinuria. In 25% hypertension was present which was significantly more common in the presence of proteinuria. Diagnosis was often delayed by failure to test urine for glucose and treatment was usually ineffective so that coma, usually non-ketotic, severe infections and gangrene occurred frequently. Although not as common as in other South Pacific countries, diabetes is increasing in Papua New Guinea. The provision of simple adequate facilities to test urine for glucose in all hospitals and the establishment of diabetic out-patient clinics in major centres to instruct both patients and other health workers are essential to improve treatment and reduce mortality and morbidity.
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PMID:The clinical characteristics of diabetes mellitus in Papua New Guinea. 29 6

One month following a cadaver renal transplant for obstructive uropathy, a 27-year-old man developed diabetes mellitus. Two years later, marked proteinuria and decreased renal function were detected. Eight months later, a second decline in function occurred. Light microscopy of graft biopsy specimens obtained after each decline in renal function showed increased mesangial cells and matrix, thickening of Bowman capsule, and tubular atrophy with basement membrane thickening. Vascular changes, interstitial infiltrate, and fibrosis were not prominent. Electron microscopic studies of the second biopsy specimen confirmed the light microscopic changes; subepithelial dense deposits were also detected. Immunofluorescent studies of both biopsy specimens demonstrated linear staining of glomerular and tubular basement membranes and Bowman capsule for IgG and albumin. Antikidney antibodies were not detected in the patient's serum. These observations suggest development of the diffuse form of diabetic nephropathy in a renal homograft following steroid-induced diabetes mellitus.
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PMID:Development of a lesion resembling diabetic nephropathy in a renal homograft. 32 61

Renal disease, particularly glomerulosclerosis, is a major cause of morbidity and mortality in patients with juvenile-onset diabetes mellitus. Signaled by the onset of proteinuria after 15 or more years of insulin therapy, progressive renal insufficiency due to glomerulosclerosis terminates in uremia within five years. Although some patients have benefited from chronic dialysis programs, the outcome in uremic diabetics has been considerably better if successful renal transplantation can be accomplished. Extrarenal complications of diabetes mellitus and recurrence of diabetic lesions in transplanted kidneys have hampered the recovery and rehabilitation of transplant recipients. Other renal diseases encountered in juvenile diabetics are reviewed.
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PMID:Grand rounds: Nashville VA Hospital--Vanderbilt University. Saturday conference: renal disease in the juvenile diabetic. 37 Oct 5

Diabetic nephropathy is a dangerous and insidious complication of diabetes mellitus. The course is variable and from the statistical point of view usually unfavorable. The pathogenesis of the complaint is not fully known. Of the numerous hypotheses, the one most favored is a defective glucose metabolism with uncontrolled inundation of the kidney cells with glucose. The predominant symptom is proteinuria. Early recognition and optimal correction of the metabolic disorder may possibly delay the manifestation of diabetic nephropathy for a time. The use of Somatostatin is attracting great attention today. With such a preparation, the stabilization of diabetes could be facilitated.
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PMID:[Clinical aspects of diabetic nephroangiopathy (author's transl)]. 40 65

In juvenile diabetes there is a renal hypertrophy: glomerular volume and capillary lumen of the individual glomeruli are about twice the size of healthy ones. The hypertrophy is associated with a hyperfunction (increased glomerular filtration and tubular reabsorption). If the diabetes is strictly controlled these changes may regress, which suggests a metabolically induced hypertrophy. Long-standing diabetes is characterized by a phase of intermittent proteinuria which gradually becomes permanent. Diabetic angiopathy is the result of many years of abnormal metabolism, presumably with involvement of the growth hormone and glucose. Whereas microangiopathy is considered specific for diabetes, it is still a matter for discussion whether a diabetic macroangiopathy exists. The results of numerous investigations suggest that it does.
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PMID:[Diabetic angiopathy. A new concept of pathogenesis (author's transl)]. 40 47

Submaximal bicycle ergometry was used in the evaluation of cardiac function in 22 patients with juvenile diabetes and 21 age-matched control subjects. Six patients had moderate to severe retinopathy and 2 had peripheral neuropathy. Half of the patients, but only 3 of the controls, were smokers. No differences were found in BP, serum cholesterol, triglycerides and serum creatinine levels between diabetics and controls. None had proteinuria. Patients with juvenile diabetes had higher heart rates (HR) at rest as well as during and after exercise than the healthy controls. Diabetics also had a reduced HR response to postural changes compared with the controls. Five diabetics and one control had a pathological exercise ECG (0.05 less than P less than 0.1) that may indicate early non-symptomatic coronary heart disease. The observed changes in HR may be due to autonomic neuropathy.
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PMID:Response to bicycle exercise testing in long-standing juvenile diabetes. 42 49

N-Acetyl-beta-D-glucosaminidase (NAG) activity has been measured in the serum and urine of primary and secondary diabetics and in primary diabetics with microangiopathy. NAG activity has also been measured in the tears of diabetics with ocular complications and diabetics with no ocular changes. Results have shown significantly higher levels of urinary NAG in diabetics with proteinuria (p less than 0.001) and proteinuria and retinopathy (p less than 0.001). There was no correlation between urinary NAG activity and serum creatinine (r = 0.28) or urinary NAG and the degree of proteinuria (r = 0.24). Increased urinary NAG levels were also observed in secondary diabetes associated with haemochromatosis and acromegaly. Significantly higher serum NAG levels were found in newly diagnosed diabetics (p less than 0.01) and significantly lower levels in chemical diabetics (p less than 0.01). Compared to non-diabetic controls tear NAG levels were significantly higher in the diabetic controls (p less than 0.01), in diabetics with retinopathy (p less than 0.01), and in diabetics with cataract formation (p less than 0.05). An assessment of this enzyme is made in relation to the development of diabetic microangiopathy.
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PMID:N-Acetyl-beta-D-glucosaminidase levels and diabetic microangiopathy. 48 3


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