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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic pyelonephritis is, by definition, a chronic interestial nephritis due to immediate or late effects of bacterial infection of the renal parenchyma. The main diagnostic criterion is recurrent or permanent bacteriuria. As a rule, bacteriuria follows as a secondary symptom a primary renal disturbance such as malformations of the urinary tract, stones, gout, analgesic abuse, diabetes mellitus or pregnancy. It is most important to eradicate predisposing factors, if possible, for successful antimicrobial therapy. In some cases, permanent intensive chemotherapy might be more harmful to the patient than untreated chronic bacteriuria, in itself.
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PMID:[Pyelonephritis]. 122 May 15

This study was made to determine whether zinc deficiency is one of the factors involved in growth retardation of infants of high-risk pregnancies. The high risk factors were hypertension of pregnancy, diabetes mellitus, congenital heart disease, chronic nephritis, rheumatic heart disease and hyperthyroidism. 102 neonatal infants were divided into 3 groups: breast fed group, 37 cases; test group, 32 cases formula-fed with supplementary zinc 1.14-2.28 mg/kg/d; and control group, 33 cases formula-fed and supplemented with Vitamin B complex as placebo. The groups were divided by double-blind and randomized method. There were no differences in the 3 groups in sex ratio, growth status and serum zinc concentration at the beginning of the study. Anthropometric data were obtained at 0, 3 and 6 months.
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PMID:Growth promoting effect of zinc supplementation in infants of high-risk pregnancies. 129 Dec 3

Interleukin-1 (IL-1) is a 17-kDa pro-inflammatory cytokine synthesized from a variety of cell types primarily in association with disease states or during host perturbation such as immune responses. At pM or even fM concentrations, IL-1 triggers various responses in nearly all cells. It appears that there is little or no major role for IL-1 in homoeostatic mechanisms. There are two IL-1's (alpha and beta) each with its distinct sequence; there are two IL-1 receptors. Disease states such as local and systemic infection, septic shock, degenerative arthritis and autoimmune diseases such as nephritis, vasculitis and inflammatory bowel disease appear to be mediated, in part, by IL-1. Organ failure, capillary leak and death occur in animals after a combination of tumour necrosis factor (TNF) and IL-1 which is more effective in inducing these changes than either cytokine alone. IL-1 is also a potent inducer of endothelial cell adhesion molecules, IL-6, and IL-8, a neutrophil chemotactic and activating factor. Strategies for reducing the effects of IL-1 have been based on suppression of transcription, translation, or secretion; more recently, receptor blockade has been a new approach. A naturally occurring IL-1-specific receptor antagonist (IL-1ra), which shares 40% conserved amino-acid homology with IL-1 beta, binds to IL-1 surface receptors with the same affinity as IL-1 but does not possess agonist activity and acts as a competitive inhibitor of IL-1. Studies using the IL-1ra to block endogenous IL-1 in a variety of animal disease models suggest that IL-1 plays a key role in triggering the cascade of inflammatory responses. In addition, the IL-1ra reduces the spontaneous production of growth factors and proliferation of leukaemic cells. The IL-1ra may be an advantageous therapy in patients with sepsis, diabetes, inflammatory bowel, arthritis and cancer.
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PMID:Reduction of inflammation by decreasing production of interleukin-1 or by specific receptor antagonism. 139 23

To ascertain the contribution of systemic hypertension in the progression of renal failure, we have studied the effects of pharmacological treatment of hypertension in rats with the remnant kidney model of renal insufficiency, streptozotocin diabetes, or nephrotoxic serum nephritis. Treatment with the angiotensin converting enzyme (ACE) inhibitor enalapril lowered systemic blood pressure in the remnant kidney and diabetic animals, but did not lower blood pressure in rats with nephrotoxic serum nephritis. Proteinuria was reduced in all three models, and creatinine clearance improved in the remnant kidney and diabetic animals, when compared with untreated controls. In the remnant kidney and diabetic models systemic blood pressure was lowered to a similar degree by treatments with a calcium blocker, with no improvement in either proteinuria, or glomerular filtration rate. Further studies of the long-term effects of enalapril have been undertaken in rats with the two kidney one clip model of hypertension. Rats treated with enalapril had a lower blood pressure and improved survival over one year of treatment, compared with untreated rats. After 1 year of treatment however the clipped kidney was small and fibrotic, and non functional. Following withdrawal of enalapril therapy there was no functional improvement of the clipped kidney. The possibility that ACE inhibitors have a specific intra-renal effect reducing the rate of progression of renal disease now needs confirmation in human studies. In renovascular hypertension however, intra-renal changes induced by ACE inhibitors may cause irreversible renal damage.
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PMID:Systemic and renovascular hypertension. 141 41

This paper describes four cats with hyperadrenocorticism. Cat 1 showed polydipsia and polyphagia. Diabetes mellitus was initially diagnosed. As the animal appeared to be insulin resistant, pituitary and adrenocortical function tests were performed and the diagnosis of hyperadrenocorticism was made. Resistance to the high-dose dexamethasone suppression test was noticed in this cat. Pathological examination revealed a pituitary chromophobe adenoma. Cat 2 presented with diabetes mellitus, which was treated with insulin. The animal had a pendulous abdomen and its coat was in a poor condition. The low-dose dexamethasone suppression test demonstrated hyperadrenocorticism. Necropsy findings of pituitary tumour and hyperplasia of the adrenal cortex confirmed the diagnosis. Cat 3 showed clinical abnormalities indicative of hyperadrenocorticism, for instance, muscle weakness, alopecia, multiple abscesses. The diagnosis of hyperadrenocorticism was confirmed by the results of the lowe-dose dexamethasone suppression test. Pathological examination revealed an adrenocortical carcinoma. Cat 4 presented with polydipsia. The cause of this symptom was not found initially. One and a half years later additional symptoms, such as nephritis and polyphagia developed. Hyperadrenocorticism was diagnosed because of a palpable mass cranial to the left kidney. The diagnosis was confirmed by the results of the lowe-dose dexamethasone suppression test and the necropsy findings.
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PMID:Hyperadrenocorticism in four cats. 141 43

