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)

Trichosporonosis due to Trichosporon beigelii or T. capitatum is an infrequent but potentially fatal invasive fungal infection in cancer patients. We studied epidemiologic, clinical, pathologic, and microbiologic features of this infection during a 7-year period at the University of Maryland Cancer Center. Fifteen patients with involvement by Trichosporon were identified: 5 were infected, 5 were possibly infected, and 5 were colonized but not infected by Trichosporon. Four of the infected patients had trichosporonemia and/or positive skin biopsy cultures as the first evidence of infection. The fifth infected patient had positive marrow and skin biopsy cultures. Serial surveillance cultures of infected patients showed preceding Trichosporon colonization in only 1 of 5 cases. Pulmonary infiltrates in 3 infected patients correlated at postmortem examination with Trichosporon pneumonia. Renal dysfunction marked by proteinuria, hematuria, red blood cell casts and azotemia correlated with widespread glomerular infiltration with the fungus. The five infected patients died of their infection, whereas the 2 possibly infected patients who died succumbed to their underlying illness. Trichosporonemia may have been averted in possibly infected patients because of a shorter median duration of profound (less than 100/microliter) neutropenia (5 days) when compared to that of infected patients (20 days). No environmental source of Trichosporon was found in environmental surveillance cultures of food, air, or inanimate surfaces. In vitro studies of three pathogenic strains showed resistance to 5-fluorocytosine but susceptibility to amphotericin B, ketoconazole, and miconazole. Norfloxacin augmented the in-vitro antifungal activity of amphotericin B. Trichosporon must be considered an opportunistic pathogen that can cause serious infections among patients with cancer.
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PMID:Trichosporonosis in patients with neoplastic disease. 352 14

A total of 10 episodes in 7 patients with leukemia or related disorders was treated with oral amphotericin B (AMPH). In 8 episodes AMPH were used prophylactically for severe neutropenia, and in the remaining 2 it was given when the patients were feverish. A daily dose of 2,400 mg of AMPH was given orally once a day and serum concentrations of AMPH were determined serially with bioassay. Two hours after administration, the mean serum concentration of AMPH rose to 0.15 microgram/ml, and reached 0.27 microgram/ml after 24 hours. The concentration was maintained between 0.23 microgram/ml and 0.39 microgram/ml through the following 7 days. These concentrations exceed the minimal inhibitory concentrations of most strains of Candida albicans. In 8 occasions of prophylactic use, no fungal infection was encountered. In a patient with pneumonia, chest X-ray and physical findings improved with administration of oral AMPH. Side effect of AMPH was seen in 1 patient, which was mild proteinuria and was eased rapidly after the withdrawal of AMPH. Clinical laboratory tests showed 1 case of proteinuria and disorder of kidney but did not clear under influence of AMPH. These results suggest that oral administration of AMPH is clinically and therapeutically effective and relatively safe for the prophylaxis or the treatment of fungal infection in patients with leukemia or related disorders.
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PMID:[Evaluation of oral amphotericin B with serial measurement of the serum concentration in patients with leukemia and related disorders]. 369 88

The clinical, laboratory and pathologic findings were studied in 62 consecutively autopsied patients with multiple myeloma between 1954 and 1975. All patients were 40 years of age or older. Bone pain was the initial symptom in 2/3 of patients. Anemia (81%), thrombocytopenia (29%), azotemia (41%), hypercalcemia (46%) and hyperuricemia (52%), were common laboratory findings at diagnosis. Ninety-seven percent had a monoclonal protein in serum or urine. Extensive plasma cell replacement of marrow was invariably seen at autopsy although in 15% of patients no abnormality was found on skeletal survey. Extraskeletal spread (67%) was due to direct extension to paraosseous tissue resulting from cortical destruction and to distant organ involvement mainly of splenic red pulp and hepatic sinusoids. The patients were susceptible to bacterial infection, mainly gram-negative, of the lung (56%), urinary tract (35%), and blood (24%). Fungal infection was less frequent and usually consisted of superficial candidal overgrowth of gastrointestinal tract ulcerations (18%). Amyloidosis (10%) was perivascular and associated with light chain proteinuria. Renal failure as a cause of death (21%) was secondary only to infection (52%). Severity of histologic findings in the kidney at autopsy had little correlation to initial BUN concentration. The median survival was 11.5 months with alkylating agent therapy (responders, 29 months; non-responders, 6 months), and 6 months with urethan. Initial azotemia (greater than 80 mg/dl) and hypercalcemia (greater than 12 mg/dl) were important prognostic indicators (median survival, less than 1 month and 3 months, respectively). A good response to alkylating agent therapy, initial BUN less than 40 mg/dl and serum calcium less than 12 mg/dl were favorable to prognostic indicators.
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PMID:Multiple myeloma: a clinicopathologic study of 62 consecutively autopsied cases. 743 54

