Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal disease was found at necropsy in 27 of 60 catheterized baboons (Papio cynocephalus). Primary diagnoses were infarcts in eight baboons, septic embolic nephritis in four, and mesangioproliferative glomerulonephritis in 15. Infarcts and septic embolic nephritis are multifocal renal diseases; mesangioproliferative glomerulonephritis is diffuse, progressive and often accompanied by severe proteinuria, hypoalbuminemia (less than 3 g/dl), and generalized edema. Five of the 15 baboons with glomerulonephritis also developed uremia and died of renal failure. Ten baboons with glomerulonephritis were given microbiological examination during their clinical course. Bacteria were isolated from the peripheral blood of eight baboons and from the catheter itself in two. The organisms isolated (in decreasing order of frequency) were Herellea sp., Streptococcus sp., Klebsiella sp., Staphylococcus sp., and Providencia sp. Prospective immunofluorescence studies were done on frozen sections from six catheterized baboons with glomerulonephritis and two uncatheterized controls. There were granular deposits of IgG in all six, IgM in five, C3 in four, and IgA and C4 in two. In the controls, only trace amounts of IgM were seen in one animal. The amount of IgG deposited in th glomeruli correlated with the severity of the glomerulonephritis. Bacterial antigens were found by immunofluorescence in glomeruli of three of five baboons examined. Glomerulonephritis in these baboons seems to be immunologically mediated, and in origin, pathogenesis and morphologic expression resembles shunt nephritis in humans with infected indwelling shunts and catheters.
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PMID:Renal pathology of catheterized baboons (Papio cynocephalus). 734 48

11 adult female dogs were given periodic intravenous injections of uranyl nitrate [UO2(NO3)2 . 6H2O] to create a syndrome of chronic uremia. Initially, dogs usually received 2.0 mg/kg of uranyl nitrate; subsequent doses were generally less. After the initial injection, there was an abrupt fall in creatinine clearance and rise in plasma urea nitrogen. Low and relatively constant creatinine clearances (10.2 +/- SD 2.7 ml/min) were easily maintained with further injections. Dogs developed proteinuria, aminoaciduria, weight loss, and plasma amino acid levels similar to those of chronically uremic humans and rats. With creatinine clearances of 4 ml/min or less, dogs became listless and lethargic, and daily activity and food intake decreased. Repeated injections of uranyl nitrate appear to be an easy and reliable method for creating a model of chronic uremia in dogs.
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PMID:Chronic uremia syndrome in dogs induced with uranyl nitrate. 736 Feb 99

The authors present a case of a 15-year-old girl with Leber's congenital amaurosis with associated nephronophthisis. The main findings in this case are: congenital blindness; enophthalmos; photophobia; nystagmus; keratoconus; cataracts; pigmentary degeneration in the fundus of both eyes; progressive uremia with absence of hematuria, proteinuria, pyuria, and glycosuria; low urinary density, normal lipidic profile; osteoporosis; absence of edema; polydipsia; polyuria; and a history of consanguinity between her parents. Tranmission of this entity allows an autosomal recessive pattern.
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PMID:Leber's congenital amaurosis with associated nephronophthisis. 739 8

The aim of the study was to document postheparin plasma lipoprotein lipase (LPL) and hepatic lipase activities and relate these to serum lipid, lipoprotein and apolipoprotein concentrations in 85 patients with kidney function ranging from normal to dialysis dependency. Strict selection criteria were applied in order to exclude conditions other than renal failure which may influence lipid metabolism. Stress was laid on minimizing proteinuria and inflammatory activity. The changes in the lipoprotein pattern were numerically strikingly modest compared to those previously reported. This probably reflected the intention to elucidate the contribution of reduced renal function as such to the dyslipoproteinemia of renal failure, a condition often associated with confounding factors. Significant increases in serum concentrations of triglycerides and apolipoprotein CIII were already observed in moderate renal failure, whereas serum concentrations of high density lipoprotein cholesterol and plasma LPL activities were decreased only in severe renal failure. Plasma LPL activities were not significantly reduced in hemodialysis patients (probably due to anticoagulation with low molecular weight heparin), but serum concentrations of triglycerides and apolipoprotein CIII were significantly increased. A multiple regression analysis, taking glomerular filtration rate, LPL and apolipoprotein CIII into account, showed that both plasma LPL activity and serum apolipoprotein CIII concentration independently predicted serum triglyceride concentration. However, serum apolipoprotein CIII concentration was a much stronger predictor than plasma LPL activity. Thus, a decrease in LPL activity does not seem to be a prerequisite for the hypertriglyceridemia of uremia, but it probably accentuates this condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that reduced lipoprotein lipase activity is not a primary pathogenetic factor for hypertriglyceridemia in renal failure. 747 64

