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)

The activities of the enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LD), creatine kinase (CK), amylase (AMS) and angiotensin converting enzyme (ACE) have been used to assess the toxic effects of xenobiotics that have hypoglycaemic action in hepatic, pancreatic, renal and muscle tissue. Using a validated experimental model of diabetes mellitus in rats, we ascertained whether this syndrome itself affected the serum activities of these enzymes over a 53-day period. Levels of hepatic enzymes AST, ALT and ALP were higher in the streptozotocin (STZ)-diabetic rats (group D), but were controlled by insulin therapy (group DI). AMS was reduced in group D and unchanged in group DI rats. Proteinuria was detected 1 day after STZ administration and partially controlled by insulin (group DI); its early presence in group D rats, and the lack of any change in serum ACE in this group, indicates that proteinuria is the better marker for microangiopathy. Microscopic examination of liver, kidney, heart and skeletal muscles (soleus and extensor digitorum longus) revealed various alterations in group D rat tissues, which were less pronounced in group DI. The liver, pancreas and kidney tissue-damage was consistent with the altered serum levels of AST, ALT, ALP and AMS and proteinuria. We conclude that: (i) rigorous control is required when these serum-enzyme levels are used as indicators of tissue toxicity in experimental diabetes, and (ii) LD, CK and bilirubin serum levels, which are unaffected by diabetes, can be used when testing effects of xenobiotics on tissues.
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PMID:Temporal response pattern of biochemical analytes in experimental diabetes. 1282 18

Abnormal glomerular glycosaminoglycan metabolism is involved in the onset of the morphological and functional aberrations of glomerulopathies. In the present study, a heparin derivative, low-molecular-weight heparin, was tested for its ability to afford renoprotection in an established model of experimental glomerulopathy. Two groups of male albino rats of the Wistar strain (140 +/- 10 g) received a single intravenous injection of adriamycin (7.5 mg/kg) to induce glomerulopathy, and one of them received low-molecular-weight heparin (Certoparin Sodium, Troparin; 300 microg/day/rat s.c.) treatment, commencing on day 8, for a week. Urinary protein/creatinine ratio, serum albumin, urea, uric acid and creatinine clearance were evaluated. Renal cell injury was assessed in terms of renal tissue lactate dehydrogenase, aminotransferases (aspartate and alanine transaminases) and alkaline phosphatase activities, as well as renal antioxidant status (superoxide dismutase, catalase and glutathione peroxidase, reduced glutathione, vitamins E and C). The kidney tissue was subjected to histopathologic examination. Low-molecular-weight heparin significantly reduced proteinuria and improved creatinine clearance and serum albumin levels in the rats with glomerulopathy. The significant rise in serum uric acid in the rats with glomerulopathy was reversed by low-molecular-weight heparin. Altered tissue enzyme activities in response to injury, oxidative stress challenged renal antioxidant system and abnormal renal histology were observed in the untreated nephrotic rats, while low-molecular-weight heparin treatment protected the nephrotic rats against these changes. Thus, in this study, low-molecular-weight heparin was evaluated for its role in combating glomerular injury, on the basis of some salient biochemical parameters, oxidative injury indices and histologic picture. The ability of low-molecular-weight heparin to restore glomerular anatamo-functional features in this nephrotoxic condition illuminates its multi-faceted renoprotective role.
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PMID:The cytoprotective role of a low-molecular-weight heparin fragment studied in an experimental model of glomerulotoxicity. 1457 5

