Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344232 (blurred vision)
 2,072 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 33 year old man developed acute oliguric failure lasting 66 days, eight days after admission with multiple gun shot wounds. On day 99 after admission, serum calcium was elevated mildly at 2.54 mmol/l (normal range 2.1-2.5 mmol/l). Serum parathormone was undetectable. He was discharged soon afterwards. He presented again on day 164 with nausea, vomiting and blurred vision. Fundoscopy revealed an ischaemic retinopathy and extensive keratopathy. Serum calcium was 3.48 mmol/l and serum creatinine 262 umol/l (normal range 40-110 umol/l). Repeat parathormone was undetectable and there was no evidence of myeloma, sarcoidosis or malignancy. Following treatment with intravenous saline and frusemide, serum calcium fell to a nadir of 3.05 mmol/l. On day 168 an infusion of sodium clodronate 300 mg was given. Twenty-four hours later serum calcium was 2.65 mmol/l and 48 hours later calcium was 2.26 mmol/l. Normocalcaemia was maintained for 17 days and severe hypercalcaemia never recurred. This is the first report in which biphosphonates have been successfully used to treat hypercalcaemia following acute renal failure thus obviating the need for further dialysis.
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PMID:Severe hypercalcaemia four months after acute oliguric renal failure--successful treatment with intravenous clodronate. 138 45

A 67-year-old white woman developed severe nausea, vomiting, diffuse abdominal cramping pain, and blurred vision followed by a syncopal episode after taking 1 tablet of quinine for leg cramps. Examination was significant for fever, elevated blood pressure, and confusion without any focal neurological deficits. Laboratory studies showed markedly elevated liver enzymes, elevated lactate dehydrogenase, anemia, thrombocytopenia, and acute renal failure. Peripheral smear showed many schistocytes and burr cells. She later recalled taking quinine more than 40 years before while on a trip to the Philippines. The patient was treated with 7 sessions of plasmapheresis with a rapid normalization of her hematological parameters. Three weeks of dialysis support were required before return of renal function to baseline. Re-exposure to quinine can cause a rapid onset of hemolytic uremic syndrome-like syndrome. We are not aware of any cases of hemolytic uremic syndrome-thrombotic thrombocytopenic purpura in response to re-exposure to a single tablet of the drug 40 years after first use.
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PMID:Quinine induced HUS-TTP: an unusual presentation. 1467 3

Thrombotic microangiopathy (TMA) is a recognized complication of malignant hypertension (HTN). Such patients have blood pressures > or = 200/140 mmHg but the condition is defined by the presence of papilledema and is frequently complicated by acute renal failure. Here we report two patients with severe HTN (systolic > or = 180 mmHg or diastolic > or = 120 mmHg), TMA, thrombocytopenia, renal failure, and, in one case, neurological changes (4 of 5 manifestations of the TTP pentad). A 50-year-old male with HTN presented with blurred vision, dizziness, headache, confusion, renal failure, and a TMA (PLT = 39 x 10(9)/L and LD = 2,781 normal <600 U/L). On presentation, BP was 214/133 mmHg and an ophthalmic exam demonstrated no papilledema. With HTN control over 7 days, his platelet count rebounded (220 x 10(9)/L), LD declined (1,730 U/L), and mental status improved. A 60-year-old female with diabetes, HTN, Lupus erythematosus, mild chronic anemia, and thrombocytopenia presented with abdominal pain, shortness of breath, renal failure, and a TMA (PLT = 83 x 10(9)/L and LD = 2,929 U/L). Blood pressures were 180-210/89-111 mmHg and ophthalmic exam demonstrated no papilledema. With HTN control over 8 days, her platelet count rebounded (147 x 10(9)/L), and LD declined (1,624 U/L). Although in both cases a diagnosis of TTP was considered because of overlap with the classic diagnostic pentad, neither received plasmapheresis. TTP is a diagnosis of exclusion, where there is no other likely diagnosis to explain the TMA. In cases of severe HTN (with or without papilledema), the diagnosis of TTP should be held in abeyance until the effect of HTN control can be assessed.
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PMID:Differentiating thrombotic microangiopathies induced by severe hypertension from anemia and thrombocytopenia seen in thrombotic thrombocytopenia purpura. 1549 50

