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)

A total of 291 urine sediments from 255 patients with various renal or urinary tract diseases have been studied by phase contrast microscopy. Based upon morphological criteria, leucocytes were distinguished from renal epithelial cells and the white blood cells were classified either as mononuclear or polynuclear in 179 patients. The percentage of the different cell types varied considerably between and within the different diseases. The median values for polynuclear granulocytes were higher than 90% in bacterial renal or urinary tract disease and in polycystic kidney disease. In interstitial nephritis, nephrosclerosis and in renal transplanted patients the percentage of polynuclear granulocytes was somewhat lower, 76-85%. In diabetes, amyloidosis, tubular nephrosis (necrosis) glomerulonephritis, lupus nephritis and endemic benign nephropathy there were 14-66% polynuclear granulocytes. 29-33% mononuclear leucocytes were found in lupus nephritis and endemic benign nephropathy. The greatest proportion of renal epithelial cells was found in endemic benign nephropathy, namely 49%. 36% renal epithelial cells were found in tubular nephrosis (necrosis) and in glomerulonephritis. The technique is rapid and inexpensive. It facilitates differential diagnostics of urinary tract disease with pyuria.
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PMID:Differential count of urinary leucocytes and renal epithelial cells by phase contrast microscopy. 110 1

There is an excess incidence of ESRD treatment among non-White North Americans that is not completely explained by the racial prevalences of the underlying diseases, including hypertension, which can potentially cause renal disease. The racial difference is particularly striking for presumed nephrosclerosis from hypertension and for nephropathy from Type II diabetes, but is not yet substantiated for ESRD attributed to polycystic kidney disease or Type I diabetes. The existing data are insufficient to support the notion that poorer blood pressure control alone is responsible for the racial differences in incident ESRD. Black race (and possibly Mexican or Native American heritage) may be a specific risk factor for ESRD, independent of hypertension and its treatment.
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PMID:Racial differences in the incidence and progression of renal diseases. 176 85

1. Graft survival rates increased about 3-5 percentage points for patients with all primary diseases in 1989-1990. 2. Patients with different diseases had 1-year graft survival rates that varied from 73% for noninsulin-dependent diabetes (NIDDM) to 83% for IgA nephropathy (IgAN). Five-year graft survival varied from 40% for NIDDM to 66% for IgAN. 3. Our findings in Clinical Transplants 1990 that IgAN patients have a high graft survival was confirmed and 1-year graft survival improved by 5% in the last 2 years. 4. There was a 20 percentage point increase in full-time work status of patients after transplantation; 68% of patients with polycystic kidney disease (PKD) and chronic glomerulonephritis (CGN) had full-time work status after 3 years whereas patients with diabetes mellitus (DM) and atheronephrosclerosis (NS) had about 50%. 5. Good early graft function (urine output during the first 24 hours posttransplant, no dialysis within the first-week posttransplant, and no rejection episodes before discharge), predicted good 1-year graft survival for patients with different diseases but patients with NS and DM had a poorer graft survival beyond the first year posttransplant. Patients who had poor early function had 20% lower graft survival than those who had good function. However, in patients with IgAN, no urine at day 1 still resulted in graft survival comparable to those that produced urine. 6. More patients with DM were transplanted within 1 year after going into ESRD than those with other diseases. Conversely, 46% of those with NS did not get transplanted until more than 2 years after developing ESRD. 7. Only 77% of NS patients had functioning grafts at discharge compared to DM (84%), PKD (81%), IgAN (81%), and CGN (80%). 8. Black patients had a statistically significant higher incidence of anuria on the first day compared with Whites. They also had a higher incidence of dialysis and rejection during the first hospitalization. This was true for CGN, DM, PKD, and NS patients. Following excellent early function, Black CGN and DM patients had a higher incidence of rejection than White CGN and DM patients.
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PMID:Outcome of renal transplantation in different primary diseases. 182 Jan 24

Studies addressing the epidemiological issues of end-stage renal disease (ESRD) and the implications for health resource allocations are valuable, especially because the Medicare ESRD program is expected to continue growing during the next decade. Studies on trends in the causes of renal failure have benefited from Medicare's extensive data files on ESRD patients. However, no studies have been published that validate the cause of renal failure field in the Medicare files. The primary disease causing renal failure for over 10,000 New York State patients in the Medicare ESRD program was compared with their hospital discharge diagnoses. Of these patients, 8,730 (83%) had a known cause of renal failure in the Health Care Financing Administration (HCFA) data files. Eighty-nine percent of these patients' primary cause of renal failure was matched with the same major hospital diagnostic code. Patients with diabetes and glomerulonephritis had the highest overall match rates (96% to 97%). Patients with polycystic kidney disease and causes of renal failure other than the four major causes had the lowest match rates (75% to 76%), but these match rates increased to 84% to 87% for patients hospitalized more than five times. Some differences in match rate by age and race were found. These findings suggest that HCFA data on the causes of renal failure of ESRD patients are reasonably accurate and can be used successfully to study a variety of issues related to the diseases leading to chronic renal failure.
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PMID:Validation of the cause of renal failure of patients in the Medicare end-stage renal disease program. 188 30