Disseminated aspergillosis is an uncommon and unpredictable complication in severely immunocompromised patients and poses a challenging problem in the management and care of seriously ill patients receiving intensive care therapy. We report an autopsied case of disseminated aspergillosis occurring ina 31-year-old female patient who was treated for HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome. She initially presented with edema and proteinuria at a pregnancy check-up. At gestational age 33 weeks and 2 days, she had right lower abdominal pain, nausea, and jaundice. The next day she delivered a male neonate transvaginally, followed by excessive postpartum uterine bleeding. Although an emergency hysterectomy was performed, her hemorrhagic diathesis could not be controlled even after transcatheter embolization of the internal iliac arteries with subsequent ligation and repeated blood transfusions totalling to 31,070 ml. She eventually died of a cerebral hemorrhage 21 days after the parturition. Autopsy showed generalized jaundice and petechiae, as well as extensive hemorrhage observed in the abdominal wall, peritoneal cavity, and retroperitoneal and pelvic spaces. In addition,there were multifocal hemorrhages found in the left temporal, right frontal and posterior lobes of the cerebrum, and pons. Disseminated aspergillosis was found in the lungs, trachea, brain, esophagus, stomach, heart, and thyroid gland. These findings suggest that systemic postoperative complications, associated with massive blood transfusions and hepatic failure, mutually contribute to the overall deterioration of host defense mechanism, and may underlie the occurrence of devastating systemic fungal infection.
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PMID:[An autopsy case of HELLP syndrome with disseminated aspergillosis]. 1077 21

A 40-year-old white woman with end-stage renal disease from idiopathic type I membranoproliferative glomerulonephritis (MPGN) developed proteinuria and renal dysfunction 7 weeks after cadaveric donor renal transplantation. At the same time, a primary cytomegalovirus (CMV) infection was diagnosed. Complement levels were low. A renal biopsy disclosed an acute exudative proliferative glomerulonephritis with influx of polymorphonuclear granulocytes (PMNs), with granular deposits of C3, C1q, IgG, and IgM. The immunofluorescence (IF) and electron microscopy (EM) findings were compatible with an early stage of a type I MPGN. CMV could not be detected in the glomeruli nor elsewhere in the kidney by IF or EM. The patient was treated with ganciclovir. In a renal biopsy 3 weeks later, the exudative lesions had disappeared, and some glomeruli now showed the characteristic lesions of a type I MPGN with an increase of mesangial cells and matrix, and reduplication of the glomerular basement membrane. Over the following period, repeated biopsies were performed. The activity of the glomerular inflammation and immune complex deposits paralleled the waxing and waning of the CMV viral load. After 10.5 months, the graft was removed because of a life-threatening systemic fungal infection. At that time, the CMV infection had cleared, and in the transplantectomy material, the membranoproliferative pattern of injury had disappeared, and in the glomeruli hardly any deposits were found. These data strongly suggest that a primary CMV virus infection can induce an apparent recurrence of type I MPGN.
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PMID:Type I membranoproliferative glomerulonephritis in a renal allograft: A recurrence induced by a cytomegalovirus infection? 1078 14

Fungal infection of the genitourinary system is a relatively uncommon presentation. Cryptococcuria has rarely been recognized in clinical practice. Patients with positive urine culture for Cryptococcus neoformans from 1992 to 2003 were retrospectively reviewed. Sixteen patients were identified. Nine (56%) patients were male, with a mean age of 44 +/- 21 (range, 16-88) years. Fifteen (94%) patients had underlying conditions such as HIV infection, diabetes mellitus, hypertension, and/or systemic lupus erythematosus. Thirteen (81%) patients had cryptococcuria as a manifestation of disseminated cryptococcosis, and the rest had only isolated cryptococcuria. Urinary analysis revealed proteinuria (75%), pyuria (31%), and budding yeast (13%). Nine (56%) patients received antifungal therapy. Other patients were misdiagnosed or died before treatment. The mortality rate was 64%. In conclusion, cryptococcuria is not extremely rare and can present as a manifestation of disseminated cryptococcosis or isolated urinary tract infection.
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PMID:Cryptococcuria as a manifestation of disseminated cryptococcosis and isolated urinary tract infection. 1550 76

