Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
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Ovarian hyperstimulation syndrome (OHSS) is a potentially fatal condition associated with the use of ovulation-inducing drugs. We describe a 28-year-old woman who presented with ascites, oliguria and vomiting. Over 2 weeks, the combination of intractable vomiting, intravenous rehydration, paracentesis, hypercatabolism and proteinuria led to severe hypoalbuminaemia with gross oedema and progressively worsening liver function. The patient's albumin dropped to 9 g/l with liver function abnormalities peaking at: alanine aminotransferase, 462 IU/l; alkaline phosphatase, 706 IU/l; bilirubin, 26 micromol/l; and prothrombin time, 19 s. The judicious use of paracentesis and commencement of total parenteral nutrition coincided with a rapid clinical improvement. One month after discharge, the patient was asymptomatic with normal liver function. This case demonstrates the severity of malnutrition and liver dysfunction that can occur with severe OHSS. Increasing use of in-vitro fertilization techniques makes it mandatory for clinicians to be aware of the clinical features, complications and treatment of this condition, and we would suggest that patients with severe OHSS should be jointly managed by physicians and obstetricians.
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PMID:A severe case of ovarian hyperstimulation syndrome with liver dysfunction and malnutrition. 1216 89

The aim of this retrospective study was to evaluate the relationship between HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome and the maternal blood groups. Five hundred and forty-seven women with severe preeclampsia were included and divided into eight groups according to their blood groups: A Rh-positive (n=203), A Rh-negative (n=38), B Rh-positive (n=83), B Rh-negative (n=10), 0 Rh-positive (n=148), 0 Rh-negative (n=21), AB Rh-positive (n=39), and AB Rh-negative (n=5). The groups were controlled by analysis of variance and found to be homogeneous with respect to parity, gestational age, blood pressure, hemoglobin, hematocrit, platelet values, prothrombin time, partial thromboplastin time, fibrinogen, creatinine, alanine aminotransferase, aspartate aminotransferase, bilirubin, uric acid, and proteinuria. Incidence of HELLP syndrome was 24% in the overall study population whereas 48% of the patients with the blood group O Rh-negative had HELLP syndrome associated with an increase in risk by a factor of 3.1. To our knowledge this is the first report of such an association.
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PMID:Distribution of ABO and Rh blood groups in patients with HELLP syndrome. 1241 Mar 71

Thromboembolic complications are often seen in patients with nephrotic syndrome. Markers of endothelial cell injury [thrombomodulin, intracellular adhesion molecule, vascular cell adhesion molecule, thrombin activatable fibrinolysis inhibitor (TAFI), protein Z, vascular endothelial growth factor, markers of thrombin and plasmin generation] were studied in 22 patients with nephrotic syndrome. All these parameters studied, except protein Z and D-dimers, were significantly higher in patients with nephrotic syndrome, whereas protein Z was significantly lower when compared with the healthy volunteers. None of the endothelial cell markers (thrombomodulin, P-selectin, E-selectin, intracellular adhesion molecule, vascular cell adhesion molecule), thrombin and plasmin generation markers (thrombin-antithrombin complexes, prothrombin fragments 1 + 2, plasmin-antiplasmin complexes, D-dimers), protein C, protein Z, vascular endothelial growth factor, and TAFI concentration and activity were directly correlated with the level of proteinuria, albumin, cholesterol, triglycerides or creatinine, except significant positive correlations between TAFI activity and serum creatinine, E-selectin and albumin as well as negative correlations between plasmin-antiplasmin complexes and proteinuria. In these patients, there is evidence of endothelial cell injury and probably secondary activation of the coagulation cascade. Elevated circulating TAFI antigen and activity might be a new link in the pathogenesis of impaired fibrinolysis and the progression of atherosclerosis in nephrotic syndrome. Protein Z deficiency might also contribute to the enhanced risk of thromboembolic complications in nephrotic syndrome.
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PMID:Markers of endothelial cell injury and thrombin activatable fibrinolysis inhibitor in nephrotic syndrome. 1243 47

