Nephropathy uric acid

Develop a pharmacotherapeutic plan for a patient with acute gouty arthritis or uric acid nephropathy that includes individualized drug selection and monitoring for efficacy and safety. 

Acute uric acid nephropathy, which is characterized by the acute overproduction of uric acid and by extreme hyperuricemia, can best be prevented with which of the following ... 

The answer is c. (Hardman, pp 649—650.) Acute hyperuricemia, which often occurs in patients who are treated with cytotoxic drugs for neoplasic disorders, can lead to the deposition of urate crystals in the kidneys and their collecting ducts. This can produce partial or complete obstruction of the collecting ducts, renal pelvis, or ureter. Allopurinol and its primary metabolite, alloxanthine, are inhibitors of xanthine oxidase, an enzyme that catalyzes the oxidation of hypo xanthine and xanthine to uric acid. The use of allopurinol in patients at risk can markedly reduce the likelihood that they will develop acute uric acid nephropathy. 

In acute uric acid nephropathy, acute renal failure occurs as a result of blockage of urine flow secondary to massive precipitation of uric acid crystals in the collecting ducts and ureters. This syndrome is a well-recognized complication in patients with myeloproliferative or lymphopro-liferative disorders and results from massive malignant cell turnover, particularly after initiation of chemotherapy. Chronic urate nephropathy is caused by the long-term deposition of urate crystals in the renal parenchyma. 

Allopurinol is the antihyperuricemic drug of choice in patients with a history of urinary stones or impaired renal function, in patients who have lymphoproliferative or myeloproliferative disorders and need pretreatment with a xanthine oxidase inhibitor before initiation of cytotoxic therapy to protect against acute uric acid nephropathy, and in patients with gout who are overproducers of uric acid. 

Risk factors for ARF include advanced age, acute infection, preexisting chronic respiratory or cardiovascular disease, dehydration, and chronic kidney disease (CKD). Decreased renal perfusion secondary to abdominal or coronary bypass surgery, acute blood loss in trauma, and uric acid nephropathy also increase risk. 

Prevention of uric acid nephropathy during vigorous therapy of neoplastic disease ... 

To prevent uric acid nephropathy during chemotherapy PO Initially, 600-800 mg/day starting 2-3 days before initiation of chemotherapy or radiation therapy. IV 200-400 mg/mVday beginning 24-48 hr before initiation of chemotherapy. Akrt Maintenance dosage is laased on serum uric acid levels. Discontinue following the period of tumor... 

Erley CM, Hirschberg RR, Hoefer W, Schaefer K (1989) Acute renal failure due to uric acid nephropathy in a patient with renal hypouricemia. Klin Wochenschr 67 308-312... 

Momose A, Kudou D, Nishimura S, Sawada Y, Kitagawa M, Funao T, Suzuki Y (1996) A case of exercise-induced acute renal failure due to uric acid nephropathy in patient with cystinuria (in Japanese). Jin-To-Tohseki (Kidney Dial) 41 853-857... 

Streptozocin is highly nephrotoxic, and renal function must be monitored carefuUy in all patients who are receiving it. Its effects include uremia, proteinuria, anuria, and proximal renal tubular acidosis (16). Uric acid nephropathy has also been reported (17). Adequate hydration has been recommended to reduce the risk of nephrotoxicity (18). 

Treatment of chronic gouty arthritis, Half-life uric acid nephropathy. Prevents or 2-3 hours... 

Allopurinol is the antihyperuricemic drug of choice in patients with a history of urinary stones or impaired renal function, in patients who have lymphoproliferative or myeloproliferative disorders and need pretreatment with a xanthine oxidase inhibitor before initiation of cytotoxic therapy to protect against acute uric acid nephropathy, and in patients with gout who are overproducers of uric acid. The major side effects of allopurinol are skin rash, leukopenia, occasional gastrointestinal toxicity, and increased frequency of acute gouty attacks with the initiation of therapy. An allopurinol hypersensitivity syndrome characterized by fever, eosinophilia, dermatitis, vasculitis, and renal and hepatic dysfunction is a rare side effect, but is associated with a 20% mortality rate. ... 

Dykman D, Simon EE, Avioh W. Hyperuricemia and uric acid nephropathy. Arch Intern Med 1987 147 1341-1345. 

Srivastava, A.S. 1970. Important insect pests of stored oilseeds in India. Int. Pest Control12,18-20,26. Starvic, B., Johnson, W.J., and Grice, H.C. 1969. Uric acid nephropathy—an experimental model. 

ATLS is potentially a catastrophic complication of chemotherapy in patients with a high tumour load. It results from cytotoxic damage to large numbers of cancerous cells. The DNA and RNA released are broken down to uric acid, which precipitates in the renal tubules causing acute uric acid nephropathy. Recent evidence suggests that recombinant urate oxidase, which converts uric acid to soluble allan-toin, is successful in the treatment and prevention of ATLS in patients with haematological malignancies. 

While this proposed mechanism may not necessarily explain all the observed facets of uric acid nephropathy, it is suggested that it does contribute further to our understanding of the pathogenetic mechanisms involved in this condition. 

The increased uric acid load, which the newborn has to cope with is probably due to the physiological fall of white and red blood cell populations seen at this age. It seems that this potential hazard of an excretion of a large uric acid load, as seen in instances of uric acid nephropathy, is facilitated by the concomitant excretion of a relatively alkaline and dilute urine. 

Reactions following initial infusions of antibody are common, but these can usually be handled by a cautious rate of infusion, appropriate hydration and diuresis, and, if necessary, praned-ication. Twenty six percent of initial reactions are reported to be mild, 48 % moderate, and 26 % severe. The initial infusion reaction to some mAbs, for example, rituximab (see below), may provoke tumor lysis syndrome, cytokine release syndrome, and systemic inflammatory response syndrome. Tumor lysis syndrome, noted particularly with rituximab, can occur following cancer treatment and sometimes without treatment. It is believed to be the result of breakdown products of cancer cells leading to increased levels of some metabolites and reflected in conditions such as hypercalcemia, hyperkalemia, hyperphosphatemia, acute uric acid nephropathy, and acute renal failure. The syndrome can occur in the early stages of mAb therapy and is potentially life-threatening. Cytokine release syndrome, also called cytokine storm, is commonly seen after... 

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