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)

A 42-year-old female was admitted to a hospital, because of acute hepatitis A. Laboratory data were GOT 8210mU/ml. GPT 4650mU/ml, LDH 11860mU/ml, total bilirubin 4.7mg/dl, BUN 19.5mg/dl and creatinine 1.9mg/dl. Urinalysis showed proteinuria 3+ and occult blood 1+. Soon after admission, she suffered from anuric acute renal failure and was transferred to our hospital for hemodialysis. Her urine-volume was under 20 ml per day. Urinalysis showed proteinuria 4+, occult blood 1+ and casts. Laboratory data showed BUN 58.2mg/dl and creatinine 8.5mg/dl. She was treated by hemodialysis for 35 days, before recovering from renal failure. However, her renal function did not recover perfectly and her 24-hour creatinine clearance remained at 50ml/min after 6 months. Renal biopsy was performed on the 17th day after admission. Examination by light microscopy revealed the findings of acute tubular necrosis and examination by immunofluorescence antibody method was negative. Urinalysis of 8 patients with acute hepatitis A showed that all patients had proteinuria at the onset. Patients with acute hepatitis A have symptoms of appetite-loss, nausea, vomiting and/or diarrhea. These symptoms cause hypovolemia, and hepatic dysfunction causes discontrol of vasoactive hormones, which gives rise to disturbance of renal circulation. Subsequently, acute tubular necrosis and acute renal failure occur.
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PMID:[A case of acute hepatitis A associated with acute renal failure from the onset]. 823 Aug 22

Clinical manifestations and laboratory findings in 40 patients with thrombotic thrombocytopenic purpura (TTP) in Japan are reviewed. The most common clinical features were central neurological sings. jaundice, fever, hemorrhagic tendency, and renal abnormalities. Laboratory tests showed anemia, thrombocytopenia, hyperbilirubinemia, high serum LDH levels, and low serum haptoglobin levels. BUN and serum creatinine levels were elevated only in about 15% of the patients, although microscopic hematuria and proteinuria were observed more frequently (about 70%). Autoantibodies, such as antinuclear antibody and rheumatoid factor, were also observed in 4% to 9% of the patients. Coagulation and fibrinolysis studies showed normal values in the majority of the patients, suggesting intravascular generation of thrombin and plasmin was minimal in TTP.
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PMID:[Clinical manifestations and laboratory findings of thrombotic thrombocytopenic purpura]. 843 12

The clinical course of multiple myeloma (MM), ranging from relatively asymptomatic form to frankly aggressive neoplasia, is more variable than that of other hematologic malignancies. The nature of tumor cells and/or the secondary effects of malignancy as anemia, hypercalcemia, and renal failure have shown to correlate with clinical behavior of MM. Prognostic variables include age, degree of anemia, morphologic subtypes, serum creatinine and calcium levels, Bence Jones proteinuria, plasma cell LI%, beta 2MG level, nucleolus-associated J chains and other laboratory prognostic factors. The plasma cell LI% is the most reliable predictor of survival. Analysis of the presenting features and the clinical characteristics indicates that there are several variants of MM with a poor prognosis, including juvenile myeloma, plasma cell leukemia, aggressive myeloma, high LDH myeloma, J chain myeloma, and amylase-producing myeloma. Four relapsing patterns have been pointed out. The appearance of an additional M-component (mutation escape) suggests the terminal or advanced stage of illness. A new lambda-type M-component can be found in patients with kappa-type myeloma. The prognostic significance of Bence Jones escape varies for different stage of illness. Bence Jones escape is an important predictor of the development of overt MM in patients with smoldering MM. The need for clearly established prognostic criteria is imperative for the choice of correct therapeutic strategies.
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PMID:[The wide variations of the clinical behavior and prognosis in multiple myeloma]. 851 Mar 30