Use-result surveillance was conducted to investigate the safety and efficacy of Acetylcysteine Oral Solution 17.6 % "SENJU" having the indication for the antidote to acetaminophen (Paracetamol) overdose. Ninety six cases (patients) were collected for the safety evaluation, and 13 cases (incidence was 13.5 %) showed 29 adverse drug reactions as follows: 4 cases of nausea; 3 cases of vomiting; 2 cases each of liver dysfunction, headache, abdominal pain, diarrhea, blood bilirubin increased; and one case each of CK increased, anaemia, prothrombin time prolonged, gamma-glutamyltransferase increased, LDH increased, body temperature increased, proteinuria, blood potassium decreased, thrombocytopenia, platelet count increased, white blood cell decreased, and blood amylase increased. One case of severe liver dysfunction which was ameliorated later was found. Neither case showing transitional chronic liver dysfunction, nor case of death was observed. Patient background analysis showed that 79.2% of the total patients was female, and that 28.1% was patients with mental disease. Gastrolavage, active charcoal administration, and extracorporeal removal of toxins were performed in cases of 71.9%, 50.0% and 7.3%, respectively. Those concomitant treatments, however, showed no influence for the incidence of adverse drug reaction or the drug effectiveness. Blood acetaminophen assay was performed in only 43.8% of the total cases. This rate indicates that the medical treatment procedure needs more consideration on the clinical standard for the antidote to acetaminophen overdose and on its practical application.
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PMID:[Post-marketing surveillance of acetylcysteine oral solution 17.6% "SENJU" for the antidote to acetaminophen overdose--use--results surveillance]. 1713 80

In August 1994, a 19-year-old woman presented to her dermatologist with a slight fever, arthralgia, and a butterfly rash. Discoid lupus erythematosus was suspected, and serological testing yielded positive results for antinuclear antibody. She was diagnosed with systemic lupus erythematosus without organ failure and was treated with only nonsteroidal antiinflammatory drugs. She became pregnant in June 2001, at age 26. In November her obstetrician noted that she had severe hypertension, edema of the low limbs, and proteinuria. On admission, she was diagnosed with severe preeclampsia, and cesarean section was performed. On hospital day 3 the patient developed sudden epigastric pain and vomiting. Laboratory tests revealed thrombocytopenia, liver dysfunction, and microangiopathic hemolytic anemia, leading to a diagnosis of HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome. Plasma exchange was performed for 5 days. The thrombocytopenia, liver dysfunction, and proteinuria diminished quickly. Later testing revealed a high titer of plasma phosphatidylserine-dependent anti-prothrombin antibody. This case is useful for exploring the relations between SLE, HELLP syndrome, and anti-prothrombin antibody.
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PMID:A case of systemic lupus erythematosus with postpartum hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome and concomitant high phosphatidylserine-dependent anti-prothrombin antibody levels. 1714 1

Tissue factor initiates the extrinsic coagulation pathway by activating coagulation factor X to factor Xa, and factor V is a cofactor for the prothrombin activation by factor Xa. As factor Xa is known to promote the proliferation of mesangial cells in culture, the roles of the coagulation pathway and factor Xa were studied in an animal model of mesangioproliferative glomerulonephritis (MsPGN). MsPGN was induced in Wistar rats by an intravenous injection of anti-Thy 1.1 monoclonal antibody, OX-7. To clarify the role of factor Xa in MsPGN, a specific factor Xa inhibitor, DX-9065a, was injected intravenously at 2.5 or 10 mg/kg at the same time as OX-7, and kidney involvement was assessed by immunohistological analyses. We also examined p44/42 mitogen-activated protein (MAP) kinase activation. Time-course study revealed that expressions of tissue factor, factor V, and protease-activated receptor 2 (PAR2) were peaked on day 3, followed by factor X accumulation and mesangial proliferation. DX-9065a treatment significantly ameliorated proteinuria in a dose-dependent manner on day 8. Histological analyses showed a significant reduction in the size of glomeruli, the total number of glomerular cells, and crescent formation by DX-9065a treatment. Macrophage infiltration, which was rapidly observed on day 1 in disease control rats was not inhibited on days 1-3 by DX-9065a treatment, however it was suppressed on days 5-8. The deposition of fibrin, the number of PCNA-positive cells, and phosphorylation of p44/42 MAP kinase were markedly increased in the disease control group, whereas they were significantly reduced in the treatment group. Tissue factor and factor V induction may accelerate MsPGN through the activation and accumulation of factor X via proinflammatory and procoagulant mechanisms, and the inhibition of factor Xa would be a promising method to regulate the disease process.
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PMID:Roles of coagulation pathway and factor Xa in rat mesangioproliferative glomerulonephritis. 1717 58

