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)

Clinical usefulness of Essential Laboratory Tests (1), proposed by Japan Society of Clinical Pathology, was retrospectively evaluated in 500 outpatients who first visited the medical clinic of a prefectural general hospital. Sixty percent of the patients were diagnosed with gastrointestinal disease or respiratory disease. Performance rates of urinalysis, blood counts, serum total protein, A/G ratio, C-reactive protein, erythrocyte sedimentation rate and fecal occult blood were 87.6%, 55.8%, 49.6%, 48.8%, 37.8%, 10.0% and 5.6%, respectively. Abnormal test results rate of urinalysis, blood counts, serum total protein, A/G ratio, C-reactive protein, erythrocyte sedimentation rate and fecal occult blood were 12.3%, 12.9%, 14.1%, 5.7%, 21.6%, 22.6% and 25.9%, respectively. The clinical diagnoses and the abnormal test results indicated that the patients general condition was assessed properly from the A/G ratio, 92% of patients with proteinuria were transient cases and urobilinogen has poor sensitivity and specificity for the diagnosis of liver diseases.
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PMID:[Clinical usefulness of essential laboratory tests]. 150 72

A 51-year-old woman had been suffering from blood-stained purulent sinusitis and antibiotic-resistant bouts of fever for 4 months. She had microhematuria and serological evidence of inflammation (erythrocyte sedimentation rate [ESR] 92/135 mm, C-reactive protein 5.0 mg/dl). When she was admitted to hospital suspected of having postinfectious glomerulonephritis she complained of spontaneous colic-like pains in the left flank. Within one day the haemoglobin concentration fell from 10 to 6.5 g/dl. Ultrasound and computed tomography demonstrated a large space-occupying lesion around the left kidney. At operation this was found to be a rupture of the kidney with perirenal bleeding which was treated without removing the kidney. No biopsy was taken, but serological tests showed antineutrophil cytoplasmatic antibodies (cANCA), indicating Wegener's granulomatosis as the cause of the compensated renal insufficiency and spontaneous renal rupture. Under immunosuppressive treatment the inflammatory signs (ESR 18/44 mm), fever, chronic maxillary sinusitis, raised serum creatinine concentration and the ANCA titre all regressed, while proteinuria of about 4 g/24 h persisted. There was no recurrence during a follow-up period of 15 months. Serological signs of marked inflammatory activity, urinary sediments of nephritis and spontaneous retroperitoneal bleeding should suggest that, in addition to lupus erythematodes and panarteritis nodosa, Wegener's granulomatosis be included in the differential diagnosis.
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PMID:[Spontaneous kidney rupture as an early complication of Wegener's granulomatosis]. 154 1

Haemostatic activation was measured in patients with either non-diabetic chronic renal failure (CRF) or diabetic nephropathy. We have investigated the relationship between these haemostatic markers and the rate of progression of renal failure. When compared with age- and sex-matched healthy controls, both patient groups showed significantly elevated plasma concentrations of D dimer, von Willebrand factor antigen (vWFAg), and C-reactive protein (CRP) (all P less than 0.001), as well as an increase in spontaneous platelet aggregation (P less than 0.01). Plasma concentration of platelet factor 4 was slightly but not significantly increased. Serum thromboxane was subnormal (P less than 0.01). Multiple regression analysis showed that in non-diabetic CRF proteinuria and serum TxB2 were independently related to the rate of progression of renal failure; in diabetic nephropathy proteinuria and vWFAg were independently related to the rate of progression. In both groups the relationship was stronger with proteinuria (standardised regression coefficients 0.56 and 0.45 respectively) than with serum TxB2 (0.29) or with vWFAg (0.37). We have found haemostatic activation in both non-diabetic and diabetic progressive renal failure. Proteinuria, and also in this study serum TxB2 and vWFAg, appear to be determining factors in the progression of renal failure, and their measurement may have prognostic value.
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PMID:Haemostatic activation and proteinuria as factors in the progression of chronic renal failure. 205 12

