Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various guanidino compounds were determined in 48 non-dialyzed patients with chronic renal failure. The patients were divided into two groups, as follows: group A, chronic glomerulonephritis and polycystic kidney; and group B, diabetes nephropathy, lupus nephritis and renal amyloidosis. Six kinds of guanidino compounds in the serum were measured by high performance liquid chromatography. Although guanidinosuccinic acid (GSA), methylguanidine (MG) and taurocyamine (G-TAU) were inversely related to deterioration of renal function, arginine and guanidinoacetic acid were not correlated with the serum creatinine and urea nitrogen (SUN) levels. GSA was increased exponentially with decrease in renal function as compared to SUN. The ratio of methylguanidine to creatinine (MG/CRN) was significantly higher in the patients of group B than those of group A (P less than 0.05) in the range of creatinine 2.0-8.0 mg/dl. MG/CRN showed a negative correlation with the progression rate of renal dysfunction (P less than 0.01). It is suggested that GSA might be a more sensitive marker for renal dysfunction than SUN at the end stage of chronic renal failure, and MG/CRN might represent another indicator reflecting the activity of the causal renal disease and progression rate of renal failure. Furthermore, G-TAU could be a potent substance indicating the disease state. From these results, it is concluded that determinations of guanidino compounds in the serum might be useful for recognizing of the state of chronic renal failure.
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PMID:Significance of guanidino compounds in non-dialyzed patients with chronic renal failure. 235 64

Fanconi syndrome is a complex of renal tubular dysfunctions defined by glycosuria without diabetes, aminoaciduria, phosphaturia, and renal tubular acidosis. It is often associated with hypokalemia, hypophosphatemia, and rickets or osteomalacia. Although it is usually found in the setting of other well-established non-renal diseases, Fanconi syndrome may present without identifiable etiology or association. Very infrequently a patient with idiopathic Fanconi syndrome will progress to chronic renal failure. This case report details the course of such a patient over the 20 years since his diagnosis and discusses the syndrome's genetic background, clinical features, putative pathophysiology, and therapeutic options, including transplantation.
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PMID:Idiopathic Fanconi syndrome with progressive renal failure: a case report and discussion. 235 24

We studied the clinical and pathological data for 334 patients age 65 or more who underwent renal biopsy for acute renal failure (ARF, n = 55), subacute renal failure (SRF, n = 72), chronic renal failure (CRF, n = 57), proteinuria (n = 137), and hematuria (n = 13). Tissue diagnoses were glomerulopathy (n = 252, 75.4%), acute tubular lesions (n = 18), interstitial nephritis (n = 23), vascular diseases (n = 36, including 14 with cholesterol emboli), and five miscellaneous diagnoses. Of the 55 patients with ARF, 23 had a glomerular lesion, 15 had acute tubular necrosis, and 8 had acute interstitial nephritis. Of 72 patients with SRF, 49 had a glomerulopathy, 12 had a vascular disorder, and six had acute interstitial nephritis. Hence, patients with ARF or SRF exhibited a high potential for reversible lesions. Only 11.3% of patients with CRF had potentially reversible causes. The most common causes of proteinuria were membranous glomerulopathy (34.3%), minimal change disease (14.6%), focal segmental sclerosis (11.7%), and amyloidosis (8.8%). Of the 25 patients with advanced nephrosclerosis, 24 had renal failure, 20 were hypertensive, and 13 had cholesterol emboli. Of 33 patients with diabetes mellitus, 66.7% were found to have lesions not related to diabetes. We conclude that renal biopsy is most useful in older patients with ARF or SRF because of potentially reversible renal disease. Old age alone is not a contraindication to performing a renal biopsy.
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PMID:Renal biopsy in patients 65 years of age or older. An analysis of the results of 334 biopsies. 235 29

