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)

The analysis of clinical, diagnostic and treatment efficacy data has been made for 160 diabetes mellitus patients (50 cases of insulin-dependent and 110 of noninsulin-dependent) with acute purulent pyelonephritis (APP). A diffuse form of the disease was detected in 100 patients (62.5%), purulent-destructive one in 60 patients (37.5%). Intoxication, resistant to insulin decompensation of diabetes mellitus, sepsis may be resultant from latent APP. Nondestructive forms of APP were responsive to antibacterial and detoxication therapy combined with catheterization of the urinary tracts. On demand, conservative therapy was reinforced with renal drainage by nephrostomy. Primary nephrectomy was recommended in purulent-destructive forms and purulent para-nephritis. Radical surgery in intensive and advanced purulent-destructive pyelonephritis produced a decrease in postoperative lethality by 26.8%. Adequate therapeutic policy provided positive results in 80% of the patients. Lethal outcomes (20%) were due to grave diabetes mellitus and APP.
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PMID:[The treatment of acute suppurative pyelonephritis in diabetes mellitus patients]. 829 30

It has been found that polycystic kidney (ADPKD) is often associated with gout. On the other hand, there are reports describing that the hyperuricemia (HU) seen in ADPKD corresponds to a reduction in renal function. We investigated the uric acid metabolism in 44 patients with ADPKD (age, 50 +/- 12.8 years; CCR, 50.5 +/- 41.1 ml/min) at our hospital. From among these 44 patients, 14 with a CCR of 80 ml/min were selected. Their data for uric acid metabolism were compared against those from the previous year's studies on various disease types (114 normal subjects, 70 with membranous nephropathy, 175 with IgA nephritis, 122 with gout, 137 with asymptomatic hyperuricemia, and 42 with diabetes mellitus). Among the 44 patients with ADPKD, the serum uric acid (SUA) was 7.7 +/- 1.9 mg/dl and HU affected 28 (63.6%). The incidence of gouty arthritis was also high (6 patients, 13.6%), revealing a positive correlation between SUA and CCR. Compared with membranous nephropathy and IgA nephritis, ADPKD exhibited an accentuated increase in SUA associated with a reduction in CCR. It is believed that this represents a factor for a high incidence of complications of hyperuricemia and gouty arthritis in ADPKD in contrast to other diseases. However, no increase in the production of uric acid was noted in ADPKD.
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PMID:A study of uric acid metabolism and gouty arthritis in patients with polycystic kidney. 833 99

The levels of urinary PIC and FDP were studied in 86 diabetics. Urinary PIC or FDP were detected only in patients representing more than (++) urinary protein, suggesting that urinary PIC is not useful for diagnosis of early stage of diabetic nephropathy. On the other hand, positive rate of urinary PIC was much higher than that of chronic nephritis not due to diabetes mellitus. Plasma levels of PIC were elevated above normal range in all patients with advanced diabetic nephropathy tested. These results suggest that urinary PIC might be derived from circulating blood and reflect the level of systemic fibrinolytic activities in diabetics.
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PMID:[Urinary-plasmin alpha 2 plasmin inhibitor complex (PIC) in patients with diabetic nephropathy]. 836 Oct 49