We conducted a retrospective study of the management and outcome for eclampsia patients in the intensive care unit (ICU) of National hospital, Abuja between November 2001 and April 2005 (42 months). The patients' case files and ICU records were used to extract the necessary data. During the study period, there were a total of 4857 deliveries, with 5051 total births (including multiple births) and 4854 live births. Forty eclamptics were admitted to the ICU, giving an ICU admission rate of 8.2/1000 live births. The records of two patients were incomplete. The average age of the patients was 28.4 years (range 17-4 years). Six patients (15.8%) were booked and 32 (84.2%) were not. The average duration of stay in ICU was 5 days. Twenty patients (52.6%) had antepartum eclampsia, 12 (31.6%) had postpartum eclampsia and six (15.8%) presented with intrapartum eclampsia. Twenty-nine (76.3%) gave birth via caesarean section and nine (23.7%) delivered per vagina augmented by oxytocin infusion. Seventeen (45%) received mechanical ventilation; 20 (53%) received oxygen via nasal prongs, nasal catheters or variable performance facemask. One patient (2%) did not receive oxygen therapy. All the patients were admitted postpartum. There were 11 maternal deaths, giving a case fatality rate of 29%. There were five (45.4%) deaths due to haemolysis, elevated liver enzymes and low platelet count syndrome and two (18.2%) due to disseminated intravascular coagulation. The remaining deaths were due to cerebrovascular accident (9.1%), lobar pneumonia (9.1%), acute renal failure (9.1%) and multiple organ failure (9.1%). All patients were admitted postpartum. This fatality rate is higher than that detailed in the reports reviewed in this study. Early referral of eclamptics or at risk patients to a tertiary care institution may help reduce morbidity and mortality. In addition, early referral to a facility providing basic essential obstetric care or comprehensive essential obstetric care is also important. Another important factor is the correct diagnosis of pre-eclampsia during antenatal and postpartum care by screening, noting blood pressure levels, performing urinalysis for protein and asking about warning signs such as headache, blurred vision, epigastric pain, etc.
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PMID:Critical care management of eclamptics: challenges in an African setting. 1830 51

A 38-year-old Caucasian male presented with a 4-week history of nose bleeds, gross hematuria and blurred vision. He was a smoker, who had used cannabis and cocaine previously. At presentation, he had features of malignant hypertension (blood pressure 220/120 mmHg), was hypoxic on room air, with no signs of fluid overload or heart failure. He had acute renal failure with radiological evidence of alveolar hemorrhage. Renal biopsy showed extensive ischemic collapse of glomeruli and severe fibrointimal thickening of the arteries with fibrinoid deposits in the wall. Auto-immune screen was negative. Serum creatinine peaked at 749 micromol/l. Adequate control of blood pressure and supportive oxygen therapy lead to a complete clinical and radiological resolution of the pulmonary hemorrhage and he did not need dialysis. Eighteen months on, his serum creatinine is stable at 279 micromol/l with good blood pressure control. Malignant hypertension is not a recognized cause of the renal-pulmonary syndrome and physicians should be aware of the possibility, if only to avoid inappropriate treatments like plasmapheresis and immunosuppression. History of cocaine use is important in the setting of an acute vascular event.
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PMID:An unusual non-immunological cause of renal pulmonary syndrome. 1982 41

We report a 57-year-old woman with concurrent tubulointerstitial nephritis and uveitis syndrome (TINU) and Fanconi's syndrome. She presented with sudden onset of bilateral ocular pain, blurred vision, acute renal failure, glucosuria and proteinuria. Slit lamp examination revealed acute bilateral anterior uveitis. Tubulointerstitial nephritis was confirmed by kidney biopsy. Laboratory examination revealed normoglycemic glucosuria, proteinuria, normal anion-gap metabolic acidosis, phosphaturia, urinary uric acid wasting and kaliuresis leading to hypokalemia. Her vision and renal function improved gradually after systemic steroid therapy. There have been rare reports of TINU syndrome which had features of Fanconi's syndrome. The prevalence of TINU syndrome may be underestimated, and its association with Fanconi's syndrome requires further investigation.
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PMID:Tubulointerstitial nephritis and uveitis syndrome (TINU) with Fanconi's syndrome. 2126 99

