Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical findings and structural alterations in the kidneys of 6 patients with sarcoidosis and an associated glomerulonephritis are described. Five of the 6 patients manifested the nephrotic syndrome during some phase of their illness. Additional clinical evidence of renal disease included persistent microscopic hematuria (5 patients), hypertension (4 patients) and progressive renal failure (3 patients). Glomerular pathology varied and included proliferative glomerulonephritis (3 patients), membranous glomerulonephritis (1 patient), and chronic glomerulonephritis (2 patients). In 2 patients sequential examination of the kidney was possible, with renal biopsies preceding autopsy examination by 3 and 6 years, respectively. Glomerular pathology had progressed in severity in each case. Immunofluorescent studies in 2 patients revealed patterns of glomerular antibody localization consistent with immune complex disease. Electron microscopic studies of 1 revealed membranous changes characterized by electron-dense subepithelial and intramembranous deposits. Totally unexpected were virus-like intraendothelial structures in the glomeruli identical to those previously reported in systemic lupus erythematosus. Since current evidence suggests that the pathogenesis of both membranous and proliferative types of glomerulonephritis is immunologic, it should not be surprising that sarcoidosis, a disease which quite possibly results from an immune response to a disseminated antigen(s), should occasionally include glomerulonephritis as a part of its histologic expression.
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PMID:Glomerulonephritis associated with sarcoidosis. 455 25

An oral glucose tolerance test and an assay of insulin receptor activity were performed in patients with chronic glomerulonephritis (CGN) to elucidate the aberration of glucose metabolism in such patients. Ninety of 123 patients with CGN without renal failure showed abnormal glucose tolerance, including 72.6% with IgA nephropathy, 81% with benign recurrent hematuria, 87% with chronic proliferative glomerulonephritis, 100% with membranoproliferative glomerulonephritis, and 80.0% with membranous nephropathy. Insulin responses in CGN patients during oral glucose tolerance tests showed lower levels of basal insulin and significantly higher levels after 90, 120, and 180 min compared with those of normal controls. The binding of radiolabeled insulin to blood mononuclear cells in 22 CGN patients with abnormal glucose tolerance was significantly (P = 0.0023) decreased in comparison with 5 normal controls. However, plasma obtained from such patients showed no significant (P = 0.4761) inhibition of the binding of insulin to normal mononuclear cells. It was concluded that glucose tolerance capacity was impaired in 80.4% of patients with CGN without renal failure. Such impairment of glucose metabolism might be due to decreased activity of insulin receptors on cells in CGN patients.
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PMID:Abnormal glucose tolerance in patients with chronic glomerulonephritis without renal failure. 635 11

Counts of the number of pores of primary collecting tubules (ducts of Bellini) on renal papillae, and values calculated by adjusting the counts of compound papillae to those of "virtual" single papillae, were determined for kidneys of patients with end-stage renal failure. Values for chronic glomerulonephritis, Alport's disease, infantile polycystic disease, trisomy 18, and trisomy 13 were not abnormal. Kidneys of patients with CUTO showed significantly low pore counts, indicating that this process in some cases is a true hypoplasia, with mean reduction of number of ducts of Bellini of 26%. FGS showed a high proportion of single papillae (80% vs. normal 60%) with high virtual pore counts, suggesting that a developmental abnormality underlies this disorder (or this outcome of nephrotic syndrome). Cystinosis showed a high proportion of compound papillae (80% vs. 40%) but low virtual pore counts, implying that this genetic disorder causes both maldevelopment and postnatal functional abnormality of the kidneys. A Jeune syndrome kidney produced very low pore counts (mean 8 vs. 16.6 for virtual pore counts), and Down's syndrome also showed low pore counts (mean VPC 15.1 vs. normal 16.6), indicating that the low kidney weights demonstrated by others with Down's syndrome reflect a true hypoplasia.
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PMID:Papillary pore counts: a method of studying developmental aberrations in diseased juvenile kidneys. 668 70

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.
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PMID:Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens. 672 98

Significant glomerular changes occur in a substantial number of renal cadaver allotransplants. Transplant glomerulopathy and recurrent glomerulonephritis account for most of the lesions whereas the development of de novo glomerulonephritis is a rare event. Only a few cases of membranous glomerulonephritis in the graft have been documented. The four patients presented all developed heavy proteinuria of 11.5 to 14 g/day 5 months to 1 year after transplantation. Three cases of de novo membranous glomerulonephritis were transplanted because of renal failure due to chronic pyelonephritis, chronic glomerulonephritis and medullary sponge kidney. One patient has recurrent membranous glomerulonephritis. Transplant biopsy revealed only minimal glomerular changes by light microscopy in all cases. Immunofluorescence and electron microscopy demonstrated typical membranous glomerulonephritis.
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PMID:Recurrent and de novo membranous glomerulonephritis in renal cadaver allotransplants. 699 Nov 85