Twenty-five patients (seven male, 18 female) were diagnosed as having the loin pain and haematuria syndrome. Presenting symptoms were either loin pain alone or pain associated with macroscopic or microscopic haematuria, and were longstanding, having been present for mean of 9.3 years in males, and 10 years in females. Ten patients described symptoms of passing gravel or renal stones but these were only demonstrated radiologically in two patients. Investigation of all patients showed anatomically normal renal tracts, normal renal function, and no significant proteinuria. Phase-contrast microscopy during episodes of haematuria revealed dysmorphic red cells in all 10 patients studied. Renal biopsies were performed in 20 patients and showed no glomerular pathology, but arteriolar and arterial hyalinosis was seen in 13 of 20 (65 per cent), fibro-elastosis in larger vessels in eight of 20 (40 per cent) and red blood cells in tubules in 13 of 20 (65 per cent) patients. The histological appearance in vessels was similar to that seen in cyclosporin A nephrotoxicity and would be consistent with the hypothesis that regional vasospasm occurs in the cortical circulation. Haematological studies in 22 patients, when compared with age and sex matched controls, showed the presence of circulating platelet aggregates, elevation of plasma beta-thromboglobulin (p less than 0.001), and increased platelet aggregation in response to serotonin and ADP (p less than 0.05 and p less than 0.03, respectively). Plasma concentrations of D dimer (p less than 0.02) and C-reactive protein (p less than 0.03) were also significantly elevated in the patient group. There was no deterioration of renal function during a mean observation period of 3.7 years and no patients developed proteinuria. Treatment was largely supportive; seven patients with intractable loin pain underwent surgical denervation with the relief of pain in four.
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PMID:Haemostatic changes in the loin pain and haematuria syndrome: secondary to renal vasospasm? 223 80

Clinical symptoms and laboratory measures of renal and liver function, coagulation, and inflammatory parameters were prospectively studied in 74 hospitalized patients (14-74 years of age) with serologic evidence of nephropathia epidemica. The most common clinical findings were acute onset of symptoms, fever (greater than or equal to 38 degrees C), thirst, headache, nausea, back pain, vomiting, myalgia, and abdominal pain. Twenty-seven patients (37%) had hemorrhagic manifestations, i.e., epistaxis, melena, hematemesis, petechial bleeding, macroscopic hematuria, or metrorrhagia. Disseminated intravascular coagulation developed in four patients. Fifty-one percent had thrombocytopenia. Proteinuria was recorded for all patients, while hematuria and glucosuria were noted for 85% and 58%, respectively. Serum creatinine levels were elevated in 71 (96%) of the patients. Levels of C-reactive protein or erythrocyte sedimentation rates were elevated in all cases, usually to levels found in serious bacterial diseases. Sixty-six (89%) of the patients were followed for up to 7 months, at which time all had recovered clinically. No patient died or required dialysis. We conclude that nephropathia epidemica in Sweden has a clinical picture similar to that of hemorrhagic fevers in other parts of the world, but with a milder course and a better prognosis.
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PMID:Clinical characteristics of nephropathia epidemica in Sweden: prospective study of 74 cases. 257 3

Serial six hourly urine collections were made for seven days on 20 patients with acute pancreatitis. Quantitative immunoassay of urinary albumin and IgG on the first urine sample after admission showed increased excretion rates in 14 and 13 patients, respectively. Urinary protein excretion rates remained normal or approached normal by seven days in 17 patients who made uneventful recoveries. The maximum urinary excretion rates of both albumin and IgG within the first 36 hours correlated with the serum C-reactive protein concentration 72 hours after admission. The highest IgG excretion rates were found in three patients who later developed severe complications. These preliminary data suggest that low proteinuria is a very early response in acute pancreatitis, and that it may reflect the severity of inflammation.
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PMID:Is low proteinuria an early predictor of severity of acute pancreatitis? 258 23

