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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glomerulonephritis has been recognized as a rare complication of diabetes mellitus. The clinical, pathologic, and laboratory findings for 18 diabetic patients were reviewed. Eight of these patients (44 per cent) were found to have primary glomerulonephritis in addition to diabetic nephropathy. Although this series may not represent the true incidence of complicating glomerulonephritis in diabetes, it is probable that the incidence of this condition has been underestimated. An additional 26 previously reported cases are reviewed.
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PMID:Primary glomerulonephritis complicating diabetic nephropathy: report of seven cases and review of the literature. 647 73

This multicenter regional study analyzes survival of a large group of patients who began chronic dialysis or received their first renal transplant during the 5 1/2-year period that ended in June 1983. Survival was determined from the onset of renal replacement therapy, irrespective of changes in treatment modality. Univariate life-table analysis was used to examine more than 35 risk factors. Age of patients at entry into the therapeutic program significantly affected survival. General survival rates were lower for patients with diabetes than for nondiabetics, irrespective of treatment modality, with the exception of those older than 60 years of age. Five-year graft survival was lower for diabetics than for nondiabetics in all age groups, irrespective of source. Patients with systemic lupus erythematosus, focal glomerulosclerosis, or glomerulonephritis had the highest survival rates, whereas those with primary renal malignant lesions, primary hypertensive disease, or diabetes mellitus as the cause of renal failure had the lowest. Concurrent morbid conditions that adversely affected survival included arteriosclerotic heart disease, peripheral vascular disease, noncutaneous malignant lesions, chronic pulmonary disease, and multiple coexisting morbid conditions. Although the objective of this study was to analyze survival for single patient characteristics, irrespective of treatment modality, analyses of survival rates by treatment modality for a control group indicated that minimal differences were evident by the third year among the four treatment groups: in-center hemodialysis, home hemodialysis, living related donor transplantation, and cadaver transplantation; however, recipients of cadaver grafts had lower survival rates than all other groups, even those maintained by in-center hemodialysis (P = 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Survival rates of 2,728 patients with end-stage renal disease. 649 73

Fifteen patients with symptomatic cryoglobulinaemia were subjected to apheretic treatment when acute renal insufficiency, glomerulonephritis, severe generalized vasculitis and polyneuropathy unresponsive to conventional therapy or complications due to steroids, such as vertebral collapse, peptic ulcer and steroid diabetes, had appeared. Treatment was performed by discontinuous flow centrifugation or cascade filtration: when discontinuous flow centrifugation was employed, a mixture of saline, gelatin and fresh frozen plasma was used for replacement. Cytotoxic drugs were administered to patients with lymphoma (4 patients) or chronic active hepatitis (5 patients) and also to patients suffering from essential mixed cryoglobulinaemia. Exchanges were organized into courses of 3 to 5 sessions over 5 to 10 days and employed as a supportive measure. No patient underwent long-term treatment. A complete resolution of kidney damage, skin involvement and neurologic signs was observed when treatment was started early in the course of the disease, whereas unequivocal but moderate improvement was obtained in the case of long-lasting symptoms such as polyneuropathy. Relapses were seen in most patients when cytotoxic drugs had been discontinued abruptly. In 8 patients the solubility of cryoglobulins was studied by a recently developed turbidimetric assay. Following treatment the solubility increased; when solubility decreased, 2 patients of this group had a relapse. On the basis of these preliminary observations it appears that the possibility of predicting relapsing disease or the need of continuing therapy can eventually be achieved.
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PMID:Plasmapheresis and cytotoxic drugs for mixed cryoglobulinemia. 653 39

A 2-year-old boy with familial extramembranous glomerulonephritis was unfortunately treated with corticosteroids (1 to 0.5 mg/kg/day) and Chlorambucil (cumulative dose: 2.5 g) over a period of 7 years. Three years later, after recovery from the renal affection, he developed fatty diarrhoea from exocrine pancreatic deficiency, followed 5 years later by the onset of diabetes with hypochlorhydric gastritis. The diagnosis of non-calcifying chronic pancreatitis was suggested by scintigraphic and ultrasonographic investigations and confirmed by the marked increase in lactoferrin levels and the lactoferrin/lipase ratio (greater 0.1 p. cent) in pancreatic juice. The etiology was more likely to be direct toxicity of corticoids and/or immunosuppressors on the pancreas than an immunologically-mediated disease.
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PMID:[Global pancreatic and gastric deficiency after a familial membranous glomerulonephritis in a child treated by corticoids and chlorambucil for a long time (author's transl)]. 681 Jul 39

The linkage of rheumatoid arthritis (RA) to infection though vague has remained a persistent notion for the past fifty years. The hypotheses that streptococcus was responsible; then M. Pneumoniae; the implication of a viral pathogenesis and, more especially, the Epstein-Barr virus, have all not withstood the test of Koch's postulates. Today, autoimmunity holds the field in the pathogenesis of RA. We know in fair detail what happens after failure of self-recognition develops. Why does synovial tissue become antigenic? Altered receptors of cell surface may be the loci of change, namely, glycoproteins and glycolipids. A hypothesis is constructed based on alteration by viral DNA of these cell surface markers that are then recognized as alien. Evidence is drawn from insulin dependent juvenile diabetes, glomerulonephritis, and Landsteiner blood groups. The initial lesion may be initiated by an infectious agent leading to a chain of events, the first link constituting change of the specific glycoprotein or glycolipid of a cell to one of antigenic challenge, thus stimulating an autoimmune reaction. The ultimate destructive-proliferative sequences of RA are then set in motion.
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PMID:Altered oligosaccharides as the initiating autoantigen in rheumatoid arthritis. 687 15