Several reports in animals, and sporadic case reports in humans, have suggested that kidneys with decreased nephron mass may be more susceptible to the development of focal-segmental glomerosclerosis. This prompted a reexamination of our previously reported group of pediatric donor-adult recipient renal transplant combinations. Data were analyzed from 31 adult recipients who had received renal transplants from cadaver pediatric donors (less than 6 years) with graft function for greater than 6 months and no evidence of chronic rejection. These were compared with a control group transplanted during the same period with adult donor kidneys. Immunosuppression consisted of azathioprine/prednisone or quadruple therapy in 16 and 15 patients respectively. End-stage renal disease (ESRD) was secondary to chronic glomerulonephritis (n = 9), diabetes mellitus (n = 6), polycystic kidney disease (n = 5), and miscellaneous causes (n = 11). Twenty patients had radiographic documentation of renal hypertrophy posttransplant. All patients had serial 24-hr urinalysis for protein and creatinine after transplantation during periods of stable renal function. Ten patients had renal biopsies performed at a mean time from transplant to biopsy of 10.4 +/- 1.6 months. Seven recipients had biopsies that revealed glomerulosclerosis at 13 +/- 6 months posttransplant. Protein excretion and serum creatinine in these patients were significantly higher than in control patients (1.6 +/- 0.37 vs. 0.49 +/- 0.15 g/24 hr and 1.96 +/- 0.11 vs. 1.64 +/- 0.09 mg%; P less than 0.03 and P less than 0.01, respectively). Only 3 of 25 control adult donor recipients developed proteinuria greater than 0.8 g/24 hr within 2 years of transplantation vs. 15/31 pediatric donor recipients. No correlations with the etiology of ESRD, age (greater than or less than 40 years), weight, sex, diabetes, hypertension, or the number of acute rejection episodes could be found. Our data suggest that adult recipients of pediatric donor renal transplants may be at greater risk for the development of glomerulosclerosis than those recipients receiving adult donor kidneys.
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PMID:The development of proteinuria and focal-segmental glomerulosclerosis in recipients of pediatric donor kidneys. 194 66

Most gas-forming infections occur in patients with diabetes. Carbon dioxide formation, resulting from fermentation of the high concentration of sugar in the urine and tissue by infecting organisms, was regarded as the key factor of gas formation in previous reports. Gas from an emphysematous infection of a polycystic kidney was analyzed to understand better the mechanisms involved in gas-forming infections of the urinary tract. The term emphysematous renal polycystic infection is proposed for this particular condition. Gas from the cysts contained 4.1% carbon dioxide, 10.5% oxygen, 67.3% nitrogen and 18.1% unknown gas. This finding is astonishingly similar to that of Wheeler in 1954 and cannot be fully explained by the sugar fermentation theory. Therefore, we propose a new hypothesis. Impaired transportation of gas produced by rapid catabolism leads to gas accumulation in the tissue, which will gradually expand and create chambers to form gas bubbles. Gas of adjacent tissues will attempt to come into equilibrium with the gas bubbles. Positive equilibrium will lead to continuous expansion of the lesion bubble. However, if the chamber is unable to withstand the increasing pressure then rupture or spontaneous drainage of the gas bubble may occur. During negative equilibrium gas in the bubble gradually simulates tissue gas with eventual shrinkage of the bubble. If the chamber is unable to sustain the pressure it collapses and the bubble disappears. However, if the chamber is capable of sustaining the pressure the bubble still may persist even when the gas content is equivalent to tissue gas. This hypothesis may lead to better understanding of emphysematous infections of the urinary tract and also may cast light on emphysematous infections of other organ systems.
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PMID:Gas-forming infection of the urinary tract: an investigation of fermentation as a mechanism. 218 58

This study was performed to determine the long-term outcome of renal transplantation in 54 patients with end-stage renal failure secondary to autosomal dominant polycystic kidney disease (ADPKD) and in 107 patients with renal diseases other than ADPKD or diabetes mellitus matched by gender, age, year of transplantation, and source of the allograft. The overall patient survival and patient survival with a functioning first renal allograft were similar in both groups. Infection and cardiovascular accidents were the leading causes of early and late death in both groups. No cause of death was greatly overrepresented in the ADPKD group. Serious complications from extrarenal manifestations of ADPKD following renal transplantation included a ruptured intracranial aneurysm in one patient, a dissection of the ascending thoracic aorta in one patient, and infected hepatic cysts in two patients. Neoplasia (other than skin or cervical) occurred in four ADPKD patients and in one control patient and included one lymphoma in each group. Two ADPKD and one control patient had monoclonal gammopathies of undetermined significance. No complications related to the retention of native kidneys were detected in 12 ADPKD patients with a mean follow-up of 3 years. Cysts were observed in the renal allografts of some patients in both groups at autopsy and in a prospective computed tomography (CT) study of the allograft. However, we failed to detect a significant difference in the occurrence and number of the cysts between ADPKD and control patients.
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PMID:Long-term outcome of renal transplantation in autosomal dominant polycystic kidney disease. 219 71

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

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

The purpose of this investigation was to study in a group of diabetics with varying degrees of renal failure, the relationship of renal size to the degree of renal function. A literature search of the past 25 years has failed to document a precise relationship between structure and function in this setting. Patients were admitted, and sex, age, race, serum creatinine levels, renal size and mean blood pressure were ascertained. Patients with polycystic kidney disease were, obviously, excluded. The group consisted of 26 diabetics, divided into two groups based on previous (prior to onset of uremia) insulin and ketone status. Interestingly, there was no significant difference between groups with insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) as regards mean blood pressure (106.5 +/- 15.3 mm Hg vs. 108.9 +/- 17.64 mm Hg; t = 0.3607892, p = 0.9). Mean kidney length was inversely related to serum creatinine level (r = 0.3980, n = 26, p less than 0.05). There was no correlation between mean renal length and mean blood pressure (r = 0.189, p greater than 0.05). However, there was a significantly higher proportion of larger kidneys (11 cm or more) in the IDDM group than in the NIDDM group (Fischer's exact test; p less than 0.0001) which was related neither to age nor blood pressure. In this paper, we show an inverse correlation between kidney length and serum creatinine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal size and function in diabetic nephropathy. 273 65


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