Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

Renal transplantation in India costs about US$5000 ($1=Rupees 48.25), azathioprine costs $200 a year and cyclosporine costs $2000. Against this the average per capita income is $279 (Rs. 12989) per year; 36% of the population earn less than $105, and only 2.2% earn more than $1000. The country cannot afford to treat end-stage renal disease. Thirty percent of chronic renal failure is due to diabetic nephropathy, and 10% each to hypertensive nephropathy and chronic pyelonephritis. Social and preventive health workers of the Kidney Help Trust administered a questionnaire at the homes of a study population of 25,000, examined the urine of every individual for albumin and reducing substances, and checked the blood pressure of every person aged over 5; 90% of the population cooperated. Six percent were hypertensive and four percent had diabetes. Eight percent of them subsequently took regular treatment. Using only reserpine, hydrallazine and hydrochlorothiazide for hypertension, and glibenclamide and metformin for diabetes (as these are the cheapest agents available), we were able to control the blood pressure to 140/90 or less in 96% of cases, and to reduce HbAIC by 10% or more of the original reading in 77%. An HbA1C of 7% was achieved in 50% of the diabetic subjects. The total cost amounts to 27 US cents for one year per capita of the study population. The Indian Government now spends $7.67 per capita on health each year, but expects patients to attend its Primary Health Centers. The patients do not attend because in doing so they lose a day's wages. We believe that domiciliary treatment is the solution for these diseases, and expect to see a fall in the incidence of chronic renal failure if this is instituted in the future.
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PMID:Prevention of chronic renal failure at the community level. 1286 81

The aim of our study was to evaluate the changes of hemodialysis (HD) service and main demographic characteristics of HD patients in Lithuania during seven years period. From 1996 to 2003 we visited annually all HD centers in Lithuania and collected data about all HD patients. There was a sharp increase in the number of HD centers (from 17 to 37), HD stations (from 25 p. m. p. (per million population) to 87 p.m.p.; p<0.001), HD patients (from 60 p.m.p. to 264 p.m.p.; p<0.001) and incidence of new HD patients (from 54.3 p.m.p. to 92 p.m.p.; p<0.01). In 1996 all 17 HD centers in Lithuania were public. Private HD centers appeared in 1998 and reached 43.2% of all HD centers (n=16) in 2003. 44.8% of HD patients were dialyzed in private HD centers. The mean age of HD patients increased from 47.2+/-16.1 years in 1996 to 57.5+/-14.9 years in 2003 (p<0.001). HD population became older. The percentage of patients over 60 years old increased from 22.8% to 49.7% (p<0.001) and over 70 years old--from 54% to 21.9% (p<0.001). The main underlying disease of end-stage renal disease was chronic glomerulonephritis but its rate had decreased from 54.5% in 1996 to 26.5% in 2003 (p<0.001). During this period there was a statistically significant increase in the incidence of end-stage renal disease due to diabetics (from 7.1% to 18.0%; p<0.01), hypertensive nephropathy (from 3.1% to 9.4%; p<0.05), and chronic pyelonephritis (from 11.2% to 18.6%; p<0.01). In summary during the last seven years HD service in Lithuania expanded significantly, and rapid development of private HD was observed. The number of HD patients was rising continuously with predominance of diabetic, hypertensive and elderly patients.
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PMID:[Development of hemodialysis service in Lithuania during (1996-2003)]. 1590 73

Metalloproteinases (MMP) and their tissue inhibitors (TIMP) play a crucial role to keep the balance between the synthesis and degradation of extracellular matrix protein. Balance disturbances of those two systems lead to abnormal tissue remodeling. There is evidence that matrix metalloproteinases activity changes in many pathological conditions, including inflammatory, degenerative disorders as well as tumor progression. Recent investigations indicate that MMPs and TIMPs play a pivotal role in pathogenesis of most of kidney diseases. Studies describing dysregulated activity of MMPs and/or their tissue inhibitors in various experimental and clinical models of kidney disease, including chronic kidney disease, glomerulonephritis, pyelonephritis, diabetic and hypertensive nephropathy, polycystic kidney disease and renal cancer are reviewed.
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PMID:[Role of matrix metalloproteinases (MMP) and their tissue inhibitors (TIMP) in nephrology]. 2103 7