An increased risk of end-stage renal disease (ESRD) among blacks has been previously shown for most causes of chronic renal failure, including diabetes. Most previous studies have not considered the higher prevalence of diabetes in the black population and have not analyzed relative risk by type of diabetes. We found that the incidence of ESRD among blacks with diabetes was 3.6 times the rate in whites with diabetes. The relative risk for blacks increases progressively with age, reaching a maximum of 6.9 in persons over the age of 65. The incidence of ESRD due to diabetes is higher in the population with type I diabetes (492 per 100,000) than in the population with type II diabetes (71 per 100,000). Blacks have a higher incidence of ESRD in both type I diabetes (odds ratio, 2.96; 95% confidence interval, 1.8 to 4.9) and type II diabetes (odds ratio, 4.9; 95% confidence interval, 3.6 to 6.5). The incidence of ESRD in patients with diabetes varies with age, race, and type of diabetes.
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PMID:Racial differences in the incidence of end-stage renal disease in types I and II diabetes mellitus. 236 96

Thirty patients with gouty arthritis were studied over 3 years. The diagnosis was established with the help of polarised light microscopy. All the patients were males, with a median age of 45 years. They belonged to the middle or upper socio-economic class and were obese (mean body mass index 29.7). Chronic alcoholism, diabetes mellitus and hypertension were present in one patient each. No patient had symptomatic coronary artery disease. Although 6 patients had a history of renal colic, only one had gouty nephropathy with chronic renal failure. Six patients had a positive family history of gout. The disease involved mostly the joints of the lower extremity and podagra was observed in 70% of patients. Eight patients had tophi at various sites. There were 17 'over producers' and 13 'under excretors' of uric acid. The treatment consisted of patient education, symptomatic control with non steroidal anti-inflammatory drugs and/or colchicine and antihyperuricaemic therapy. The overproducers were treated with allopurinol while the under excretors were treated with [corrected] sulfinpyrazone. In general, there was a good response to therapy as indicated by lowering of serum uric acid and the number of painful episodes per year. The overall profile of the disease appears similar to that seen in the West.
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PMID:Clinical profile, therapeutic approach and outcome of gouty arthritis in northern India. 238 54

Mucormycosis is an uncommon infection caused by fungi of the order Mucorales. During an 8-year period, mucormycosis was diagnosed in 13 patients from three Madrid hospitals. There were 8 males and 5 females, with ages ranging from 21 to 75 years (mean 45 years). There were several underlying diseases, and 4 patients had more than one. Five had diabetes mellitus, 4 chronic renal failure, 2 acute myeloblastic leukemia, 2 were narcotic abusers and were infected by the human immunodeficiency virus (HIV), 1 had non-Hodgkin's lymphoma, 1 was a carrier of a renal allograft and 1 had systemic necrotizing vasculitis. There were different clinical presentations: rhino-orbital in 3, paranasal in 2, cutaneous in 2, pulmonary in 2, primary cerebral in 2, rhinocerebral in 1, and peritoneal in 1. The diagnosis was made during the first week in 6 patients, in the second week in 4, and it was delayed for more than one month in 2. Fresh examination of clinical samples was carried out in 3 patients and hyphae were visualized in all 3. Cultures were taken in 10 patients and they were positive in 7. All isolates were identified as Rhizopus sp. One patient died within 24 hours without being treated, 12 were treated with amphotericin B and 9 received surgical therapy. Six patients (46%) died. The involvement of central nervous system and the absence of surgical therapy were associated with a poor outcome. These results indicate that mucormycosis can develop in several clinical contexts and has a varying clinical presentation. It is a potentially curable infections when early diagnosed and appropriately treated.
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PMID:[Mucormycosis. The disease spectrum in 13 patients]. 239 7