Cronkhite-Canada Syndrome is a non-inherited, non-congenital disease characterized by juvenile hamartomatous gastrointestinal polyps with a typically late onset. In the case described herein the disease was diagnosed in a 17-year-old male with type I diabetes and thalassaemia minor, in coincidence with severe symptomatic intestinal candidiasis. Following the disappearance of the mycosis and correction of the protein and electrolyte imbalance, the ectodermal abnormalities returned to normal and the patient remained asymptomatic during a 7-year follow-up period, despite proteinuria resulting from membranous glomerulopathy. The concept that Cronkhite-Canada Syndrome is a late-onset disease should probably be reconsidered as it may remain asymptomatic, and thus not diagnosed, for a long a time.
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PMID:Is Cronkhite-Canada Syndrome necessarily a late-onset disease? 1614 64

A 76 year-old woman was admitted to our hospital because of pyrexia and fatigue. One year earlier, she was diagnosed as nephrotic syndrome(NS) caused by focal segmental glomerulosclerosis and immunosuppressive therapy was started with marked amelioration of proteinuria. Thereafter, her renal function worsened, but only supportive treatment was continued. After admission, a cerebrospinal fluid (CSF) examination revealed Cryptococcus neoformans (C. neoformans) by india ink staining and a subsequent CSF culture confirmed C. neoformans infection. Accordingly, we made the diagnosis of cryptococcal meningitis and immediately started multiple anti fungal drugs with dosage modification according to her impaired renal function. Immunosuppressive therapy for NS was temporarily terminated. The inflammatory signs and symptoms soon were markedly improved, but the anti cryptococcal antibody titer in the serum and CSF remained high. Immunosuppressive therapy was started again at a low dosage because urinary protein had increased again. One hundred and eight days from admission, she was discharged with a regimen of multiple anti fungal drugs. Proteinuria and renal insufficiency was almost stable during hospitalization. Most fungal infection develops in patients in an immunosuppressive state induced by immunosuppressive drugs, HIV infection and so on. Patients with NS are frequently in an immunosuppressive state because of urinary loss of immunoglobulins and the use of immunosuppressive drugs. Therefore, it should be remembered that patients with NS are at a high risk of suffering from fungal infection.
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PMID:[A case of cryptococcal meningitis with nephrotic syndrome and renal insufficiency under immunosuppressive therapy]. 1729 87

A knowledge of the causes and risk factors of fatal infection in childhood lupus nephritis (LN) patients treated with intravenous cyclophosphamide (IVCY) is important to enable optimal treatment. During an 11-year period (1996-2007), severe infection cases occurred in 31/84 (36.9%) patients with 64 infection episodes in our central referral institution in southern Thailand. Fatal infections occurred in 13/31 (41.9%) patients, most (11/13, 84.6%) during the first infective episode. The major causative organisms of the fatal infections were fungus and Gram-negative bacilli. Fatal infections were more likely to occur in patients with a prior history of treatment with pulse methylprednisolone and in patients with more active LN, as evidenced by the higher proteinuria and serum creatinine levels and lower hemoglobin and lymphocyte counts in this group than in patients with non-fatal infections. Multivariate analysis indicated that factors associated with fatal infection were prior treatment with pulse methylprednisolone [odds ratio (OR) 11.2, 95% confidence interval (CI) 1.9-61.0], renal failure (OR 5.9, 95% CI 1.0-34.8), and fungal infection (OR 23.9, 95% CI 1.9-298.2). Cases of active LN treated with IVCY and pulse methylprednisolone who later develop severe infection that fails to respond to antibiotics should be carefully investigated for fungal infection.
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PMID:Fatal infection in children with lupus nephritis treated with intravenous cyclophosphamide. 1928 Feb 26

Disseminated histoplasmosis is an invasive fungal infection that can be fatal in patients with weak immune system. The goal of our exploratory study was to evaluate differences in urinary protein profiles among samples of healthy individuals, patients with proteinuria (PRU), and histoplasma antigenuria (HIS), and to identify physiological pathways associated with the excreted proteins. Urine samples were depleted of abundant proteins, deglycosylated, digested with trypsin, fractionated and analyzed by nano-LC-QTOF. The total number of human proteins identified in the samples was 117, of which 20 and 23 were unique to the samples from patients with PRU and HIS, respectively. Pathway analysis of proteins identified in samples of PRU and HIS patients suggested increased levels of proteins associated with acute response signaling, coagulation system, prothrombin activation, glucocorticoid regulation and the lipid antigen presentation signaling pathway networks. The obtained data provide information on protein expression associated with HIS, and suggest that further more rigorous studies aimed at the identification of proteins associated with proteinuria of different causes are feasible.
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PMID:Exploratory study of proteins in urine of patients with histoplasma antigenuria. 2196 77


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