Tubulointerstitial nephritis and uveitis (TINU) syndrome is due to a disregulation of cell-mediated immunity and genetical predisposition due a particular molecular characterization. We report the case of a 50-year-old woman who was admitted for acute renal failure. She had recently taken flurbiprofen for 10 d for recurrent bronchitis. A renal biopsy revealed acute tubulointerstitial nephritis. Prednisone was started and prognosis was favorable. Three months later the patient developed transitory blurred vision. The diagnosis was bilateral uveitis and she received topic and systemic corticosteroid therapy, with resolution of ocular symptoms. Recurrent episodes of uveitis experienced during the next 12 months were treated with same therapy. Genomic haplotype in our patients was HLA A*0278/2631,-B*1517/3802,- Cw*0701/1202, -DRB1*0101/1359 (DRB3* 52), -DQA1*0102/0102, DQB1*0603/0603. TINU syndrome is characterized by tubulointerstitial nephritis that tends to be selflimiting, whereas uveitis tends to relapse. HLA-DQA1*01 and -DQB1*06 haplotypes are strongly associated with TINU syndrome. This is the first report of TINU syndrome induced by flubiprofen intake. Our case emphasizes the importance of the association between drug exposure and strong susceptibility to TINU syndrome giving the molecular characterization.
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PMID:Drug-induced TINU syndrome and genetic characterization. 2287 12

A 63-year-old man was admitted for investigation of blurred vision and multiple ring-enhancing lesions on cranial MRI. Histopathological examination of tissue obtained at brain biopsy showed multiple Toxoplasma gondii cysts. He was started on a combination of sulphadiazine and pyrimethamine for cerebral toxoplasmosis and was subsequently diagnosed with HIV-1 infection. He then developed acute renal failure and flank pain and was diagnosed with bilateral vesico-uretric calculi requiring bilateral stent insertion. The retrieved renal calculi were negative for the common stones that are routinely tested for in our laboratory and had the macroscopic characteristics of a sulphadiazine stone. His renal failure responded to cessation of the sulphadiazine.
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PMID:Sulphadiazine-induced renal stones in a 63-year-old HIV-infected man treated for toxoplasmosis. 2300 Oct 98

A 25-year-old woman presented with acute bilateral blurred vision and history of headache, dizziness, and syncope for three days. Her visual acuity was 20/60 in both eyes. Fundoscopy revealed multiple bilateral peripapillary yellow-white patches like cotton wool spots, intraretinal hemorrhages and macular edema. The patient was diagnosed with Purtscher-like retinopathy based on the retinal findings and lack of trauma history. She was urgently admitted to the nephrology clinic due to thrombotic microangiopathy findings (hemoglobinemia, thrombocytopenia, and acute renal failure). After excluding thrombotic microangiopathy, the patient was diagnosed with atypical hemolytic uremic syndrome (aHUS) with the clinical and laboratory findings. Eculizumab treatment was added to hemodialysis and plasmapheresis therapy. Three months after starting treatment, retinal lesions regressed and visual acuity increased to 20/20 in both eyes. To the best of our knowledge, this is the first reported case of Purtscher-like retinopathy associated with aHUS.
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PMID:Purtscher-Like Retinopathy Associated with Atypical Hemolytic Uremic Syndrome. 2932 53

Posterior reversible encephalopathy syndrome (PRES) was described in 1996. Herein, we aimed to report an immunosuppression- related PRES case. A 34-year-old woman was diagnosed as t-cell acute lymphoblastic leukemia and allogeneic hematopoietic stem cell transplantation (HSCT) was performed. Cyclosporine was given for GVHD prophylaxis in addition to the other routine medications of HSCT. She was hospitalized for acute renal failure and due to the possible contribution of acute renal failure cyclosporine was stopped. Tacrolimus was started for GVHD prophylaxis at a dose of 1 mg/day. However, fifteen days after the initiation of tacrolimus, blurred vision occurred in our patient. Petechial bleeding sites were detected in bilateral cerebral and cerebellar hemisphere by MR imaging. Tacrolimus dosage was reduced to 0.5 mg/day. She had hypertension which was difficult to control and followed-up in the intensive care unit. She had seizures. Control cranial MR resulted as diffusion limitation in bilateral cerebellar hemisphere, bilateral occipital and frontal-parietal regions with vasogenic edema findings; contrast involvement in left frontal-parietal and right cerebellar regions. She had vision loss and lethargy. Control cranial MR favored PRES syndrome secondary to immunosuppression. Hypertensive state was taken under control with antihypertensive treatment and all immunosuppressive agents were stopped. Two weeks later her clinical condition was slightly improved. MR test which was conducted 2 weeks after the diagnosis revealed the regression of PRES lesions. The characteristic signs on neuroimaging are the symmetrical white matter edema in the posterior cerebral hemispheres, particularly the parietal- occipital regions. In conclusion, PRES rarely develops secondary to the immunosuppressive agents and the clinicians should suspect and promptly diagnose PRES which might cause otherwise serious irreversible clinical complications.
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PMID:Immunosuppression-associated posterior reversible encephalopathy syndrome in an acute leukemia case. 3054 27


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