The concentration and molecular form of pancreastatin-like immunoreactivity (PST-LI) in urine of normal subjects and patients with noninsulin-dependent diabetes mellitus or chronic renal failure were examined. PST-LI output (mean +/- SEM) in urine of normal subjects was 74.6 +/- 8.5 pmol/day and 87.1 +/- 11.7 pmol/g creatinine. That in patients with noninsulin-dependent diabetes mellitus was 78.1 +/- 9.0 (SEM) pmol/day and 85.6 +/- 9.0 pmol/g creatinine and was not significantly different from that in normal subjects. Gel filtration analysis showed that PST-LI molecules excreted in urine of these two groups were smaller than human pancreastatin (43-52) (hPST-10) of C-terminal fragment. The PST-LI molecular forms were deduced to be nonbioactive from the result that hPST-10 did not inhibit pancreatic exocrine secretion. PST-LI excretion in patients with chronic renal failure was 258.5 +/- 62.9 pmol/day and 713.2 +/- 219.6 pmol/g creatinine. A molecular form corresponding to hPST-52 and a larger form eluted in the high mol wt region (approximately mol wt 15 K) were detected by gel filtration of urine from these patients, indicating that PST-LI is excreted in urine without degradation in patients with chronic renal failure. These results support the suggestion that the kidney may play an important role in PST degradation or metabolism.
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PMID:Pancreastatin-like immunoreactivity in urine. 240 13

The distribution of total serum zinc between serum albumin and alpha 2-macroglobulin was evaluated by ultracentrifugation in patients with cirrhosis of the liver, insulin-dependent diabetes mellitus, or chronic renal failure. We found that the alpha 2-macroglobulin bound zinc fraction amounts to approximately 6 and 5% of the total serum zinc in patients with cirrhosis of the liver and diabetes mellitus, which corresponds to the distribution in controls. In patients with chronic renal failure, however, the alpha 2-macroglobulin-bound zinc fraction only constitutes approximately 2%, which is significantly less than in controls. Our findings indicate that most of the total serum zinc is bound to serum albumin.
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PMID:Distribution of serum zinc between albumin and alpha 2-macroglobulin in patients with different zinc metabolic disorders. 241 56

Histomorphometry was performed on transiliac bone biopsies, double-labeled with tetracycline, from 60 consecutively admitted patients (20 women) at various stages of chronic renal failure (CRF). Eleven patients (1 woman) had normal bone resorption and formation indices. Bone resorption and osteoid formation increased with progression of renal failure, but abnormal values were seen even at slightly elevated creatinine levels. Mineralization lag time increased with CRF duration; prolonged values were only seen in patients with polycystic kidney disease or chronic pyelonephritis with advanced CRF. All patients with impaired mineralization also had increased bone resorption. Diabetes mellitus did not protect against skeletal lesions. The biochemical tests were too insensitive to predict type or severity of bone disease, and hand X-rays had no diagnostic value in early stages of renal osteodystrophy.
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PMID:Renal osteodystrophy in predialysis patients without stainable bone aluminum. A cross-sectional bone-histomorphometric study. 245 77

We evaluated an enzyme immunoassay (Novo BioLabs) for determination of hemoglobin A1c and measured the contribution of carbamylated hemoglobin to the hemoglobin A1c results obtained by HPLC for patients with chronic renal failure. The reference interval, determined for blood donors, was 0.035-0.050 (i.e., 3.5% to 5% of the total hemoglobin). For non-diabetic patients with chronic renal failure, on hemodialysis, the mean proportion of hemoglobin A1c was 0.038 (SD 0.0045); for umbilical cord blood it was 0.006-0.009. For diabetic patients with normal or near-normal renal function, results by enzyme immunoassay (y) and HPLC (x) correlated well (r = 0.83): y = 0.99x - 0.005. Added fetal hemoglobin or carbamylated hemoglobin did not interfere with enzyme immunoassay, but added carbamylated hemoglobin co-chromatographed with hemoglobin A1c. Measurements for patients with chronic renal failure, with or without diabetes, by enzyme immunoassay and by HPLC, were compared with measurements for patients with diabetes mellitus but no renal failure. Carbamylated hemoglobin contributed 0.019 to the hemoglobin A1c results obtained by HPLC for patients with chronic renal failure.
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PMID:Enzyme immunoassay of hemoglobin A1c: analytical characteristics and clinical performance for patients with diabetes mellitus, with and without uremia. 246 21


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