Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 36-year-old with end-stage renal disease secondary to hypertensive nephrosclerosis had a two-day history of epigastric pain and nausea. Soon after admission, multiple grand mal seizures uncontrolled by intravenous phenytoin sodium and diazepam developed. His calcium level was 14 mg/dL and his amylase level was 2,230 mg/dL; lumbar puncture was normal. Hemodialysis lowered his calcium level to 10.7 mg/dL but failed to control his seizures. Secondary hyperparathyroidism was thought to be the cause of his malignant hypercalcemia, and an emergency subtotal parathyroidectomy was performed. Postoperatively, his grand mal seizures resolved. Confusion and aphasia also developed, but they resolved over the ensuing three weeks. Microscopic examination of the parathyroid glands revealed diffuse chief cell hyperplasia. Preoperative parathormone level was 2,196 pg/dL (normal, less than 450 pg/dL). A review of the literature has failed to reveal a similar case.
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PMID:Secondary hyperparathyroidism manifesting as acute pancreatitis and status epilepticus. 728 72

This report describes a patient with acute renal failure that resulted from the ingestion of djenkol beans. Features of acute djenkolism include nausea, vomiting, bilateral loin pain, gross hematuria, and oliguria. The blood urea level was 16.2 mmol/L and the serum creatinine was 460 mumol/L. Phase contrast microscopy of the urinary sediment indicated that the hematuria was nonglomerular. Ultrasound of the kidneys showed slightly enlarged kidneys with no features of obstruction. Renal biopsy showed acute tubular necrosis similar to the single animal study reported in the literature. With conservative therapy, which included rehydration with normal saline and alkalinization of the urine with sodium bicarbonate, the acute renal failure resolved. Based on its chemistry, djenkol bean-associated acute renal failure may be analogous to acute uric acid nephropathy.
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PMID:Djenkol bean poisoning (djenkolism): an unusual cause of acute renal failure. 781 May 35

Effective renal plasma flow (ERPF) was evaluated, using continuous-infusion p-aminohippurate clearance (CLPAH) and single-injection plasma clearance of technetium-99m mercaptoacetyltriglycine (99mTc-MAG3; CLMAG3) methods. Simultaneous clearance determinations were made in 6 dogs: 2 determinations for each dog before, and 1 determination after renal failure was induced by administration of amphotericin B. Linear regression analysis was used to derive an equation to estimate ERPF from CLMAG3 after the single IV injection. A Student's t-test was used to compare pharmacokinetics between the dogs when they were healthy and when they were in renal failure. An F-test was used to determine the appropriate Student's t-test. Results indicated that CLMAG3 correlated reasonably well (r = 0.83, P < 0.0001) with ERPF obtained from the CLPAH value. The volume of distribution and elimination of 99mTc-MAG3 decreased during renal failure. Although there was minimal binding of 99mTc-MAG3 to erythrocytes, it was significantly (P = 0.0008) lower during renal failure. Protein binding was not significantly different during renal failure. All dogs had signs of nausea and emesis at variable times after injection of 99mTc-MAG3. Determination of CLMAG3 after a single injection provides an adequate means to rapidly assess ERPF in dogs. The technique could easily be performed in dogs with renal disease, thus providing valuable information regarding progression of naturally acquired renal failure.
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PMID:Evaluation of the single-injection plasma disappearance of technetium-99m mercaptoacetyltriglycine method for determination of effective renal plasma flow in dogs with normal or abnormal renal function. 788 6

Although serologic studies have identified hantaviral infection in the United States, acute disease has not been recognized. This study describes 3 cases of domestically acquired hemorrhagic fever with renal syndrome (HFRS) in the United States. Infection was due to a local strain of Seoul virus (Baltimore rat virus). A review of the clinical features indicated a mild illness characterized by nausea, vomiting, renal and liver failure similar to HFRS described elsewhere for rat-borne viruses. Follow-up of 2 patients identified persistent hypertension and renal disease providing further evidence of an association between past hantaviral infection and hypertensive renal disease.
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PMID:Domestic cases of hemorrhagic fever with renal syndrome in the United States. 799 Oct 40

Seventy-five non-dialized patients with chronic renal failure (CRF) and severe renal anemia were enrolled in a study, receiving r-HuEPO subcutaneously thrice weekly for 6 months. In 64 patients (85%) 7 weeks of treatment with a weekly dose of 158 U/kg were required to achieve Hb concentrations within the target range of 10 to 12 g/dl. Of the 11 patients (15%) who failed to achieve the target Hb range, none were considered to be non-responders as they were excluded for unrelated reasons prior to week 16 (8 cases), or were iron deficient (2 cases), or had bleeding complications (1 patient). Maintaining the Hb concentration at a level of 10.5 g/dl required a mean r-HuEPO dose of 92 U/kg per week. Adverse events were generally mild or moderate. The most commonly reported were hypertension (8%), viral infection/including flu-like syndrome (7%), nausea (7%), and dizziness (5%). Statistically significant increases in mean creatinine concentrations observed after 12 and 24 weeks were most likely due to the progression of renal disease. These results confirm that 50 U/kg of r-HuEPO given 3 times per week subcutaneous provide a safe and effective therapy for anemic predialysis patients.
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PMID:Effectiveness and safety of recombinant human erythropoietin (r-HuEPO) in the treatment of anemia of chronic renal failure in non dialysis patients. European Multicentre Study Group. 807 Sep 41