Amyloidosis is a pathological process which encompasses a spectrum of diseases that result from extracellular deposition of pathological fibrillar proteins. Clinical presentations vary depending on the organs involved. There is no documented case of amyloidosis presenting as small bowel encapsulation. A previously healthy 62-year-old man developed a small bowel obstruction in 1997. At surgery, a peculiar membrane encasing his entire small bowel was discovered. This appeared to have no vascularity and was removed without difficulty, exposing a grossly normal bowel. Histopathology revealed thick bands of collagen overlying the peritoneal surface, which was congo red positive and showed apple green birefringence. The findings were consistent with encapsulating peritonitis due to amyloidosis. There was no history or symptoms of any chronic inflammatory condition and he became symptom-free postoperatively. An abdominal fat pad biopsy failed to demonstrate amyloidosis. Endoscopic duodenal biopsies revealed classical primary amyloidosis. Quantitative immunoglobulins, lactate dehydrogenase, C3, C4 and beta-2 microglobulin were normal. Protein electrophoresis identified monoclonal paraprotein, immunoglobulin G lambda 3.7 g/L. Bone marrow biopsy and aspirate revealed only a mild plasmacytosis (5% to 10%). Echocardiogram and skeletal survey were normal. He had mild proteinuria. Complete blood count, C-reactive protein, calcium, albumin and total protein were normal. No specific therapy was instituted. In January of 1998 the patient remained asymptomatic with no gastrointestinal, cardiovascular or constitutional symptoms. He had developed nephrotic range proteinuria (3.95 g/24 h), microalbuminuria, hypoalbuminemia and a renal biopsy consistent with renal amyloidosis. In 1999 there was an increase in the monoclonal paraprotein (6.2 g/L). The remaining investigations were normal except for an echocardiogram which showed left ventricular hypertrophy but a normal ejection fraction and no diastolic dysfunction. He went on to have high-dose chemotherapy and an autologous stem cell transplant in September, 2000. He has subsequently developed renal insufficiency. To our knowledge this is the first reported case of primary amyloidosis presenting as small bowel obstruction from encapsulating peritonitis.
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PMID:Primary amyloidosis presenting as small bowel encapsulation. 1505 90

The explosive RDX (hexogen, cyclonite) is usually used for the production of C-4 explosive. The rare occurrence of accidental and intentional RDX intoxications has been reported during manufacturing process or in wartime. In this article, the authors report 5 cases of accidental oral RDX poisoning. On admission, observed signs and symptoms included repetitive generalized tonic-clonic convulsions, postictal coma, lethargy, confusion, hyperreflexia, postictal amnesia, nausea, vomiting, abdominal tenderness, sinusal tachycardia, dysrhythmia with frequent ventricular premature beats, generalized muscle spasms, and myoclonus. Leukocytosis, mild anemia, methemoglobinemia, elevated levels of blood glucose, serum aspartate transaminase, alanine transaminase, lactic dehydrogenase, creatine phosphokinase, amilase, hypokalemia, metabolic acidosis, proteinuria, glucosuria, and myoglobinuria were also noted. Plasma RDX concentrations were 268 to 969 ng/mL at 3 hours of ingestion. For management, supportive and symptomatic measures were taken. Whole-bowel irrigation might have been an effective therapeutic procedure due to probable slow gastrointestinal absorption of RDX. Three patients who developed severe metabolic acidosis underwent urgent hemodialysis. All patients were discharged 7 to 21 days after admission without any sequelae. Plasma RDX levels were strongly correlated with the clinical and laboratory manifestations. The available toxicological data on this rare accidental poisoning are reviewed in light of the literature.
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PMID:Accidental oral poisoning caused by RDX (cyclonite): a report of 5 cases. 1518 66

We report a case of non-Hodgkin lymphoma (NHL) with acute renal failure. A 62-year-old man was admitted to our hospital on March 8, 2002 with leg edema and dyspnea on effort. About 3 weeks before admission, he was found to have slightly high serum creatinine (Cr) and high lactate dehydrogenase (LDH) levels by another home doctor. Physical examination revealed anemic conjunctivae and leg edema, but the urinary volume was preserved. Blood examination showed high BUN (64 mg/dl) and Cr levels (3.91 mg/dl). Urinary analysis showed proteinuria (1.05 g/day) and high BMG (14,434/microg/day) and NAG (4.55 U/day) levels, suggesting severe tubulointerstitial injury. On ultrasonography of the kidney, the bilateral kidneys showed marked swelling without hydronephrosis. To investigate the genesis of renal failure, we performed a renal biopsy. The specimen showed normal glomeruli, but a large number of cells infiltrated in the tubulointerstitial area with normal tubulointerstitial structure. The cells stained positively with anti-leukocyte antigen and L26 (B cell marker), and negatively with cytokeratin and UCHL-1 (T cell marker). These findings indicate that the interstitial cells were non-Hodgkin lymphoma with B cell diffuse large cells. Chemotherapy was performed with VAD (vincristine sulfate, doxorubicin hydrochloride, dexamethasone) considering his renal dysfunction. To avoid tumor lysis syndrome after chemotherapy, hemodialysis was performed on days 1-4 after the initiation of chemotherapy. After a series of chemotherapy, the urinary volume increased and serum Cr levels decreased to 2 mg/dl. After additional therapy with 4 courses of CHOP, he improved and was discharged on day 180 after admission.
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PMID:[Case of non-Hodgkin lymphoma with acute renal failure successfully treated with chemotherapy]. 1564 40