We describe a 10-year-old severe hemophilia B boy with a stop codon mutation of exon 2 in the factor IX gene who developed high inhibitor of 70 Bethesda units (BU) from 12 months of age after exposure to prothrombin complex concentrate for 14 days. The inhibitor spontaneously disappeared within 3 months. The patient, however, exhibited anaphylactic reaction to the administration of prothrombin complex concentrate and factor IX concentrate at ages 15 and 23 months, respectively. Although recombinant activated factor VII was alternatively given, he suffered from progressive hemophilic arthropathy. At the age of 10 years, the boy underwent desensitization to factor IX concentrate and could tolerate factor IX concentrate of 40 U/kg administered on day 9 of desensitization. Unfortunately, the inhibitor of 16 BU was detected on day 6 and rapidly increased to 180 BU on day 9 of desensitization. Rituximab 375 mg/m2 per week was therefore immediately initiated on day 10 and a total of four doses were given. The inhibitor gradually decreased to 21.5 BU after the fourth dose of rituximab. The daily factor IX concentrate administration of 40 U/kg was continued for 1 month and decreased to three times per week for another month, and then to once to twice per week for the remaining 14 months of desensitization. The patient was able to attend regular school and the most recent inhibitor ranged from 4.4 to 10 BU. No proteinuria or alteration of renal function was found. In conclusion, rituximab is a helpful adjuvant to immune tolerance therapy in a hemophilia B boy with inhibitor and anaphylaxis to factor IX concentrate.
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PMID:The use of rituximab as an adjuvant for immune tolerance therapy in a hemophilia B boy with inhibitor and anaphylaxis to factor IX concentrate. 1838

Pre-eclampsia is a pregnancy-associated disease of the second part of the pregnancy, occurring mainly after 20th weeks gestation. The prevalence of hypertension in pregnancy is between 5 to 11% and affects mainly women under 20 years of age. An inadequate invasion of trophoblasts with consequential placental ischemia as a result of insufficiently dilated uterine spiral arteries is thought to be an initial cause in the pathogenesis of pre-eclampsia. The clinical symptoms of pre-eclampsia, such as loss of intravascular volume and edema, are caused by generalized endothelial dysfunction. These symptoms are potentiated by hypertension and reduced colloid osmotic pressure in the plama. The organs being affected by pre-eclampsia are those of the vascular-, hepatic-, renal-, cerebral- and coagulatory systems. The prognosis is much more severe when pre-eclampsia develops very early in the pregnancy. The symptoms include elevated blood pressure (over 140 mmHg systolic, 90 mmHg diastolic) combined with proteinuria. Frequent symptoms are hyperreflexia and edema. The etiology of pre-eclampsia has not been clearly defined. Risk factors/triggers for the development of pre-eclampsia can include chronic hypertension, advanced maternal age at first pregnancy (over 35 y), nephropathy, thrombophilia (heterozygous factor V Leiden mutation, antiphospholipid syndrome, heterozygous prothrombin mutation and homozygous MTHFR), multiple gestation and prior pregnancy with preeclampsia. The incidence of preeclampsia is higher in nulliparous than multiparous women. In many countries pre-eclampsia is still most frequent cause of maternal perinatal mortality. HELLP-Syndrome (haemolysis-elevated liver enzyme- low platelets) is a severe progressive course of this disease. Eclampsia, characterized by generalized tonic-clonic convulsion, is the most dangerous complication of pre-eclampsia, and may develop before or after delivery. This form of pre-eclampsia is associated with higher maternal and fetal mortality. Constant maternal hypertension potentially alter vascular integrity of the placenta with further consequences in fetal blood supply leading to growth restriction or zero growth and subsequently resulting in low birth weight or fetal death. The sooner the disease is detected and confirmed, the better the maternal and fetal prognoses are. This is the reason why it is major importance, together with the employment of preventive measures, to identify patients with risk factors with pre-eclampsia though an adequate screening method, thereby detecting the disease earlier and ensuring better pregnancy outcomes for both mother and child.
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PMID:[Pre-eclampsia screening in first and second trimester]. 1897 29