Nodular duodenum, frequently described as nodular duodenitis, is endoscopically characterized by multiple erythematous nodules in the proximal duodenum and may represent a variant of duodenal inflammation. This study examines the incidence, clinical presentation, histologic correlates, natural history, and response to therapy of nodular duodenum in 83 patients who presented with epigastric pain, heartburn, early satiety, bloating, nausea, vomiting, or gastrointestinal bleeding. There was a previous history of peptic ulcer disease in 58% of patients and gastroesophageal reflux in 33%. None of the patients had associated end-stage renal disease. Endoscopically, in addition to nodular duodenum, esophagitis was found in 17% of patients and gastritis in 32%. Histology of duodenal nodules revealed chronic inflammation in 58% of patients, Brunner's gland hyperplasia in 9%, gastric heterotopia in 7%, and normal mucosa in 26% of patients. In a group of 34 patients studied prospectively, high dosage (300 mg orally bid) therapy with the H2-antagonist ranitidine for 8 wk significantly improved symptoms and endoscopic appearance (p < 0.05). In 26 patients who completely or partially failed H2-antagonist therapy, continuation of therapy with omeprazole (40 mg orally qd) for 8 wk significantly improved symptoms and endoscopic findings (p < 0.05) in 10 patients. These therapeutic approaches led to improvement in the endoscopic findings, but to no statistically significant changes in the underlying histologic appearance of the duodenum. We conclude that nodular duodenum is an endoscopically distinct entity that may respond clinically to antisecretory therapy, but remains difficult to eradicate completely.
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PMID:Clinical and pathologic features of the nodular duodenum. 831 6

Diet and nutrition are integral to the management of individuals with renal disease. Uremia engenders anorexia, nausea, meat aversion, and emesis, disturbances that ultimately reduce appetite and cause weight loss and malnutrition. Protein restriction can alleviate these uremic symptoms and improve patient health and vigor, but overly zealous protein restriction may, itself, produce malnutrition. This is particularly likely when energy intake is restricted by either design or anorexia. End-stage renal disease patients require renal replacement therapy for survival, and although dialysis is life sustaining, it neither replaces normal kidney function nor obviates the need for dietary management. In this setting of controlled, persistent uremia, undernutrition can develop surreptitiously. Dialysis physicians have long regarded malnutrition as a sign of uncontrolled uremia and failing health. This supposition has now been validated by epidemiologic studies demonstrating that serum albumin and protein catabolic rate (PCR) discriminate between dialysis patients at high and low risk of death or illness. This correlation of undernutrition with health and survival persists across wide ranges of age, medical diagnoses, and dialysis prescriptions. Because PCR is readily measured using urea kinetic analyses, it has been promoted as a patient monitoring tool and under steady-state conditions it is a reliable method of determining protein intake. Although a single PCR measurement does not integrate day-to-day dietary and metabolic fluctuations and contains an inherent uncertainty of +/- 20%, sequential measurements can be used to assess changes in an individual's dietary protein intake. PCR defines nitrogen losses and, when normalized to a realistic index of metabolic activity (metabolically active body size), it can disclose subtle individual variances in nitrogen utilization. These normalized protein catabolic rates (NPCR) do not, however, measure or describe overall nutrition. The normalization schemes employed are based on population averages and only approximate an individual's true metabolic activity. Thus, using NPCR to define nutritional needs can result in overfeeding obese and underfeeding wasted subjects. Instead, nutritional adequacy should be defined by clinical inspection and comparison with defined standards. Once that state is defined, and desirable protein and calorie intakes are determined, NPCR can be used to monitor the patient's ability to maintain homeostasis.
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PMID:The significance of protein intake and catabolism. 859 Nov 24

Six patients are with inappropriate secretion of antidiuretic hormone syndrome are reported (two with bacterial acute meningitis, two with bacterial pneumonia, one with oat cell lung carcinoma, other with mediterranean fever boutonneuse) and the clinical manifestations were: mind changes (four cases) nausea-vomiting (two cases) and inappetence (six cases). All patients presented hyponatremia criteria, serum decreased osmolarity, urinary sodium and osmolarity increased, without edemas, renal disease endocrine (hypophysis, thyroids, adrenal) without diuretic treatment. Treatment was, effective water restriction in three patients and hydrochloride of demeclocycline in other three patients.
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PMID:[Inappropriate ADH secretion syndrome]. 867 42

