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

Hyperlipidemia and lipoprotein abnormalities are often encountered in patients with nephrotic syndrome or chronic renal disease and also in those undergoing haemodialysis and with renal transplant. Even though the significance of lipid deposition in renal tissue and the role of lipoproteins in the pathogenesis of renal disease in man is unclear, experimental and clinical data indicate a possible damaging effect of a disturbed lipid metabolism on the kidney. In humans, glomerular lipid deposition is observed in genetic diseases such as Fabry's disease, lecithin:cholesterol acyltransferase activity (LCAT) deficiency and arteriohepatic dysplasia, and in diseases with acquired disturbance of lipid metabolism such as nephrotic syndrome and cholestatic liver disease. Studies on animals with lupus nephritis, aminonucleoside nephrosis, reduced renal mass, diabetes mellitus or systemic hypertension have shown that cholesterol can increase the incidence of glomerulosclerosis. As most of these studies have been performed in the rat, which has a different lipoprotein profile to that of man, these results should be carefully interpreted with regard to their relevance for humans. In vitro cell culture studies on human glomerular cells have given some preliminary insights into the cellular mechanisms of lipid induced glomerular damage. Apo E-containing lipoproteins, which are pathologically elevated in many renal diseases, are avidly taken up by human mesangial cells. These cells seem to play a central role in the initiation of glomerulosclerosis by inducing proliferation and production of excess extracellular matrix. Lipoproteins are able to stimulate DNA synthesis in these cells, and increase the synthesis of mitogens and extracellular matrix protein. The pathogenic role of oxidized lipoproteins has not yet been defined. Human mesangial cells do not seem to take up these modified lipoproteins. However, macrophages infiltrate glomeruli and may constitute the stimulus for the generation of minimally modified lipoproteins and their cellular uptake. The data from animal experiments suggest that treatment that corrects hyperlipidemia may have an ameliorative effect on renal function. Thus, there are strong indications that lipoproteins may play a critical role in mediating the development of glomerulosclerosis.
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PMID:The role of lipids in nephrosclerosis and glomerulosclerosis. 794 52

This study was conducted to determine whether overproduction of triglyceride-rich lipoprotein is an obligatory factor for experimental hypertriglyceridemia in nephrotic rats. Nephrosis was induced in male Wistar rats by administration of 150 mg/kg puromycin aminonucleoside. Nephrotic rats had slightly increased triglyceride secretion rate (TGSR) estimated using Triton WR1339 (0.53 +/- 0.05 vs. 0.45 +/- 0.04 mg/min, P < 0.05 vs. control rats) and marked hypertriglyceridemia (330.4 +/- 78.6 mg/dl). Rats made diabetic by 40 mg/kg streptozotocin were normotriglyceridemic (66.3 +/- 12.1 mg/dl) but had suppressed TGSR (0.33 +/- 0.09 mg/min). Experimental nephrosis was induced in diabetic rats. Their TGSR remained suppressed (0.35 +/- 0.06 mg/min) but they had marked hypertriglyceridemia (296.6 +/- 72.4 mg/dl) suggesting further impairment of triglyceride removal from the circulation in diabetic rats caused by nephrosis. Endogenously radiolabeled very low density lipoprotein (VLDL)-triglyceride from donor rats was reinjected into normal recipient rats. [3H]VLDL from the experimental groups (the rats with nephrosis, diabetes with nephrosis, and diabetes alone) were more slowly cleared by normal rats than VLDL from normal rats. These results suggest that circulating insulin is essential for increased triglyceride secretion in experimental nephrosis and that nephrotic hypertriglyceridemia can be induced only by a triglyceride removal defect. Therefore, hypersecretion of triglyceride-rich lipoprotein is not an obligatory factor for nephrotic hypertriglyceridemia.
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PMID:Hypertriglyceridemia in nephrotic rats is due to a clearance defect of plasma triglyceride: overproduction of triglyceride-rich lipoprotein is not an obligatory factor. 835 53