We report the case of a 47-year-old man with the simultaneous occurrence of clinical and laboratory features consistent with acute poststreptococcal glomerulonephritis (APSGN), hemolytic uremic syndrome (HUS), and nephrotic syndrome. Acute nephritic syndrome occurred 3 weeks after having pharyngeal pain and diarrhea. He presented with edema and hypertension on admission. Laboratory evaluation showed hemolytic anemia with fragmentation, thrombocytopenia, elevated lactic dehydrogenase level, low haptoglobin level, low complement C3 level, and elevated antistreptolysin-O titer. Serum creatinine level was 1.22 mg/dL (108 micromol/L), and urinalysis showed marked proteinuria, with protein of 8.7 g/d, and hematuria. The renal biopsy specimen was characteristic of APSGN, but not HUS. Moderate expansion of the mesangial matrix, moderate proliferation of epithelial and endothelial cells, and marked infiltration of neutrophils was seen by means of light microscopy, and many subepithelial humps were seen by means of electron microscopy. Neither fibrin deposition nor evidence of thrombotic microangiopathy was found. Complement C3 deposition along the capillary wall and tubules was seen in an immunofluorescence study. The patient was administered plasma infusion at 320 mL/d and antihypertensive drugs. Serum complement C3 and haptoglobin levels returned to normal within 3 weeks. This is a rare case of the simultaneous occurrence of APSGN, HUS, and nephrotic syndrome.
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PMID:An adult with acute poststreptococcal glomerulonephritis complicated by hemolytic uremic syndrome and nephrotic syndrome. 1618 9

Everolimus is a proliferation signal inhibitor (PSI)/mammalian target of rapamycin inhibitor that is structurally similar to sirolimus, but with a number of important pharmacokinetic differences, including a shorter half-life and time to steady state. In clinical trials, the efficacy of everolimus 1.5 mg/day and 3.0 mg/day combined with ciclosporin (CsA) and steroids in de novo renal transplant recipients is similar to that of mycophenolate mofetil, with one study showing a significantly lower risk of antibody-treated acute rejection with everolimus. When combined with reduced-dose CsA, everolimus is associated with improved renal function compared with full-dose CsA, with no decrease in efficacy. Thus, everolimus may play an important role in calcineurin inhibitor (CNI)-sparing regimens for renal transplant recipients. Studies with sirolimus have shown that CNI withdrawal is associated with a significant improvement in renal function, although there may be an increase in the risk of acute rejection. however, patient and graft survival are not adversely affected by CNI withdrawal. Notably, proteinuria <800 mg/day before conversion is a strong predictor of successful response to sirolimus treatment, and hypertensive therapy and serum lactate dehydrogenase levels may also predict response. Adverse events commonly associated with the PSIs include dyslipidaemia, proteinuria and anaemia, although these can usually be managed without difficulty. Data are also available to suggest that the PSIs are associated with a lower risk of malignancy than other immunosuppressive agents. In conclusion, everolimus may permit reduced exposure to CNIs in renal transplant recipients, with the potential to improve tolerability and renal function.
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PMID:Everolimus in clinical practice--renal transplantation. 1681 52