The associations or linkages between the polymorphisms of the Gm and Km immunoglobulin allotypes and the susceptibility to autoimmune diseases, including diseases with immuno-pathological pathogenesis are reported in this review. These diseases include multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, insulin-dependent diabetes mellitus, Crohn's disease, coeliac 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. Immunoglobulin allotypes are described as well as the statistical methods used to analyse the data.
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PMID:Gm and Km allotypes in autoimmune diseases. 162 73

The aim of the present study was to further elucidate acute and chronic manifestations of Yersinia enterocolitica infection. During the period 1974-83, 458 hospitalized patients were diagnosed by antibody response and/or isolation of the microorganism. 64 patients had suffered from chronic conditions as rheumatic disease, inflammatory bowel disease, hepatitis, nephritis or thyroid disease for some time. Acute hepatic, renal, cardiac, pulmonary, pancreatic or neurologic involvement were observed in a substantial portion of patients; several had multiorgan disease. Acute insulin-dependent diabetes was seen in 2 patients, malignant mesothelioma in 2, and specific lymph node inflammation in 1. The patients were followed for 4-14 years (1987). 36/160 readmitted patients had abdominal pain and 26 had diarrhea; chronic colitis was demonstrated in 4. Some patients developed rheumatic conditions; others developed chronic disease of liver, kidneys, heart, pancreas, thyroid or nervous system. Chronic liver disease, in 22 patients, was correlated with positive tests for antinuclear antibody and rheumatoid factor; and might influence development of malignant disease, and mortality. A variety of acute and chronic clinical pictures may be associated with Y. enterocolitica infection, and further clinical research is required in this field.
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PMID:A survey of acute and chronic disease associated with Yersinia enterocolitica infection. A Norwegian 10-year follow-up study on 458 hospitalized patients. 176 49

Following 689 percutaneous renal biopsies, membranous glomerulonephritis was proved in 68 patients. In 16 (23.5%) an underlying primary disease was verified, and thus the glomerulonephritis the secondary form. The primary disease was SLE in 5 cases, diabetes mellitus in 5 cases, rheumatoid arthritis in 3 cases, chronic active hepatitis in 2 cases, an ulcerative colitis and eosinophilic angiolymphoid hyperplasia in 1 patient. As initial sign, nephrotic syndrome emerged in 87.5% of the 16 cases. Microscopic haematuria was observed in half of the patients, as was hypertension, while acute renal failure presented in only 1 case. Histologically, in 13 cases the predominance of early glomerular alterations was characteristic, while in 9 cases the picture proved to be equivocal and accompanied by some degree of interstitial alterations. During combined treatment, remission was achieved in 75%. Two patients with SLE died, but not as a consequence of renal failure. Transient side-effects of the treatment were registered in 5 cases. The principal pathogenetic and clinical differences between the individual secondary nephritis forms, and the difficulty of their differentiation from the idiopathic cases, even on repeated examination, are emphasized. In 3 patients the possibility of secondary renal processes was suggested by the histological picture, and this was proved by the detailed clinical findings.
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PMID:[Secondary membranous glomerulonephritis]. 199 1

To find how diabetes affects the processes of proliferative glomerulitis, we induced anti-glomerular basement membrane (GBM) nephritis by injection of anti-GBM antiserum in rabbits with alloxan diabetes (the DM-GN group) and in rabbits without the diabetes (the GN group), and compared the glomerular lesions between the two groups. Rabbits with alloxan diabetes only (the DM group) were also studied as control. Morphological examination showed that in the acute phase, the DM-GN and GN groups underwent histolysis of the glomerular loops, which gave rise to proliferative glomerulitis. In the later stages of glomerulitis, proliferating cells were crowded toward the axial portion of glomerular loops with an increase of intercellular matrix, and glomerular capillaries in the periphery of the glomerular loops recanalized. The amount of intercellular matrix of the axial portion increased more in the DM-GN group than in the GN group. Some of the glomerular lesions in the DM-GN group showed a formation of large nodules. The results suggested that diabetes could accelerate the formation of the intercellular matrix of glomerular loops in proliferative glomerulitis in rabbits, resulting in accelerated glomerulosclerosis.
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PMID:Accelerated glomerulosclerosis in alloxan-induced diabetic rabbits with anti-glomerular basement membrane nephritis. 206

In the period 1973/74-1983 a prospective observation was carried out on 4591 out-patients (2095 males and 2496 females) aged 18-68, with predominantly non-insulin treated diabetes of 1-10 years' duration. During the ten years period over a third of initial cohort died. Age-standardized mortality rate was twice that for the general population of Warsaw for the median year 1978. The risk of death rose with decreasing age, especially in females. The most frequent causes of death were cardiovascular diseases, particularly coronary heart disease, standardized mortality ratios amounting to 2.7 and 2.4 respectively. Among diabetic cohort the risk of death was also higher for nephritis, nephrosis, cirrhosis of the liver and pneumonia. No excess death rate could be found for tuberculosis, malignant neoplasms, and diabetes itself. Diabetic patients were less frequently exposed to accidental deaths than the general population of Warsaw. The mortality diabetic patients in Warsaw was similar to that seen in most of the developed countries with the exception of the higher mortality due to cirrhosis of the liver and smaller due to accident, trauma and poisoning.
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PMID:[Mortality among patients with diabetes mellitus in Warsaw--a 10-year prospective study]. 262 53


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