In 1982 Weinstein coined the term HELLP syndrome to describe a special group of pre-eclamptic women who had evidence of hemolysis, elevated liver enzymes and low platelets. The question of whether the HELLP syndrome exists as a distinct entity or is a part of a spectrum of pregnancy complications has long been a source of speculation and debate among obstetricians and internists. A review of the literature indicates that the syndrome occurs in post-partum from 20% to 30% of the cases; maternal mortality from 1% to 4% and perinatal mortality from 5% to 40%. Hypertension and proteinuria are frequently associated with HELLP syndrome, but may also be absent. The syndrome is a group of clinical and pathological manifestations resulting from an insult that leads to intravascular platelet activation (thrombocytopenia) and micro-angiopathic hemolytic anemia (elevated total bilirubin and LDH). Endothelial damage and vasospasm are responsible of hepatic hypoperfusion that results in liver damage, as indicated by a rise in circulating liver enzymes. Since natural evolution of HELLP syndrome is the disseminated intravascular coagulation (CID), the interruption of pregnancy is mandatory and irrespective of the gestational age. This is the reason of an high incidence of cesarean section. Visser and Wallemburg (1995) treated 128 pre-eclamptic patients with HELLP syndrome with volume expansion and pharmacologic vasodilatation under invasive haemodynamic monitoring; they tried to delay delivery with the aim of enhancing fetal maturity. A complete reversal of HELLP occurred in 43% of patients. Further investigations will be necessary to confirm this interesting experience.
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PMID:[The HELLP syndrome. Notes on its pathogenesis and treatment]. 876 57

We encountered a patient with enterohemorrhagic Escherichia coli (EHEC) O157:H7 infection and secondary hemolytic uremic syndrome (HUS). The patient was a 79-year-old woman with hypertension, constipation, and asymptomatic cholelithiasis. She complained of nausea and abdominal pain, and had bloody stool EHEC O157 was detected by fecal culture. The bloody stool resolved after treatment with antibiotics, but the patient was hospitalized on July 23, 1996 because of abdominal distention. HUS was diagnosed because of proteinuria, hematuria, thrombocytopenia, hemolytic anemia, fragmentation of red blood cells, and increased serum LDH. Treatment was focused on plasma exchange, administration of antibiotics, large doses of gamma-globulin, haptoglobin replacement, and anticoagulation. Within about 2 weeks, the level of hemoglobin, the number of platelets, and the serum LDH had normalized, and the patient recovered from HUS. The decreased intestinal movement continued. On August 23, acute cholecystitis was diagnosed, and percutaneous transhepatic gall bladder drainage was done. Another exacerbation was noted on October 13, and cholecystectomy was done on November 12, when the patient's status had improved after instillation of antibiotics. Macroscopically, the gallbladder wall was thickened. Histopathological examination showed diffuse infiltration of lymphocytes into the mucosa, chronic cholecystitis was diagnosed. Because the postoperative course was satisfactory, the patient was discharged from the hospital on December 15. Acute exacerbation of chronic cholecystitis might have been caused by decreased cholic excretion after the marked decrease in intestinal movement due to O157 infection and secondary HUS. Because elderly people frequently have anamnesis of the digestive system, considerably attention should be paid to the management of anamnesis, as well as O157 infection and secondary HUS.
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PMID:[Enterohemorrhagic Escherichia coli O157 infection in an elderly patient with secondary hemolytic uremic syndrome who developed recurrent acute exacerbation of chronic cholecystitis]. 977 57