The New Zealand Obese (NZO) mouse was studied as a potential model for autoimmune diabetes. NZO mice develop obesity, glucose intolerance, and insulin resistance, and have low-titer IgM antibodies to the insulin receptor. It is shown that they have circulating antibodies to both native DNA and denatured, single-stranded DNA. The antibody levels are higher in females, and, up to 6 mo of age, are comparable to those found in the related NZB X NZW F1 (NZB/W) mouse, a model for systemic lupus erythematosus. After 6 mo of age the antibody levels in NZO mice fall toward normal, in contrast to the persistently elevated levels in NZB/W mice. NZB/W mice are known to succumb to immune complex-mediated proliferative glomerulonephritis before 1 yr of age, whereas NZO mice survive. NZO kidneys exhibit light microscopic features of both diabetic and lupus nephropathies: glomerular proliferation, mesangial deposits, mild basement membrane thickening, glomerulosclerosis, eosinophilic nodules in some glomeruli, occasional hyalinization of the glomerular arterioles, and healing arteriolar inflammation. These changes are associated with glomerular deposition of immunoglobulin, especially IgM, in a granular pattern on fluorescent staining. The NZO mouse, therefore, has evidence of a generalized immune disorder and provides a model for studying the relationship between autoimmunity, obesity, and diabetes.
Diabetes 1980 Oct
PMID:Diabetes is associated with autoimmunity in the New Zealand obese (NZO) mouse. 700 65

The behavior of blood pressure was investigated in 65 transplantation (Tx) patients in a nephrological outpatient service for an average of 18.6 months after Tx. Before Tx 2/3 of the patients exhibited hypertension, after Tx this was reduced to 1/2. No correlation was found between behaviour of blood pressure and such factors as renal function, incidence of rejection episodes, prednisolonee dose, diabetes mellitus and urinary function, incidence of rejection episodes, prednisolon dose, diabetes mellitus and urinary tract infection of the Tx. Only in patients with glomerulonephritis as original renal disease there was in increased incidence of hypertension before and after Tx. Causes of hypertension are discussed and demonstrated in the case of Tx arterial stenosis.
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PMID:[Observation on the course of arterial hypertension after kidney transplantation]. 703 94

Although most forms of glomerulonephritis in man are thought to have an immunopathogenesis, certain clinical and experimental observations support the role of other non-immunologic mechanisms in the progression of these diseases. 1. Intra-renal vascular disease thought to be secondary to hypertension, may be responsible for ischemic glomerular sclerosis. 2. Hypertension may damage the diseased glomerulus directly, as has been demonstrated in experimental glomerulonephritis, in the remnant kidney, and in experimental diabetes mellitus. 3. Alterations in glomerular structure and function in the remnant kidney suggest that adaptations to nephron loss may contribute to further renal damage. 4. Glomerular sclerosis occurs under circumstances where immunologic mechanisms are highly unlikely, such as aging, reflex nephropathy, chronic aminonucleoside administration, and protein loading. 5. Preservation of renal function can be achieved by phosphorus restriction in the remnant kidney and in nephrotoxic serum nephritis.
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PMID:Mechanisms of progression in glomerulonephritis. 703 41

The low graft survival rate in black recipients (36 +/- 2% at 1 year) as compared with the graft survival rate in white recipients (48 +/- 1%) might be secondary to a higher incidence of vascular lesions, inducing hypertensive disease, in blacks than in whites. The relative frequency of malignant hypertension in black recipients was six times that of white recipients, and recipients with malignant hypertension had a significant lower graft survival rate (43 +/- 2%) than recipients with glomerulonephritis (54 +/- 1%). In addition, patients with vascular lesions (diabetes, malignant hypertension, and glomerulonephritis) showed significantly lower graft survival rates in black than in white recipients, in contrast to patients with primary tubular or interstitial lesions (polycystic kidneys and pyelonephritis), who showed similar graft survival rates in blacks and whites. Only a small fraction of this racial effect could be traced back to the higher incidence of Lewis-negative phenotypes in black recipients and a similar beneficial effect of transfusions, on graft survival, was observed in both black and white recipients. The effects of graft survival of age (6%), race (9%), and transfusions (18%) were significant in good (A) and poor (B) centers. No overlap between A and B centers was observed for any of these three parameters when analyzed separately. However, when the cumulative effects of these three risk parameters were analyzed together a partial overlap appeared, i.e., higher graft survival rates were observed in low-risk recipients that received transplants in B centers than in high-risk recipients that received transplants in A centers. Consequently, the selection of the recipient may play a role in the overall results of different transplantation units, leading to their classification into A or B centers, but cannot explain all of the differences between A and B centers.
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PMID:Influence of the original disease, race, and center on the outcome of kidney transplantation. 703 19

Two patients with long-standing diabetes mellitus and diabetic retinopathy were evaluated for declining renal function and heavy albuminuria. Initially, diabetic glomerulosclerosis was suspected as the cause of progressive glomerulopathy. However, in both patients the rate of loss of glomerular filtration rate was greater than that usually seen in diabetic glomerulosclerosis, and the urine sediment contained many RBC casts. These findings led to renal biopsy, which demonstrated crescentic glomerulonephritis superimposed on diabetic glomerulopathy. Both patients were treated with prednisone and cyclophosphamide and both experienced substantial improvement in renal function. These experiences demonstrate the importance of searching for evidence of a superimposed treatable glomerulopathy in the diabetic patient with glomerulopathy and advancing renal insufficiency.
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PMID:Rapidly progressive glomerulonephritis superimposed on diabetic glomerulosclerosis. Recognition and treatment. 705 37


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