Acute hepatitis A (AHA) is one of the most common infectious diseases; it is usually a self-limiting disease affecting the liver. Although extrahepatic manifestations are not common, some cases have been reported associated with acute renal failure. We reviewed the clinical features of patients with AHA complicated by acute renal failure (ARF group) and compared them with patients with noncomplicated AHA (non-ARF group). The medical records of 208 consecutive patients with AHA who were diagnosed between January 2003 and October 2008 were reviewed. We identified 15 patients (7.2%) with ARF associated with AHA. There were no differences between the ARF and non-ARF group with regard to gender and age. The peak value of alanine aminotransferase (ALT) (median: 6060 IU/L vs 1792 IU/L, P < 0.001), prothrombin time (PT) (International normalized ratio, median 1.72 vs 1.10, P < 0.001), and total bilirubin level (median: 9.6 mg/dL vs 6.3 mg/dL, P = 0.04) were significantly higher in the ARF than in the non-ARF group. Twelve patients (80%) recovered completely with haemodialysis (seven patients, 46.7%) or only conservative management (five patients, 33.3%), while one patient underwent liver transplantation because of fulminant hepatic failure, and two patients died because of fulminant hepatic failure. There were no deaths among patients with noncomplicated AHA in the non-ARF group. Five patients underwent kidney biopsy; two patients were diagnosed with acute tubular necrosis, two patients with acute interstitial nephritis with IgA nephropathy and one patient with acute tubulointerstitial nephritis. All patients in the ARF group had microscopic haematuria and proteinuria (100%vs 31.1%, P < 0.001). Urine sodium levels were more than 10 mEq/L in 10 patients. The findings of high urinary sodium concentrations, microscopic haematuria and proteinuria did not support the diagnosis of hepatorenal syndrome (HRS). Patients with AHA with ARF had higher ALT levels, more prolonged PTs, and higher total bilirubin levels. The prognosis for these patients was poorer than for those without ARF. However, the patients with ARF and nonfulminant AHA had recovered with proper treatment and should not be confused with patients that have HRS.
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PMID:Clinical features of acute renal failure associated with hepatitis A virus infection. 1982 44

Factor X (FX) deficiency is a rare hereditary coagulation disorder. This is the first case report on the association of FX deficiency and membranoproliferative glomerulonephritis (MPGN) type I. The patient, a 17-year-old male, presented with edema, hypertension, and microscopic hematuria, followed by a mild upper respiratory tract infection. Laboratory tests revealed: serum creatinine 1.6 mg/dl, serum albumin 2.80 g/dl, C3 16 mg/dl and proteinuria (1,800 mg/day). The renal biopsy showed MPGN type I. The coagulation profile prior to percutaneous renal biopsy revealed prolonged prothrombin time and activated partial thromboplastin time values. The patient was given fresh frozen plasma and vitamin K before the biopsy. Further evaluation showed the functional activity of FX was 7% of the norm. This case emphasizes the need for routine coagulation screening before percutaneous renal biopsy.
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PMID:Membranoproliferative glomerulonephritis and a rare bleeding disorder: Factor X deficiency. 2085 84


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