Forty-two patients with the nephrotic syndrome were grouped according to the absence or presence of renal failure and/or diabetes mellitus. All patients had a similar degree of hypoalbuminemia and urinary protein losses. A lipid and apoprotein pattern was generated in serum and ultracentrifugally isolated lipoproteins. Low-density lipoprotein composition was essentially normal in uremic patients while in the other patients with the nephrotic syndrome, a considerable lipid enrichment was noted. The very-low-density lipoprotein content in lipids was uniformly increased in nephrotic patients irrespective of the presence of complications. High-density lipoprotein cholesterol and serum apolipoprotein A I and E concentration was significantly reduced in uremic patients with respect to normal subjects and to the other groups considered. Serum apolipoprotein A II and B levels were also decreased in uremics. All patients had increased serum apoprotein C II and C III concentration. We conclude that diabetes mellitus does not affect the pattern of hyperlipoproteinemia of nephrotic syndrome while the characteristic lipoprotein and apoprotein pattern of uremia is present irrespective of nephrosis in uremic, nondiabetic patients.
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PMID:Pattern of hyperlipoproteinemia in human nephrotic syndrome: influence of renal failure and diabetes mellitus. 836 82

In summary, ANP exerts its action in the kidney directly and indirectly. Its qualitative importance in body fluid regulation remains unsettled. It appears that its role is more important in pathophysiological conditions such as CHF in which plasma ANP is elevated. Paradoxically, kidneys in heart failure, nephrosis and diabetes are characterized by diminished responsiveness to exogenous ANP. Further studies are needed to ascertain whether this involves an alteration at the receptor or postreceptor site. The cellular mechanisms for receptor regulation and postreceptor signalling in physiology and pathophysiology need further investigation. Finally, a paracrine mode for the action of ANP and other natriuretic peptides has been proposed. Whether they act locally to facilitate sodium excretion and how much importance they have compared to circulating ANP remain to be clarified. The potential role of ANP as a growth inhibitor is also intriguing.
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PMID:Biological significance of atrial natriuretic peptide in the kidney. 844 32

1. Glomerulosclerosis and tubulointerstitial damage are common histological abnormalities of many renal diseases that progress to end-stage renal failure. 2. In some models of renal damage, glomerulosclerosis seems to be associated with increased glomerular capillary pressure. 3. Due to the positive correlation of glomerulosclerosis and proteinuria in both experimental models and in humans, abnormal permeability to macromolecules has also been considered a possible determinant of glomerulosclerosis. 4. Abnormally filtered macromolecules have an intrinsic toxicity to the kidney due to protein over-reabsorption, possibly leading to tubulointerstitial damage. 5. Endothelin-1 (ET-1) is a vasoconstrictor peptide that induces mitogenesis and the accumulation of matrix proteins by mesangial cells. 6. Evidence is available that ET-1 plays a role in progressive renal disease in different experimental models, including renal mass reduction, lupus nephritis, streptozotocin-induced diabetes and puromycin-induced nephrosis.
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PMID:Endothelin is a key modulator of progressive renal injury: experimental data and novel therapeutic strategies. 871 73

Intravenous immunoglobulin (IVIG) is currently used for an increasing number of indications where an immune-medicated disorder is suspected. It is considered as a safe and efficacious treatment but several cases of severe acute renal failure (ARF) have been described since 1987. We report four cases of IVIG-induced ARF and the literature on the subject is reviewed. The chronological and semiological characteristics of this rare adverse effect are analysed. A sudden and marked increase of serum creatinine within the 2 to 4 days following institution of IVIG therapy, especially when the patient becomes oligo-anuric, is very suggestive of IVIG renal toxicity. The recovery of renal function is often obtained in 10 to 15 days after discontinuation of the drug. Histological changes are characterized by osmotic nephrosis injuries. Patients generally presented numerous risk factors such as over 65 years, particularly in men, pre-existing renal disease, long-standing diabetes mellitus or hypertension, volume depletion, quick infusion rate, body-weight adjustment of IVIG doses in fat subjects. The mechanism of renal injury remains speculative but an oncotic overloading of kidney probably occurs. These results indicate the need for research and investigation of risk factors before starting IVIG therapy. Close monitoring of serum creatinine and diuresis should be carried out during and after treatment.
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PMID:[Acute kidney failure secondary to intravenous immunoglobulin administration. 4 cases and review of the literature]. 913 86

A glomerular endothelial function with its hemodynamic impact is proposed to determine disease progression. In the clinical settings associated with an intact endothelial function, such as minimal-change steroid-sensitive nephrosis, the early phase of diabetes mellitus and the early stage of an experimental model of renal ablation in animals, it was observed that adequate renal perfusion correlates with the intact structure and function of the nephron with no evidence of disease progression. In contrast, the clinical settings associated with endothelial dysfunction, such as chronic glomerulonephropathy, the late stage of diabetes mellitus and a renal ablation model in animals, are usually associated with a reduction in renal perfusion. The magnitude of renal hypoperfusion observed in all forms of chronic glomerulonephropathies is proportional to the degree of clinical severity. A progressive pattern of renal hypoperfusion is uniquely observed when disease severity progresses. In this context, a new therapeutic maneuver aiming to improve renal perfusion is proposed for treating glomerulonephropathy with disease progression and preventing it from developing to end-stage renal disease.
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PMID:Glomerular endothelial dysfunction determines disease progression: a hypothesis. 942 51

