PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “NEPHROSCLEROSIS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,117 records · Page 62Linked to original sources

Special considerations with regard to the dosage of tranexamic acid in patients with chronic renal diseases.

Tranexamic acid is a potent antifibrinolytic drug frequently used in the treatment of haematuria and a number of other haemorrhagic conditions. Since it is eliminated mainly in the urine, the drug accumulates in patients with uraemia. The excretion of tranexamic acid in patients with renal failure has been investigated and dosage recommendations are given for tranexamic acid therapy in cases of renal failure.

Biological Availability↗

Diabetic microangiopathy in patients with pancreatitic diabetes mellitus.

Clinically evident diabetic microangiopathy (retinopathy and nephropathy) occurred in 18% of diabetic patients with acute pancreatitis and 14% of diabetic patients with chronic pancreatitis. The presence of diabetic retinopathy and nephropathy in patients with pancreatitic diabetes without a family history of diabetes mellitus suggests that these patients have "primary" diabetes mellitus unmasked by the pancreatitis. The occurrence of diabetic microangiopathy is significantly correlated with the duration of diabetes. The frequency of these diabetic complications seems to increase when there is a family history of diabetes in patients whose pancreatitis is simultaneous with or precedes the onset of diabetes. The majority of patients with diabetic microangiopathy were on insulin therapy, but the need for insulin treatment is an indication of the severity of the diabetes, rather than the insulin being a causative factor of the microangiopathy. The degree of steatorrhea in diabetic patients with chronic pancreatitis did not protect against the development of microangiopathy.

Acute Disease↗

Search for a biochemical basis of diabetic microangiopathy.

Diabetic microangiopathy, particularly as seen in the renal glomerulus, is characterized by morphological and biochemical alterations of the capillary basement membrane. Observations from a number of disciplines have indicated that the microvascular disease is not a separately inherited entity but a true consequence or "complication" of insulin deficiency. An evaluation of the biochemical events which could be responsible for the basement membrane lesions of diabetes indicates that the hyperglycemia or plasma somatotropin elevation of this disease alone, or in combination, may play an important role.

Animals↗

The different forms of glomerulonephritis morphological and clinical aspects, analyzed in 2500 patients.

Comparative morphological and clinical studies of 2,500 patients suffering from glomerulonephritis, enabled us to divide the different forms of diffuse glomerulonephritis into 3 distinct groups and to separate these groups from the focal glomerulonephritides. The different forms of diffuse glomerulonephritis in group I are: 1. endocapillary (acute) glomeruloenphritis (of the post-streptococcal type), 2. mesangioproliferative glomerulonephritis, 3. mesangioproliferative glomerulonephritis with focal crescents, 4. mesangioproliferative glomerulonephritis with focal scarring, 5. minimal proliferating intercapillary glomerulonephritis without nephrotic syndrome. It is emphasised that these forms can transform into one another, that they seldom occur with nephrotic syndrome, and with varying frequency with hypertension. Group II consists of: 1. minimal proliferating intercapillary glomerulonephritis with nephrotic syndrome, 2. focal sclerosing glomerulonephritis, 3. perimembranous glomerulonephritis, 4. membranoproliferative glomerulonephritis, 5. lobular glomerulonephritis. It is stressed that these glomerulonephritis forms usually do not develop out of group I type glomerulonephritis forms, and that in this group a nephrotic syndrome is the most prominent clinical syndrome. In the third group are 1. mesangioproliferative glomerulonephritis with diffuse crescents, 2. necrotising glomerulonephritis. It is shown that this form of glomerulonephritis does not usually develop from either group I of II forms. The fourth group of focal glomerulonephritis is uncommon. This disease is characterized by a necrotising and proliferative inflammatory lesion found segmentally and focally in the glomeruli. Most of the other glomeruli appearing normal. It is emphasised that in the literature the diagnosis focal glomerulonephritis is made far too often. This is because glomeruli in which the inflammatory process in a few lobules is of varying prominence, are included in the focal glomerulonephritis group. The classification of the different forms of glomerulonephritis into 3 groups here described, is thought of as a basic classification. It is compared with Ellis' classification (1942), with which it has much in common.

Basement Membrane↗

Effects of glycosaminoglycans on the glomerular changes induced by Adriamycin.

Glycosaminoglycans can stimulate the synthesis of glomerular basement membrane (GBM) proteins by glomerular cells and correct biochemical alterations of the GBM. In this study we examine the effects of heparin and low-molecular-weight heparin (LMWH) on glomerular permeability to proteins and glomerular structure in Adriamycin-treated rats. One Adriamycin dose of 5 mg/kg body weight was administered i.v. to 38 female Wistar rats. Eleven animals were also treated with heparin (250 U) administered s.c. twice daily and 7 with LMWH 6 mg/kg body weight administered s.c. twice daily. Urine samples were collected before and 30 and 60 days after the beginning of treatment to quantify albumin excretion and to characterize urinary proteins by gel filtration and electrophoresis in sodium dodecyl sulfate polyacrylamide gels. Blood samples were also collected on day 60 from these rats to estimate renal permeability by gel filtration; the rats were then killed and the kidneys removed for histological analysis. Heparin administration caused a reduction in urinary albumin excretion and in the incidence of segmental glomerulosclerosis in Adriamycin-treated rats. However, heparin did not modify the selectivity of the GBM to proteins of different molecular weights. These data suggest that the effect of heparin on albuminuria may be due to changes in the negative GBM charges induced by this drug.

Albuminuria↗