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)

In a retrospective study the incidence and consequences of acute renal failure were evaluated in 324 renal transplantations performed in our centre. The overall incidence of acute renal failure was 31.2%. In recipients with acute renal failure, patient and graft survival were significantly worse than in those without acute renal failure (P less than 0.02 and P less than 0.0001 respectively). Acute renal failure also increased the morbidity during the first 3 months after transplantation. Three months after transplantation renal function as determined by serum creatinine and proteinuria, was less satisfactory. Factors influencing the incidence of acute renal failure appeared to be: match grade on the AB locus, percentage of antibodies, duration of dialysis, number of blood transfusions prior to transplantation, anastomosis time and total ischaemia time. Recipients transplanted for the first time were less likely to develop acute renal failure, but also for this group total ischaemia time was a prognostic factor for the development of acute renal failure. When recipients were allocated to different classes of total ischaemia time it appeared that the incidence of acute renal failure differed, especially between groups with total ischaemia time 32-36 h (27%) and 36-40 h (38%). The difference in acute renal failure between these groups was also reflected in a difference in graft survival for total ischaemia time less than 36 h and greater than 36 h. Thus, it appears that acute renal failure has a detrimental effect on graft survival and postoperative morbidity in renal transplantation. Total ischaemia time is one of the prognostic factors for the development of acute renal failure. To improve renal transplantation results it is worth attempting to shorten total ischaemia time.
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PMID:Detrimental effect of acute renal failure on the survival of renal allografts: influence of total ischaemia time and anastomosis time. 177 54

Five patients (median age 63 years) with severe crescentic glomerulonephritis had acute renal failure (median plasma creatinine 930, range 690-1390). Following induction of immunosuppressive treatment all patients achieved recovery of adequate renal function (median creatinine 440, range 290-570 mumol/l). After 3-6 months of continuous remission, all patients, despite stable renal function developed increasing proteinuria (median 4.4 g/24 h, range 3.2-6.1), and enalapril (5-20 mg per day) was substituted or introduced as antihypertensive therapy. Immunosuppression was not altered. After 1 year, renal function remained stable in four patients and plasma creatinine increased initially in one patient before becoming stable: proteinuria was reduced substantially in all patients to a median of 0.8 g/24 h, range 0.2-1.3). Patients with severe crescentic glomerulonephritis may develop persistent or increasing proteinuria despite successful treatment of acute disease. We have used enalapril to reduce proteinuria and maintain function in such patients.
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PMID:Effect of enalapril on proteinuria and renal function in patients with healed severe crescentic glomerulonephritis. 179 92

A 31 year old man first developed steroid-resistant idiopathic membranous glomerulonephritis in 1981. Stable normal renal function was maintained until August 1988 when he suffered a clinical relapse with heavy proteinuria and declining renal function. Immunosuppressive therapy with prednisolone and cyclophosphamide was instituted in an attempt to arrest this relapse. Despite this, he later developed acute renal failure with histological evidence of crescentic transformation of his nephritis. This unusual transformation was not associated with features of systemic vasculitis or positive anti-glomerular basement membrane and anti-neutrophil cytoplasmic antibodies.
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PMID:Crescentic transformation in primary membranous glomerulonephritis. 192 31