During 1984 to 1991, 54 out of 569 lupus nephritis patients at Siriraj Hospital were male (F:M sex ratio = 10:1). Mean age of the males was 29.8 +/- 14.6 years, range 12 to 69. The three most common extrarenal manifestations were anemia, cutaneous, and musculoskeletal involvement (74.5, 51.1, and 43.9%, respectively). The major renal manifestations were edema (75.9%) with heavy proteinuria over 3.5 g/day in 62.2% and nephrotic/nephritic findings in 51.9% of cases. Hypertension was found in 35.2%. Mean serum creatinine was 2.0 +/- 1.4 mg/dl while 60.5% of cases had creatinine clearance below 50 ml/minute. Mean serum albumin was 2.6 +/- 0.8 g/dl, cholesterol 262.8 +/- 129.5 and triglycerides 343.2 +/- 244.6 mg/dl. Interestingly, hypercholesterolemia (> 250 mg/dl) was found only in 44.8% of cases with nephrotic syndrome. Antinuclear antibody was demonstrated in 91.5%, anti-dDNA antibody in 64.4% and LE cells in 40.4% of cases. Renal biopsy was done in 45 patients and 30 cases (66.7%) were classified as diffuse proliferative nephritis (WHO type IV), 15.6% of type II, 6.7% each of type III and V, with the rest of type V plus IV (4.4%). Tubulointerstitial inflammation was found in 77.3% of cases. During the follow-up period (42 +/- 35.8 months), 6 patients died. The cause of death were uremia in 3, infection in 2, and cardiac failure in 1. By life-table analysis, the probabilities of survival for 1 and 5 years were 89.5 and 80.6%, respectively. In comparison between sexes, except for a higher amount of urinary protein excretion (4.5 +/- 3.1 vs 3.5 +/- 3.0 g/day, p < 0.05), there were no statistically significant differences in clinical and pathological parameters, and probability of survival.
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PMID:Lupus nephritis in males: 8-year experience at Siriraj Hospital. 761 14

The prognosis of lupus nephritis patients in Thailand has been reported to be poorer than that in Western countries since 1978. After a great evolution in management, we re-evaluate the long-term outcome in patients who were treated and followed up at Siriraj Hospital in Bangkok from 1984 to 1991. Clinical and pathologic records were collected from 569 patients (515 females and 54 men) who were followed up for a mean period of 38.7 +/- 34.6 months. The mean age was 28 +/- 10 years and the median duration of symptoms prior to admission was 7 months. Hypertension was diagnosed in 32.4% of patients and 41.3% had serum creatinine greater than 1.5 mg/dL. Nephrotic-range proteinuria was found in 43.6% of patients and creatinine clearance less than 50 mL/min was found in 58.0%. Of the 314 patients who underwent renal biopsy, the most common histologic finding was diffuse proliferative glomerulonephritis (61.5%). The overall probability of survival was 76.5% at 60 and 90 months after diagnosis. Initial presence of hypertension, renal insufficiency (creatinine clearance < 25 mL/min), and World Health Organization histology class IV and III in the biopsied patients were the three independent factors significantly associated with lower survival probability. Neither gender nor amount of proteinuria was the predictive factor for poor outcome. During the follow-up period, 89 patients died and two patients entered a chronic dialysis program. The two leading causes of death were infection (50.5%) and uremia (28.6%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lupus nephritis in Thailand: clinicopathologic findings and outcome in 569 patients. 764 34

Chronic spinal cord injury, when complicated by chronic suppurative infections, has replaced chronic tuberculosis as a leading cause of secondary amyloidosis. Renal involvement with secondary amyloidosis is characterized by the presence of nephrotic range proteinuria and an increased incidence of renal vein thrombosis. Two cases of acute renal vein thrombosis associated with secondary amyloidosis in patients with spinal cord injury are presented. In both cases, a past history of extensive decubitus ulcerations and urinary tract infections preceded the development of nephrotic range proteinuria. In case 1, nonoliguric acute renal failure occurred after the development of acute bilateral renal vein thrombosis. The patient declined dialytic therapy and expired with uremia. In case 2, worsening renal function and increased proteinuria resulted after the development of acute unilateral renal vein thrombosis. These cases include the clinical and anatomic findings of acute renal vein thrombosis that occur as a complication of secondary amyloidosis. Acute renal vein thrombosis should be considered whenever an acute change in renal function or increase in proteinuria is noted in this setting.
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PMID:Case report: acute renal vein thrombosis in patients with spinal cord injury and secondary amyloidosis. 804 53