Arterial hypertension, which represents a common problem in patients with renal transplant, contributes to the cardiovascular morbidity and mortality of these patients. The most usual immunosuppressive drugs (cyclosporine and FK-506) collaborate on the development of hypertension. Calcium channel blockers are the most habitually used antihypertensive drugs in this population, although its long-term hemodimamycs effects could be deleterious especially in transplanted patients with chronic graft nephropathy. Losartan, a specific blocker of angiotensin II (AT1) receptors, has demonstrated a potent antihypertensive effect with a good safety and tolerance profile. The glomerular effects of losartan could be useful in transplanted patients. The present open, prospective and multicenter study evaluated the efficacy and safety of losartan in the treatment of hypertension in a group of patients with a renal transplant. Seventy-six patients with systolic blood pressure > or = 140 and/or diastolic blood pressure > or = 90 mm Hg, and/or patients on therapy with one antihypertensive drug and related side effects were included. After inclusion, therapy with losartan 50 mg/24 hr was started, discontinuing the previous antihypertensive therapy and/or therapy which caused the side effects. At four weeks, if blood pressure (BP) was not controlled, hydrochlorothiazide 25 mg or furosemide 40 mg/24 hr was added. At baseline and at weeks 2, 4, 8 and 12, the following parameters were monitored: BP, creatinine, hematocrit, hemoglobin, glucose, ions, uric acid, cholesterol, triglycerides, bilirubin, SGOT, SGPT, GGT, LDH, calcium, phosphate, alkaline phosphatase, proteinuria, and both cyclosporine and FK-506 levels in whole blood. Sixty-seven patients completed the 12-week study period. Mean blood pressure decreased from 113 +/- 10 to 102 +/- 9 mm Hg at the end of the study (P < 0.0001); 38 of the 67 patients (56.7%) who completed the study had a SBP lower than 140 mm Hg and a DBP lower than 90. These blood pressures were obtained in 30 patients on monotherapy with losartan (78.9%). Proteinuria decreased significantly at week 4 and was confirmed at week 12, especially in patients with proteinuria > or = 300 mg/24 hr. Nine patients were withdrawn during the study period for different reasons. Serum creatinine showed a slight, non-clinically significant increase at week 4, remaining stable until the end of the study. Two patients developed a mild normocytic anemia, and three others presented a mild impairment of pre-existent anemia. No interactions with cyclosporine or FK-506 were described. These results indicate that losartan is effective in reducing BP in hypertensive patients with a renal transplant. It has a good tolerance profile and does not interfere with immunosuppressive therapy.
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PMID:Efficacy and safety of losartan in the treatment of hypertension in renal transplant recipients. 983 98

We report on a series of 26 patients diagnosed with primary (de novo) plasma cell (PC) leukemia (PCL) in whom we analyzed the clinicobiologic characteristics of the disease together with the immunophenotype, DNA cell content, proliferative index, and numeric chromosomal aberrations of the neoplastic PC, and compared them with 664 multiple myeloma (MM) patients at diagnosis. The median age, sex ratio, and bone lesion extension were similar, but PCL cases displayed a higher prevalence of clinical stage III, extramedullary involvement, and Bence Jones cases, with fewer IgA cases than for MM patients. In addition, according to several prognostic indicators (beta2-microglobulin serum level, proportion of S-phase PCs, proteinuria, calcium serum level, lactate dehydrogenase [LDH] and renal function), the incidence of adverse prognostic factors was significantly higher in PCL versus MM. Immunophenotypic expression was similar for CD38, CD138, CD2, CD3, CD16, CD10, CD13, and CD15, but PCL differed from MM in the expression of CD56, CD9 HLA-DR, CD117, and CD20 antigens. Twenty-two PCL cases were diploid and one was hypodiploid, while most MM cases (57%) showed DNA hyperdiploidy. With the fluorescent in situ hydridization (FISH) technique, 12 of 13 PCL cases displayed the numeric aberrations, -13 (86%), +/-1 (57%), +18 (43%), and -X in women (25%), but they lacked several numeric aberrations usually found in MM such as +3, +6, +9, +11, and +15. PCL cases had a lower overall response to therapy than MM cases (38% v 63%, P =.01332). Among PCL patients, a trend for a worse response was observed in cases treated with melphalan and prednisone (MP) versus polychemotherapy. Overall survival was significantly worse in PCL versus MM patients (8 v 36 months, P <.0001), but it was significantly better in PCL patients treated with polychemotherapy versus MP (18 v 3 months, P =.0137). By contrast, MM patients did not show significant differences in overall survival according to the treatment used, MP or polychemotherapy. Ten variables seemed to predict survival in PCL patients, but only the beta2-microglobulin level and S-phase PCs retained an independent value in multivariate analysis. In summary, our study illustrates that PCs from PCL display singular phenotypic, DNA cell content, and cytogenetic characteristics that lead to a different disease evolution versus MM.
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PMID:Primary plasma cell leukemia: clinical, immunophenotypic, DNA ploidy, and cytogenetic characteristics. 1061 Jan 15