Patients with end-stage renal disease commonly develop secondary hyperparathyroidism. Calcitriol may be administered to such patients to decrease the synthesis and secretion of parathyroid hormone (PTH) and to help maintain calcium and phosphorus homeostasis. However, the doses of calcitriol required to suppress serum PTH concentrations can lead to hypercalcemia or hyperphosphatemia in many patients undergoing hemodialysis. Paricalcitol is a new vitamin D analogue that is safe and effective in suppressing elevated concentrations of PTH in patients with established hyperparathyroidism who are maintained on chronic hemodialysis. As with vitamin D, the biologic action of paricalcitol is mediated through activation of the vitamin D receptor (VDR). The VDR functions as a ligand-induced transcription factor regulating the rate of expression of genes that are involved in controlling not only calcium homeostasis and bone remodeling but also hormone secretion, inhibition of cell growth, and induction of cell differentiation. In vitro studies have shown that paricalcitol inhibits PTH secretion from bovine parathyroid cells in a dose-dependent manner. Studies in renally insufficient rats demonstrated that paricalcitol caused approximately 10 times less elevation of serum calcium concentrations than calcitriol. In clinical studies, paricalcitol effectively decreased PTH by about 60% over a 12-week period. Mean serum concentrations of calcium were significantly increased but remained within the normal range. There were occasional (5/414 determinations) transient elevations in serum calcium above the upper limit of normal in some (5/401) patients. Serum phosphorus values did not change significantly compared with baseline, although they tended to be slightly higher in the paricalcitol-treated group than in the group receiving placebo. Elevations of the calcium-times-phosphorus product were relatively few but occurred more often in the paricalcitol than in the placebo group. The terminal half-life of paricalcitol was 5 to 7 hours in healthy subjects; in patients undergoing hemodialysis, it was 14 hours. Adverse events associated with paricalcitol use included, among others, chills, feeling unwell, fever, sepsis, palpitations, dry mouth, gastrointestinal bleeding, nausea, vomiting, edema, light-headedness, and pneumonia. Paricalcitol should be considered as an alternative to calcitriol in the treatment of patients who are undergoing maintenance hemodialysis for end-stage renal disease, as it has a decreased potential to induce hypercalcemia and hyperphosphatemia. Additional studies are required to determine the long-term effects of therapy.
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PMID:Paricalcitol, a new agent for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis. 1032 13

The most frequent cause of upper urinary tract infection remains E. coli. Other organisms are found in complicated infections associated with diabetes mellitus, instrumentation, stone, and immunosuppression. The pathogenesis of acute pyelonephritis is reviewed herein, with an emphasis on the virulence factors responsible for its initiation, including urothelial adhesion by P-fimbriae of E. coli and other common factors including hemolysin and aerobactin. Renal damage does not always ensue following such infection. It is seen when toxic oxygen radicals are released during the ischemic episode and the respiratory burst of phagocytosis is marked and prolonged. These events occur when effective antibacterial treatment is delayed when the diagnosis is not made early or when socioeconomic factors prevent treatment. The scarring of chronic pyelonephritis leads to the loss of renal tissue and function and may progress to end-stage renal disease. With effective antibacterial therapy, the immune response by both T and B lymphocytes leads to antibodies that assist in bacterial eradication. Therapy must be both rapid and effective. In many instances, antibacterial agents may be used as outpatient therapy. If the Gram stain shows only gram-negative organisms and if the infection is community acquired, oral outpatient therapy with trimethoprim/sulfamethoxazole or a fluoroquinolone may suffice if the patient has no nausea. When the patient is septic, hospitalization and treatment with parenteral antibiotics are needed. Both ceftriaxone and gentamycin are cost-effective parenteral therapy because only once-daily dosing is needed. If gram-positive organisms are found, an enterococcus should be suspected, and a beta-lactam penicillin such as piperacillin or a third-generation cephalosporin such as ceftriaxone is indicated. If penicillin allergy exists, vancomycin should be used. If the patient does not improve rapidly, diagnostic studies including ultrasound and CT will assist in the diagnosis of obstruction, abscess, or emphysematous pyelonephritis. Most of these complications are now rapidly treated percutaneously, with surgical therapy following as needed. Complicated infections, such as those occurring in patients with anatomic abnormalities, stone, or immunosuppression, are often caused by organisms other than E. coli, and long-term antibacterial therapy often leads to fungal infections such as candidiasis. A recrudescence of tuberculosis is occurring, often with resistance to antituberculous drugs. The increased incidence has been associated with the immunosuppression of AIDS but is also occurring in intravenous drug users, perhaps because of poor nutrition but also owing to noncompliance with treatment. The symptoms of renal tuberculosis are usually limited to fever, frequency, urgency, and dysuria. Hematuria with sterile pyuria is the usual laboratory finding. The young urologist should remember this renal disease in the differential diagnosis of hematuria, because medical therapy can provide a cure.
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PMID:Management of pyelonephritis and upper urinary tract infections. 1058 16


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