The renal concern in a multiple myeloma (MM) case has a frequency of 50% and causes a worsening of the disease with a survival average of about 12 months. The monoclonal light free chains (CLL) produced in excess by the plasmacytes are present in the urine as proteinuria of Bence Jones (PBJ) in 60-70% of patients affected by MM. They represent the major pathogenetic factor of the nephropathy in course of MM as they can deposit in shape of intratubular "casts" in the myeloma casts nephropathy (MCN). In some worse cases, dehydration or hypercalcaemia can cause an irreversible acute renal insufficiency (RI). It is therefore important in a patient affected with MM with PBJ to prevent, locate and opportunely treat these situations which worsen the nephropathy. Beside the tubular cast nephropathy, the CLL "accumulate" in the kidney even though with a lower frequency compared to MCN, in the light chains deposition disease (LCDD) and in the amyloidosis AL (AL). LCDD is characterized by a deposit of nodular amorphous materials PAS positive in the glomerulus and sometimes even in the tubulus. It usually presents itself as a chronic RI and a proteinuria causing nephrotic syndrome (NS). This quickly evolves into uraemia and its evolution can be lessened by the MM treatment. AL in course of MM also reveals with a chronic RI and NS. CLLs deposit in the typical fibrillar structure, on the vessel walls, in the glomerulus, in the mesangium and can be marked out with the Congo red colouring and the subsequent green birefringence through microscope with polarized light. Prognosis of AL is extremely severe and no benefit is given by the treatment of the hematological illness. It is therefore absolutely necessary to study the renal histology through biopsy when MM is grade B, that is, with serumal creatinine above 2 mg/dl as: MCN imposes the MM treatment programme in order to reduce the tubular excess of PBJ and to attempt to make RI reversible; MCN with tubular atrophy and interstitial fibrosis results in an unfavourable prognosis as it expresses a nephropathic irreversibility due to the loss nephrons. It will therefore necessary to start on a renal substitutional treatment programme. Renal damage in course of MM is not always tubular, rather an unexpected glomerular damage of LCDD or amyloidosis AL type can be found.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The kidney in multiple myeloma. The physiopathological and clinical aspects]. 818 90

We observed 12 boys and 1 girl, 5-15 years old, presenting with acute renal failure (ARF) and severe hypertension. They constituted 4.9% of all patients with ARF. There was no preceding diarrheal or respiratory prodrome. Clinical and laboratory findings were indicative of hemolytic uremic syndrome (HUS) in 4, but obscure in 9 others. Renal biopsies revealed variably severe occlusive thrombotic microangiopathy (TMA) affecting predominantly interlobular arteries in 8 and both arteries and glomeruli in 5 cases. Glomerular crescents and cortical necrosis were not seen. Following supportive therapy, 8 progressed to or died of uremia; 2 showed persistent proteinuria, 1 moderate hypertension and 2 complete recovery. Our observations indicate that renal TMA without a prodromal illness and typical features of HUS may present with ARF, proteinuria and severe hypertension, and is associated with high mortality.
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PMID:Acute renal failure and severe hypertension in children with renal thrombotic microangiopathy. 819 Jan 82

Kidney tissue of acceptable quality was available from autopsies of 55 patients who had been followed prospectively for 3 to 15 years as participants in the University Group Diabetes Program, a study of vascular disease in Type 2 (non-insulin-dependent) diabetic patients. Slides were prepared for light microscopic reading by uniform histologic techniques, and then were randomly intermixed and coded with tissues identically prepared from matched non-diabetic subjects (morphologic controls). After independent review by three morphologists, the results were tabulated and assigned to one of four diagnostic groups: 1) typical diabetic nodular glomerulosclerosis; 2) mesangial changes suggestive of diabetes (diffuse lesion); 3) non-diabetic renal disease; 4) normal for age. Of the diabetic cases 31% (17 of 55) were found to show nodular glomerulosclerosis, and another 47% (26 of 55) showed suggestive changes; none of the morphologic control slides was read as showing nodular glomerulosclerosis, but some were judged to show suggestive mesangial (diffuse) changes. Although only 4 of the 17 diabetic patients with nodules had died of uraemia, many had hypertension, which may have contributed to their deaths from vascular disease. The patients with nodular glomerular changes also showed, on the average, the highest blood glucose levels during life. Type 2 diabetes in later life appears to be associated with a high risk for typical tissue changes of diabetic kidney damage, which may contribute significantly to morbidity and mortality and may be present before azotaemia and qualitative proteinuria have been recognized.
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PMID:Glomerulosclerosis in type 2 (non-insulin-dependent) diabetes mellitus: relationship to glycaemia in the University Group Diabetes Program (UGDP). 824 55


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