Acute renal failure (ARF) or renal dysfunction (RD) associated with germanium-induced nephrotoxicity has been reported in 18 patients since 1982. In 2 of these cases the patients died of acute renal and cardiogenic failure. In 17 of 18 cases biopsies showed vacuolar degeneration in renal tubular epithelial cells in the absence of glomerular changes, without proteinuria or hematuria. Accumulated elemental Ge intake in 17 patients over a period of 4 to 36 months ranged between 16 and 328 g, or more than 100 to 2000 times the average estimated dietary intake of Ge for man (1.5 mg/d; range 0.40 to 3.40 mg/d). The biological half-life of Ge is 4.5 days for kidneys, the highest retention level of any organ. The mean concentration of Ge in healthy adult kidneys is 9.0 mg/kg wet weight. In 3 patients studied with Ge-induced RD or ARF, urinary Ge excretion was 9, 15, and 60 ng/mL, compared to greater than 5 ng/mL in healthy controls, and remained elevated even 12 months after discontinuing supplemental Ge intake. The mechanism for Ge-induced nephrotoxicity remains unknown, although the suspected cause is the inorganic Ge salts, such as germanium dioxide. Sufficient evidence for a role of organogermanium compounds, such as carboxyethyl germanium sesquioxide or citrate-lactate germanate, in Ge-induced nephrotoxicity remains lacking. The recent introduction of over-the-counter Ge "nutritional" supplements in some countries increases the risk of additional cases of Ge-induced nephrotoxicity, especially if appreciable levels of inorganic Ge salts are present and consumed for long periods (greater than 3 months) at levels above the average daily estimated dietary intake for Ge.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nephrotoxicity in humans by the ultratrace element germanium. 192 11

A 37-year-old Caucasian male homosexual presented with hematuria and rapidly progressive acute renal failure. He was found to have proteinuria and microscopic hematuria as well as RBC casts. Investigations revealed polyclonal gammopathy with five times normal serum IgA levels as well as elevated serum IgG. Renal biopsy showed evidence of crescentic IgA nephropathy with ultrastructural changes of tubuloreticular inclusions described in HIV nephropathy. He was found to be positive for human immunodeficiency viral antibodies. Renal function improved during follow-up after two doses of 1 g each of methylprednisone. In our opinion, this is the first case of HIV-related crescentic IgA nephropathy. HIV testing should be performed more frequently in patients presenting with acute glomerular diseases.
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PMID:Crescentic IgA nephropathy as a manifestation of human immune deficiency virus infection. 180 45

We present two patients with Hantaan virus infection, admitted to the Department of Nephrology, Skopje, at the same time, with the same clinical presentation (chills, fever, abdominal pain, hemorrhages, nausea, headache, proteinuria, hematuria, oliguria, acute renal failure) but with different pathohistological findings and different disease courses. In the first case diffuse proliferative glomerulonephritis was found, with a complete recovery of renal function after a month, with a mild proteinuria and erythruria during the second and the third month. In the second case, glomeruli were normal in general, with slight mesangial proliferation found in two out of twenty, but interstitial edema, lymphocyte infiltrations and tubular changes were noted. Complete recovery was not noted after 3 months of follow-up. The patient is now without hemodialysis treatment, with polyuria, in the stable phase of chronic renal failure which is not improving.
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PMID:Different pathohistological presentations of acute renal involvement in Hantaan virus infection: report of two cases. 198 98

Acute glomerulonephritis is characterized by the presence of hematuria, proteinuria and edema, and often hypertension and acute renal failure. Acute post-streptococcal glomerulonephritis is the prototypic disease of acute glomerulonephritis. It is seen after both streptococcal pharyngeal and skin infections with a latency period from infection to presentation of 7-14 days and 14-21 days respectively. Approximately 90 percent of post-streptococcal glomerulonephritis occurs in young children. The diagnosis is made by supporting evidence of recent streptococcal infection, a positive ASO-titer or Anti-DNAase B titer, with associated hypocomplementemia. The disease is self-limited and generally requires only supportive therapy with resolution occurring over a period of weeks to months. There are generally no permanent sequelae in children. Adults may have a higher incidence of hypertension and chronic renal failure as a result of post-streptococcal glomerulonephritis.
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PMID:Acute post-streptococcal glomerulonephritis. 200 61