We have prospectively evaluated the clinical and immunological features of serum sickness in 35 patients treated for bone marrow failure with anti-thymocyte globulin (ATG 15 mg/kg/day) and methylprednisolone (1 to 1.5 mg/kg/day). Twenty-one patients were treated for 10 days and 14 were treated for 28 days. Clinical evidence of serum sickness developed in 30 patients (86%) and included fever and malaise (100%), cutaneous eruptions (93%), arthralgias (67%), gastrointestinal complaints (67%), cephalgia (57%), blurring of vision (37%), arthritis, (30%) and lymphadenopathy (13%). Clinical serum sickness began on day 7 +/- 1 (X +/- S.E.M.) and lasted for 10 +/- 2 days in the 18 affected patients receiving the shorter course of ATG. In the 12 affected patients receiving the longer course of ATG, serum sickness began on day 9 +/- 1. The earliest manifestations of serum sickness were fever, malaise, and cutaneous eruptions. Cutaneous findings consisted of morbilliform eruptions (n = 19) and urticaria (n = 1) or a combination (n = 8) that lasted 10 to 14 days. Twenty-one patients (75%) developed a highly characteristic serpiginous band of erythema and purpura along the sides of the fingers, toes, palms and soles 12 to 48 hours before other symptoms of serum sickness. Biopsies of lesional skin during the course of serum sickness revealed immune deposits (IgM, IgE, IgA and C3) in dermal vasculature in 7 of 9 patients. Immunological changes that occurred during the course of serum sickness included increased serum levels of IgG, IgM, IgA, and IgE. Circulating immune complexes, as measured by the C1q-binding assay, increased from a mean value of 12% to 45% on day 13 +/- 1. Complement levels (C3, C4, and CH50) decreased 50 to 80% from their baseline levels on day 10 +/- 2. Acute phase reactants increased: erythrocyte sedimentation rate, C-reactive protein and beta-2 microglobulin. Abnormal urinalysis developed in 17 patients (57%) over the course of serum sickness and included proteinuria, hematuria and hemoglobinuria on day 10 +/- 3. Hematopoietic response occurred in 43%. All 5 patients who did not develop serum sickness recovered from bone marrow failure. Our data document the clinical and immunopathological findings in human serum sickness and suggest that the principles of antigen-antibody interaction, complement activation, and resultant inflammatory response as seen in the previous animal studies are directly applicable to studies of patients with serum sickness.
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PMID:Human serum sickness: a prospective analysis of 35 patients treated with equine anti-thymocyte globulin for bone marrow failure. 325 88

Daily blood and 24-hour urine samples from 6 runners were studied for 2 days before and for 5 days after a 42.2 km. marathon footrace run in cool environmental conditions. Although the race caused muscle damage as shown by the increased post-race serum creatine kinase activity and C-reactive protein levels, renal function measured by urine flow rates, creatinine clearance and protein excretion was normal during the race. Sodium and fractional sodium excretion decreased during the race despite a maintained osmolar clearance, and remained low for the next 48 hours, whereas osmolar clearance decreased sharply for the remainder of the race day but it was significantly elevated on days 2 to 4 after the race. Creatinine clearance was increased significantly 24 hours after the race, and reached its peak 3 days after the race, while urine flow rates were elevated from days 2 to 5 after the race. Urea excretion was significantly decreased 3 to 5 days after the race, while creatinine excretion was increased significantly on day 3 after the race. Glomerular proteinuria occurred 24 hours after the race with no associated reduction in tubular reabsorption of the low molecular weight protein beta-2-microglobulin. This study shows previously unrecognized substantial delayed effects of prolonged exercise on renal function. The nature of these changes may reflect catabolic followed by anabolic processes in muscle as well as changes consequent on excess sodium retention and related fluid compartment shifts.
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PMID:The immediate and delayed effects of marathon running on renal function. 377 85

It is reported on the course of histologically ascertained Wegeners' granulomatosis in 4 patients. After initial affection of the upper respiratory tract in form of necrotizing and granulomatous inflammations in all cases a generalisation of the disease with above all early and severe participation of the kidneys developed. Maximum acceleration of sedimentation, C-reactive protein, anaemia, leucocytosis, eosinophilia, thrombocytosis, enlargement of the number of alpha 2-globulins, increase of creatinine, proteinuria, erythrocyturia and leucocyturia are the most frequent pathological laboratory findings, whereas LE-cells, ANF, rheumatoid factor and decrease of the complement never could be proved. By reason of a pathogenic immunoreaction a combined glucocorticoid therapy and immunosuppressive therapy with prednisolone and cyclophosphamide may favourably influence the course of the disease which is otherwise prognostically infaust.
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PMID:[Wegener's granulomatosis with pronounced kidney involvement]. 725 36

Since 1987, we have experienced 11 children with acute renal failure (ARF) associated with Yersinia pseudotuberculosis (YP) infection. The illness began with the sudden onset of high fever, skin rash and gastrointestinal symptoms. Later in the course, periungual desquamation developed, mimicking Kawasaki disease. Elevated erythrocyte sedimentation rate, C-reactive protein and thrombocytosis were noticeable, and mild degrees of proteinuria, glycosuria and sterile pyuria were common. ARF, which typically developed about 1-3 weeks after the onset of fever, underwent a benign course with complete recovery. The renal biopsies mainly revealed findings of acute tubulointerstitial nephritis. YP should be considered as one of the causes of acute tubulointerstitial nephritis causing ARF, especially in children.
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PMID:Acute renal failure associated with Yersinia pseudotuberculosis infection. 747 20


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