A large body of clinical experience on the adverse consequences of cytokine administration has accumulated since the last decade. Side-effects reported after the therapeutic use of cytokines has provided evidence that activation of the immune response may sometimes have deleterious consequences. Several effects appeared as a direct consequence of the immune activation induced by cytokines, e.g. flu-like reactions, vascular leak syndrome. Cytokine-induced exacerbation of underlying diseases or immune dysregulation were other complications of growing concern. Interferon-alpha (IFN-alpha) treatment has now been clearly linked with the exacerbation or the occurrence of several types of autoantibodies or autoimmune diseases (thyroiditis, systemic lupus erythematosus, hematologic disorders, insulin-dependent diabetes mellitus) or diseases involving altered cell-mediated immune functions (inflammatory dermatologic diseases, nephritis, pneumonitis, colitis). By contrast immunological side-effects of IFN-beta and IFN-gamma have been seldom reported. However, the extent of clinical experience with both of these cytokines is still very limited. Interleukin-2 (IL-2) has also been implicated in various conditions that may involve immunopathological processes (thyroid disorders, rheumatoid arthritis, dermatological diseases, interstitial nephritis). Growth factors have been more specifically linked with the development or the exacerbation of dermatological inflammatory diseases through neutrophils, monocytes/macrophages or eosinophils activation (e.g. cutaneous vasculitis and generalized cutaneous eruption, Sweet's syndrome, bullous eruption, psoriasis). Exacerbation of autoimmune thyroiditis was described with granulocyte-macrophage colony-stimulating factor (GM-CSF) only. The immunogenicity of cytokines is also of great relevance and the occurrence of antibodies binding IFN-alpha and IFN-beta, IL2 and GM-CSF have been reported. While the clinical significance of non-neutralizing antibodies is not clearly established, an absence of response or reversal of clinical efficacy has been described in patients developing neutralizing antibodies. Finally, several isolated reports have recently suggested that IFN-alpha treatment may be associated with several immunosuppressive effects while IL-2 is clinically associated with an increased incidence of infectious complications.
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PMID:Immune-mediated side-effects of cytokines in humans. 863 83

Recipient vessels from the head and neck region were histologically examined in 30 patients who had undergone extensive tumor resection necessitating microvascular tissue reconstruction. Past illnesses considered to be risk factors included hypertension, myocardial disease, lung disease, cirrhosis, diabetes, nephritis, as well as extensive nicotine and alcohol abuse. Blood vessels chosen for microsurgical anastomosis were exclusively examined histologically in this study. Patients undergoing microvascular surgery demonstrated vessel abnormalities in 93%. The frequency of dysplasia was higher in the arteries than in the veins (73% and 26%, respectively). Marked thickening of the blood vessel wall and severe exfoliation of the endothelial cells were observed in most arteries. Fibrodysplasia and exfoliated endothelial cells were more frequently observed in the recipient arteries than the graft arteries. Only slight thickening of the vessel wall and mild fibrodysplasia were seen in the veins. Two graft failures were correlated to technical errors rather than pre-existing vessel lesions. This study revealed that most patients undergoing microsurgery in the head and neck region demonstrate pre-existing damage in vessels, which generally hinders anastomosis. Although the study tried to identify fully the interrelationships between the extent of dysplasia, past medical history, preoperative therapy, risk factors and factors that cause free-graft failure, pre-existing changes in the recipient and graft vessels may cause technical difficulties and must be regarded as additional factors contributing to graft failure.
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PMID:Histological changes in vessels used for microvascular reconstruction in the head and neck. 870 38

To characterize the phenotypic modulation of mesangial and glomerular epithelial cells, we investigated the expression of a nonmuscle type myosin heavy chain, SMemb, and alpha-smooth muscle actin (alpha-SM actin) in rat experimental glomerular diseases, which included anti-Thy 1 nephritis, 5/6 nephrectomy, diabetes, and anti-glomerular basement membrane nephritis. SMemb was only slightly expressed in normal glomerular epithelial cells but not in mesangial cells. In the anti-Thy 1 nephritis rats, both SMemb and alpha-SM actin were most conspicuously induced in mesangial cells. However, the expression profile was shifted from alpha-SM actin to SMemb dominant pattern over the course of glomerulonephritis. The expression of SMemb was also increased in epithelial cells in this model. In the other three models, glomerular cells did not express alpha-SM actin, but did so for SMemb. In the nephrectomized and the diabetic rats SMemb was newly expressed in mesangial cells at earlier stages, but at later stages was remarkably enhanced in epithelial cells when severe glomerular hypertrophy developed. In the anti-GBM nephritis rats, SMemb expression was increased in epithelial cells. In all models examined, mesangial and epithelial expression of SMemb was confirmed by immunoelectron microscopy, and enhanced expression of SMemb mRNA in glomeruli was verified by RNase protection assay. We conclude from these results that glomerular cells change their phenotypes differently depending on various types of glomerular diseases. These phenotypic changes in glomerular cells can be revealed by the combined immunostaining for SMemb and alpha-SM actin. SMemb is especially useful to detect both mesangial and glomerular epithelial cell activation in these glomerular disease models. Understanding the functional difference and regulatory mechanisms of these cytoskeletal proteins will provide insight into the pathogenesis and progression of glomerular diseases.
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PMID:Expression of a nonmuscle myosin heavy chain in glomerular cells differentiates various types of glomerular disease in rats. 873 Oct 86