We report a rare case with multiple renal infarction associated with lupus anticoagulant and SLE. A 20-year old woman presented with remitent fever, butterfly rash and, abdominal pain. Laboratory findings showed leukopenia, positive antinuclear and anti-DNA antibodies, and biological false positive for syphilis. Despite a therapy with prednisolone 25 mg/day, the patient showed hypocomplementemia, high titer of anti-DNA antibody and a development of proteinuria and an elevation of serum creatinine. Renal biopsy revealed no abnormalities. She presented abdominal pain with an elevation of serum LDH. Abdominal dynamic computed tomography demonstrated multiple perfusion defects in both kidneys indicating multiple renal infarction. Brain MRI showed multiple micro infarction in the anterior lobes. She was treated with 80 mg of aspirin and have been in remission for two years. Although there have been reported 18 cases with renal infarction associated with antiphospholipid syndrome, this is the first report in Japan. Renal infarction should be differentiated from renal involvement in patients with SLE who have antiphospholipid antibodies.
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PMID:[Multiple renal infarction associated with lupus anticoagulant in a patient with systemic lupus erythematosus]. 1043 52

A 81-year-old woman was admitted to our hospital because of edema and massive proteinuria on September 26, 1995. On admission, the palpebral conjuctiva were slightly anemic, and edema of the eyelids and legs was observed. Laboratory findings were as follows, urine protein(3+), occult blood(3+), WBC 2,600/microliter, Hgb 10.0 g/dl, reticulocytes 20@1000, TP 5.0 g/dl, Alb 2.7 g/dl, T-Cho 376 mg/dl, TG 194 mg/dl, LDH 763 U/l, haptoglobin < 93 mg/dl, Ham's test(+), sugar water test(+), and indirect coombs (+). The erythrocytes of this patient showed a negative population consisting of double negative erythrocytes evaluated by flow cytometric two-color analysis using monoclonal antibodies specific to CD55 and CD59. From these findings, the diagnosis of paroxysmal nocturnal hemoglobinuria(PNH) was made. The patient showed nephrotic syndrome and a renal biopsy was performed. The histological findings of renal biopsy showed focal and segmental sclerosis and adhesion of glomerular tufts. Interstitial fibrosis with atrophic tubules and lymphocyte infiltration were also observed. There was no specific staining of immunoglobulins and complement by immunofluorescence. The diagnosis of focal segmental glomerular sclerosis(FSGS) was made. There have been only three case reports of glomerular disease in patients with PNH, such as purpura nephritis, IgA nephropathy and membranous nephropathy. The complication of FSGS and PNH is every rare and there has been no report of FSGS in a case with PNH. The onset of PNH resulted from the loss of CD55 and CD59, which was critical in the onset of FSGS in the present case.
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PMID:[A case of paroxysmal nocturnal hemoglobinuria combined with focal segmental glomerular sclerosis]. 1121 17

Renal proximal tubular epithelial cells (PTEC) are target for LPS during sepsis and renal infections. In the present study, we evaluated whether stimulation of human PTEC by LPS is modulated through the soluble or the membrane form of the LPS receptor CD14. We found that PTEC lacked expression of the membrane form of CD14 and did not release soluble CD14 (sCD14). sCD14 was detected in the urine of normal subjects and it was increased in patients with renal sepsis or with proteinuria. In the presence of sCD14 and LPS binding protein (LBP), PTEC were 10 to 100-fold more sensitive to LPS activation, resulting in cytokine production (IL-6, IL-8 and TNF-alpha) and NO release. We found that sCD14 purified from urine was biologically active on PTEC. Moreover, the presence of sCD14 and LBP was required for cytotoxicity induced by low concentrations of LPS (1-10 ng/ml) in PTEC. Cell death showed the characteristics of both necrosis and apoptosis, as demonstrated by LDH release and by TUNEL and acridine orange staining and caspase-3 activation. Whereas the LPS alone was sufficient to induce necrosis, sCD14 and LBP were required for apoptosis. Our results suggest that sCD14 excreted in urine may participate with endotoxin in the activation and injury of renal proximal tubules. In particular, sCD14 may contribute to the tubulo-interstitial injury in clinical settings characterised by proteinuria and enhanced susceptibility to infections such as in diabetes.
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PMID:Urinary soluble CD14 mediates human proximal tubular epithelial cell injury induced by LPS. 1223 91


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