Diabetes mellitus is often complicated by nephropathy with progression to renal failure. Various forms of glomerulonephritis have been associated with diabetes, sometimes resulting in more rapid deterioration in renal function and occasionally dictating alternative management of these patients in attempts to reverse or contain nephrosis or renal failure. We report the occurrence of Type I membranoproliferative glomerulonephritis (MPGN) with hepatitis C virus (HCV) infection in two patients, in association with diabetic nephropathy. One patient had cryoglobulinemia and cryoglobulin deposits in the kidney. A brief review of the literature on glomerulonephritides occurring in patients with diabetes mellitus is also presented. Clinicians should be aware of the possible occurrence of Type I MPGN and cryoglobulinemia in patients with diabetes mellitus and HCV infection with the appropriate history and physical findings. The therapeutic approach to managing patients with two distinct concurrent lesions remains unresolved.
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PMID:Diabetic nephropathy with concurrent hepatitis C virus infection related membranoproliferative glomerulonephritis. 998 47

Fifteen isolates of Mycobacterium kansasii in Showa University Fujigaoka Hospital between 1982 and 1995 were investigated. Comparing by gender, 13 were isolated from male patients and only two were isolated from female patients. The average of cases was 48 years old and 14 out of 15 cases (93%) were isolated from respiratory tract specimens. The rate of the smear- and culture-positives was 64%, which was significantly higher than that (26%) of M. avium complex (p < 0.01 by chi 2 test). All 4 isolates were susceptible to rifampicin (10 micrograms/ml) by drug susceptibility testing using Ogawa egg medium, and only 1 was resistant to ethambutol (2.5 micrograms/ml). Seven out of 10 patients whose medical record was available were diagnosed as pulmonary infection with M. kansasii. Two out of 4 patients with primary infection type had underlying diseases such as diabetes mellitus and leukemia, while the remaining two patients did not have any underlying disease. Two out of 3 patients with secondary infection type had a medical history of tuberculosis and the remaining 1 patient had infected pulmonary cyst. Such as Pseudomonas aeruginosa, Enterobacter aerogenes and Flavobacterium spp., and Branhamella catarrhalis, associated with M. kansasii, bacteria more than 10(7) cfu/ml were isolated from the sputa of 3 patients with leukemia, infected pulmonary cyst and post-tuberculosis, respectively. M. kansasii, Stenotrophomonas maltophilia (10(7) cfu/ml) and Candida albicans were detected from the sputum of 1 patient with nephrosis, for which steroid (predonin) and antibiotics (piperacillin and latamoxef) were administrated, however, this patient was not diagnosed as a case of M. kansasii infection. These findings suggest the fact that M. kansasii inhabits among compromised hosts of a city hospital.
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PMID:[Evaluation of Mycobacterium kansasii isolates from a clinical laboratory in a city hospital]. 1006 52

This report describes a patient not suspected of having Klinefelter syndrome during life but diagnosed with it following postmortem examination using fluorescent in situ hybridization (FISH) for sex chromosomes and hormone serum analysis. A 49-year-old Japanese man had a history of nephrosis, heavy alcohol consumption, diabetes mellitus, and liver cirrhosis and had been undergoing dialysis for 10 years. He died of ruptured esophageal varices. Autopsy revealed hypogonadism, suggesting Klinefelter syndrome. This was confirmed by FISH, which showed a mosaic 46XY, 47XXY karyotype, and by serum analysis, which revealed high luteinizing hormone and follicle-stimulating hormone and low testosterone levels. Autopsy also revealed a nodular, bilateral, testicular Leydig cell hyperplasia. This report illustrates the value of postmortem laboratory investigations, particularly FISH for sex chromosomes and serum hormone analysis, for the demonstration of clinically uncertain or "occult" Klinefelter syndrome.
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PMID:Postmortem diagnosis of "occult" Klinefelter syndrome in a patient with chronic renal disease and liver cirrhosis. 1186 Mar 15


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