In most cases of glomerulonephritis (GN) long-term course lead to chronic renal failure. The cause of inevitably gradually progress of GN to end-stage renal disease (ESRD) is unclear. The histological abnormalities seen in patients with progressive renal failure consist of focal and segmental glomerulosclerosis and tubulointerstitial nephritis. At present it is considered that tubulointerstitial changes attends almost all forms of progressive glomerular and vascular injury. It was known that chronic tubulointerstitial nephritis is characterized morphologically by tubular atrophy, interstitial fibrosis and interstitial inflammation of variable severity. The pathomechanism of this changes is complicated. Tubular ischaemia results from obliteration of peritubular capillaries, adaptation of tubular function with increased oxygen consumption and increased glomerular capillary permeability to macromolecules are reasons of chronic tubular damage. Injured tubules release growth factors and cytokines, which induce interstitial fibroblast proliferation, chemo-attraction and proliferation of infiltrating cells, and disruption of the balance between synthesis and degradation of cellular constituents. The consequences of these processes are tubular atrophy and interstitial fibrosis. Because of many studies concurred that tubulointerstitial changes determinant the progression of GN, tubular injury markers were searched for. Although over 50 enzymes were detected in human urine, only a few have been used for diagnosis in renal disease. The most widely used are lysosomal enzyme N acetyl-beta-D-glucosaminidase (NAG) and brush border enzymes alanine-aminopeptidase (AAP) and gamma-glutamyltransferase (GGT). tubular damage in hypertension, diabetes and in diagnostics of renal disease. AAP and GGT, brush border enzymes seem to be sensitive markers of renal injury too. Pathological value of GGT was observed even in the early stage of disease. Measurement of urinary excretion of low molecular weight proteins was valuable supplement in estimation of tubulointerstitial system malfunction. These proteins are readily filtered by normal glomeruli and virtually completely reabsorbed by normal proximal tubules. Favour are alpha-1-microglobulin (alpha-1-m) and retinol-binding protein (RBP) because they are less affected than beta-2-microglobulin (beta-2-m) by low urine pH. Above presented review confirm that further research in correlation between activity of disease, histological picture, deterioration in renal function and changes in urinary excretion of markers proteins (for example alpha-1-m, AAP, NAG, GGT) is advisable, and can contribute to use in clinic diagnostics of GN.
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PMID:[The role of tubulointerstitial changes in progression of kidney function failure in patients with chronic glomerulonephritis (GN)]. 875 11

GM and KM immunoglobulin (Ig) allotypes and their interactions with HLA antigens have been analyzed in various autoimmune diseases: multiple sclerosis, rheumatoid arthritis, insulin-dependent diabetes mellitus (IDDM), systemic lupus erythematosus, coeliac disease, Crohn's disease, Graves' disease, atrophic thyroiditis, Hashimoto's thyroiditis, myasthenia gravis, chronic active hepatitis, alopecia areata, uveitis, vitiligo, Turner's syndrome, glomerular nephritis, Berger's disease and idiopathic dilated cardiomyopathy. This review reports published results about associations or linkages, as well as the origins of the populations, the numbers of patients and controls tested. The possible role of Ig polymorphisms in the physiopathology of autoimmune diseases is discussed. Ig allotypes and statistical methods used to analyse the HLA and Ig data are also described.
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PMID:Immunoglobulin allotypes (GM and KM) and their interactions with HLA antigens in autoimmune diseases: a review. 878 16