We performed a retrospective chart analysis on 449 AIDS patients admitted to Bellevue Hospital Center from 1983-1986 to characterize the etiologies and clinical course of acute renal failure (ARF) and to define the incidence and clinical course of AIDS-associated nephropathy (AAN) in an unselected hospitalized AIDS population. Defining ARF as a rise from baseline serum creatinine of at least 2.0 mg%, we found 88 cases (a prevalence of almost 20%) or 14.5 cases per 100 admissions. Volume depletion was the most common etiology and was as severe a cause of ARF as other etiologies. There were 21 cases of ARF in 17 patients with a peak serum creatinine greater than or equal to 6.0 mg%. Volume depletion accounted for 7/21 of these cases. Baseline renal insufficiency existed in 9/17 patients (12/21 cases) and volume depletion was the cause of ARF in 3 of these cases. Only 4 cases required dialysis. There were 34 patients (prevalence of 7.6% or 3.0 cases per 100 patient-years) with otherwise unexplained chronic renal insufficiency and/or persistent qualitative or quantitative proteinuria and thus were defined on clinical grounds to have AIDS-associated nephropathy. Thirty-two of these patients (94%) had evidence of AAN at or within 1 year of presentation. Eleven patients (32%) reached ESRD (serum creatinine greater than or equal to 6.0 mg%); 9 patients did so within 1 year of presentation and 3 required dialysis. In those with adequate follow-up (9 cases), the mean survival from time of ESRD was 25.5 days and all cases died within 6 months of reaching ESRD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute and chronic renal disease in hospitalized AIDS patients. 160 80

There are currently no reliable early markers of renal tubular damage. Since aminoaciduria is an accompanying feature of this condition, the usefulness of increased urinary amino acid excretion as a marker was investigated by inducing renal tubular necrosis in male Wistar rats by the administration of gentamicin (40 mg/kg/d) for 14 d. Plasma amino acids, urea, creatinine, protein and electrolytes, and urine amino acids, protein and N-acetylglucosaminidase (a lysosomal enzyme) were measured over a 20 d period. Amino acid excretion increased dramatically within 24 h of the initial dose for 14 of the 16 amino acids measured. The conventional renal disease markers listed above did not increase until after day 7. Glomerular damage caused by puromycin aminonucleoside did not induce aminoaciduria until marked proteinuria occurred (day 9), and even then amino acid excretion was much less than that caused by gentamicin. To distinguish whether the gentamicin-induced aminoaciduria was a consequence of tubular damage or inhibition of amino acid transport, isolated rat kidneys were perfused with a Krebs-Henseleit albumin buffer with and without gentamicin for 20 min, during which time urinary amino acids were quantitated. Gentamicin did not inhibit amino acid reabsorption. Thus, it appears that in the rat-gentamicin model of acute renal failure, urinary amino acids are early markers of renal tubular damage.
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PMID:Aminoaciduria is an earlier index of renal tubular damage than conventional renal disease markers in the gentamicin-rat model of acute renal failure. 206 Jan 88

The patient was a 74 years-old male who had suffered arthralgia since April 1986. Gold therapy was performed from June 1986 based on a diagnosis of rheumatoid arthritis (RA). This treatment was ineffective and administration of D-penicillamine (D-Pc) was started from March 1987, which alleviated the arthralgia. However, proteinuria appeared, and the nephrotic syndrome (NS) and acute renal failure (ARF) gradually developed. Four items, not including the renal symptoms, fulfilled the diagnostic criteria for systemic lupus erythematosus (SLE). Thereafter, D-Pc was withdrawn, and the symptoms were improved by hemodialysis and steroid therapy. This case was considered to be NS and ARF caused by treatment of RA with rather small doses of D-Pc (18.3 g in total), but the involvement of other factors could not be ruled out. Since the four items conforming to the SLE diagnostic criteria were alleviated by steroid therapy, the case was considered to be drug-related lupus-like syndrome. In recent years, D-Pc has frequently been used in the treatment of RA and its effects have been confirmed. However, side effects often appear, and considerable caution is required in the presence of drug-related SLE as well as proteinuria. When drug-related SLE is suspected, withdrawal of the drug concerned and steroid therapy appear to be useful.
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PMID:[A case report of rheumatoid arthritis which showed acute renal failure, nephrotic syndrome and drug-related lupus-like syndrome caused by D-penicillamine]. 208 56


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