Patients with sickle cell anemia (SCA) may develop a glomerulopathy with proteinuria and progressive renal insufficiency, leading to ESRD. Albuminuria is a sensitive marker of glomerular damage in this population and precedes the development of renal insufficiency. For determination of the prevalence of glomerular damage in SCA and the clinical correlates of renal insufficiency, 300 adult patients with SCA were studied (hemoglobin SS = 184; and 116 with other sickling hemoglobinopathies: SC, SD, and S-beta thalassemia); albumin excretion rates (AER) and renal function (Cockroft-Gault formula) were determined, and clinical and hematologic evaluations were conducted. In hemoglobin SS disease, increased AER (micro- and macroalbuminuria) occurred in 68% of adult patients, and macroalbuminuria occurred in 26%. In other sickling disorders, increased AER occurs in 32% of adults, and macroalbuminuria occurs in 10%. The development of graded albuminuria was age dependent, so at 40 yr, 40% of patients with SS disease had macroalbuminuria. There were no differences in hematologic parameters (hemoglobin levels, white blood cell count, percentage of reticulocytes, platelet counts, or lactate dehydrogenase levels) between patients with normoalbuminuria and those with micro- or macroalbuminuria. By multivariate analysis, albuminuria correlated with age and serum creatinine in SS disease but not with BP or hemoglobin levels. In other sickling disorders, albuminuria tended to be associated with age but not with hemoglobin or BP levels. The diastolic BP was lower in patients with SCA than in African American control subjects, and the development of renal insufficiency, which was present in 21% of adults with SS disease, was not accompanied by significant hypertension. It is concluded that glomerular damage in adults with SCA is very common, and a majority of patients with SS disease are at risk for the development of progressive renal failure. The development of micro- and macroalbuminuria is not related to the degree of anemia, suggesting that sickle cell glomerulopathy is not solely related to hemodynamic adaptations to chronic anemia. In contrast to other glomerulopathies, the development of systemic hypertension is uncommon in SS disease with renal insufficiency.
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PMID:Glomerular involvement in adults with sickle cell hemoglobinopathies: Prevalence and clinical correlates of progressive renal failure. 1683 35

Renal lymphoma occurs most often as a part of a multi-systemic disseminated lymphoma or as a recurrence of the tumor. Renal involvement usually occurs late in the course of the disease and is clinically silent. Acute renal failure (ARF) from lymphomatous infiltration has been described but is quite rare. We report a 50-year-old Caucasian woman, who presented with features of ARF. Physical examination showed that her arterial blood pressure was 190/100 mm Hg with no lymphadenopathy or hepatosplenomegaly. Her urine output was about 100 ml/day, and urinanalysis revealed + proteinuria and microscopic hematuria. Biochemical findings revealed severely impaired renal function with a serum creatinine of 693 micromol/L. The patient's lactate dehydrogenase was elevated at 632 U/L. An abdominal ultrasound showed bilateral, large non-obstructed kidneys and a hypoechoic mass arising in the right lobe of the liver. An ultrasound-guided percutaneous liver biopsy showed typical features of B-cell lymphoblastic lymphoma. The patient expired two days later, even before any specific treatment could be started.
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PMID:Acute renal failure due to lymphomatous infiltration: an unusual presentation. 1697 Feb 62

Renal thrombotic microangiopathy (TMA) is an uncommon vascular complication of severe hypertension. Until now, its clinical-pathological characteristics and renal survival have been unclear. Twenty-one patients with biopsy-proven renal TMA and with severe or malignant hypertension were retrospectively studied. All the patients exhibited severe hypertension, with systolic blood pressure at 200-280 mmHg and diastolic pressure at 110-180 mmHg. No patients had hemorrhagic manifestations. Elevated lactate dehydrogenase and thrombocytopenia were found in 6 and 5 patients, respectively. Significant proteinuria (>3 g/day) was present in 2 patients and microscopic hematuria in 18 patients. All patients presented with renal insufficiency (creatinine 3.1+/-2.1 mg/dL). The level of von Willebrand factor:antigen (vWF:Ag) in patients was not significantly higher than that in the healthy subjects, while the ADAMTS13 (a disintegrin and metalloprotease, with thrombospondin-1-like domains) activity was not significantly lower than that in the healthy subjects. Renal histology showed a TMA involving preglomerular arterioles and/or interlobular arteries characterized by fibrin deposits and vascular wall sclerosis. Fibrin glomerular microthrombi were not observed in these patients. Four patients required hemodialysis upon admission for severe acute renal failure. On follow-up, 3 patients had recovered normal renal function and 14 had mild renal insufficiency (creatinine 1.8+/-0.3 mg/dL), while 4 patients still required persistent hemodialysis. In conclusion, compared with patients having hemolytic uremic syndrome/thrombocytopenic purpura, our patients showed a low incidence of thrombocytopenia and better renal outcome.
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PMID:Renal thrombotic microangiopathies induced by severe hypertension. 1849 67


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