Thyroid cancer patients are treated with up to 9.9 GBq of 131I to ablate remnant thyroid tissue and/or any functioning metastases that may be present. Radioiodine therapy is repeated as often as required. However, only a small fraction of the 131I is taken up by remnant thyroid and metastases, the remainder being eliminated by the kidneys, which are therefore subject to irradiation. External radiation therapy to the kidneys is known to lead to nephritis and albuminuria. The study included 113 patients treated with one to four doses of 131I (1.1-9.9 GBq each dose) and followed up 1 month to more than 8 years later. Spot samples of urine were collected and microalbuminuria measured by in-house radioimmunoassay. Twelve patients had elevated levels (normal range up to 34 micrograms ml-1), but their clinical history revealed such predisposing factors as diabetes and/or hypertension and proteinuria before therapy commenced. The remaining patients had normoalbuminuria. Grouping the patients based on the total dose of 131I administered resulted in a median microalbuminuria of 2.4-12.9 micrograms ml-1. Hence, this study showed that the dose of 131I normally used in treating thyroid cancer does not increase microalbuminuria to any significant extent.
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PMID:Screening for microalbuminuria by RIA in 131I-treated thyroid cancer patients. 882 54

Isolated hypoaldosteronism is found in 75% diabetics where the disease has persisted for 10 or more years. Sporadically it is found in congenital autonomous neuropathy, in acute glomerulonephritis, in gouty kidney, tubulointerstitial nephritis, after transplantation of the kidney, on mytomycin etc. During dynamic testing of the response of plasma renin activity and aldosterone to the administration of furosemide and a vertical position in diabetics a significantly reduced response was recorded as compared with non-diabetic hypertonic subjects. In 18.3% no response was observed (decompensated form of IHH). Diabetic hypertonics behaved like control hypertonics on long-term beta-blocker treatment. In the decompensated form of IHH after administration of drugs interfering with the activity of SNS-RAAS activity (ACEI, spirolactone etc.) a hyperkalaemic crisis may develop which threatens the patient with acidosis, dehydration, myoplegia, muscular spasms, however, in particular with fatal disorders of the cardiac rhythm. A similar effect may be exerted also by blockers of prostaglandin synthetase (non-steroid antirheumatics) and other drugs. The cause of IHH in diabetics is the coincidence of several pathogenic factors: 1. hypersecretion of ANF with hyperosmolar hyperglycaemic hypervolaemia and hyperfiltration already at the onset of DN, 2. early development of autonomous neuropathy of the sympathetic nerve, 3. reduced renin and prostaglandin formation already in the early stages of DN, 4. reduced extrarenal isorenin formation, 5. reduced conversion of prorenin into active renin, 6. reduced reactivity of the zona glomerulosa to AII, hyperkalaemia and ACTH for its functional reconstruction as a result of periodic activation of contraregulative hormones by fluctuations of the blood sugar level in diabetic patients, 7. reduced response of the distal renal tubule to aldosterone because of tubulointerstitial changes. IHH is thus another serious but rarely diagnosed late complication of diabetes which depends only partly on the stage of DN. It must be, however, diagnosed and respected with regard to the selection of drugs for the treatment of arterial hypertension and the syndrome of insulin resistance and the 5H syndrome resp., i.e. the association of hyperinsulinism which compensates insulin resistance with hyperglycaemia (NIDDM), hypertension, hyperlipoproteinaemia and hirsutism in women (so-called Stein-Leventhal syndrome).
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PMID:[Diabetic nephropathy and isolated hyporeninemic hypoaldosteronism]. 892 9


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