Chronic renal failure associated with hypercalcemia and hypophosphatemia was diagnosed in 6 horses. The renal lesions in 5 of the horses were classified as chronic glomerulonephritis and in the sixth, as chronic interstitial nephritis/pyelonephritis. There was no evidence of primary hyperparathyroidism or pseudohyperparathyroidism, thus suggesting that hypercalcemia associated with advanced renal failure in horses is related to a unique role of the equine kidney in calcium homeostasis.
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PMID:Paradoxic hypercalcemia and hypophosphatemia associated with chronic renal failure in horses. 706 1

Thirty-one patients who developed nephrotic syndrome when greater than 60 yr of age and who underwent renal biopsy are presented. In this group of the patients the most common histologic diagnosis was membranous nephropathy (52%); other diagnoses were amyloidosis (16%), end-stage renal disease (13%), chronic glomerulonephritis (9%), minimal change disease (6%), and lupus nephritis (3%). The prognosis in all these patients was poor; most of them died or were in terminal renal failure during the following-up period.
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PMID:Nephrotic syndrome in the elderly. 717 67

Of 570 patients operated on for hyperparathyroidism, 18 subsequently died (between one day and 12 yr after operation). Pathological findings at necropsy in these patients have been reviewed. Four necropsies on patients with untreated hyperparathyroidism have also been reviewed for comparison. Of these 22 cases, 14 had renal failure at the time of death. This was attributed to the following: nephrocalcinosis 6; chronic glomerulonephritis 4; analgesic nephropathy 1; cystinuria 1; sarcoidosis 1; and polycystic disease 1. Of those with renal failure due to nephrocalcinosis, three had persistent hypercalcaemia after operation; the other three survived only for a short time. There was no evidence of residual nephrocalcinosis producing progressive renal failure if the plasma calcium concentration was corrected. In those with chronic glomerulonephritis, cystinuria, and polycystic disease, the hyperparathyroidism was considered to be tertiary to the renal disease but renal failure was not always present at the time of diagnosis.
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PMID:Progressive renal failure in surgically treated hyperparathyroidism. 726 1

A 39 year old man with 4 of the 5 cardinal features of the Laurence-Moon-Biedl syndrome (LMBS) had proteinuria and moderate renal failure. Excretory urography showed small cysts communicating with the dilated calyceal system. Renal biopsy showed diffuse mesangial sclerosis and cellular proliferation. Excretory urograms in 22 of 24 reported patients demonstrated similar findings. Review of renal pathology reports on 16 patients revealed either chronic glomerulonephritis or severe tubulo-interstitial disease with cysts or both in 8 of 9 who died from uremia and 2 of 7 who died from other causes. The abnormalities seen on excretory urography occur more frequently than 2 of the cardinal features, and as uremia is often the cause of death for these patients, renal disease should be considered a cardinal feature of LMBS.
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PMID:Renal disease-a sixth cardinal feature of the Laurence-Moon-Biedl syndrome. 729 73

A 3-year survey of patient referrals and case material in pediatric nephrology is evaluated to provide a data base for future projection of patient needs. In the 3-year period between January 1978 to December 1980, 538 pediatric patients with renal and electrolyte disorders were evaluated and treated. The principle reasons for the referrals were: hematuria (23%), hypertension (5%), nephrotic syndrome (7%), non-acute glomerulopathies (11%), acute glomerulonephritis (3%), fluid-electrolyte disorders (29%), urinary tract infections (6%), and others. Of the 538 patients, 99 underwent percutaneous renal biopsies under ultrasound guidance. The indications and results of the renal biopsies were also reviewed. The accrual of 18 chronic dialysis patients over a 36-month period is analyzed and presented. The ages of the patients were 4 to 16 years. They weighed from 16 to 51 kg. The primary renal diseases were objective uropathy, chronic glomerulonephritis, membrano-proliferative nephritis, chronic pyelonephritis, focal glomerulonephritis, lupus nephritis and others. All children, except 9 received kidney transplantations. The annual incidence of end-stage renal failure was 4 per million population.
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PMID:A 3-year survey of referral pattern and case material in pediatric nephrology. 734 35


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