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Nephrolithiasis treatment

Urinary lithiasis is a disease in which calculi form in the kidney and urinary tract. Roughly 5 % of the human population suffers to some degree from urinary lithiasis. A number of severely afflicted patients (e.g. ca. 60,000 in West Germany and more than 100,000 in the U.S.) are hospitalized yearly for major surgical treatment. Obviously, nephrolithiasis is not only a common ailment but also an issue of great social and economic consequence. [Pg.131]

The answer is a. (Katzung, pp 255-256.) Thiazide diuretics can be used in the treatment of nephrogenic diabetes insipidus. Its other uses include the treatment of hypertension, CHF, and nephrolithiasis due to idiopathic hypercalcuria. [Pg.218]

Urinary oxalate Some patients may develop increased levels of urinary oxalate following treatment. Exercise caution in patients with a history of hyperoxaluria or calcium oxalate nephrolithiasis. [Pg.1390]

Some patients receiving indinavir exhibit nephrolithiasis/urolithiasis including flank pain that may be accompanied by hematuria. The frequency of nephrolithiasis is dependent on the period of treatment with indinavir. Other side effects associated with indinavir include insulin resistance, hyperglycemia, asymptomatic hyperbilirubinemia, HIV lipodystrophy syndrome and skin abnormalities. Indinavir should not be coadministered with drugs that affect the cytochrome P-450 system (CYP3A4). Antacids are not recommended within 2 h of its administration, specifically didano-sine containing an antacid buffer. [Pg.189]

Systemic side effects reported with oral CAIs have generally not been seen with topical CAIs. Paresthesias, electrolyte imbalance, and CNS side effects, including malaise and fetigue, have not been reported with dorzolamide. Bitter taste is experienced in approximately 25% of patients taking topical dorzolamide. Three cases of nephrolithiasis have been attributed to topical dorzolamide. Onset was from 21 days to 8 months after treatment began. Two patients, however, had previously received systemic CAIs. Because there may be an increased risk of developing nephrolithiasis, a careful history of renal calculi should be obtained. [Pg.165]

Original attempts to market zonisamide in the USA were halted by reports of nephrolithiasis, but successful marketing in Japan resulted in renewed interest elsewhere (1). Zonisamide has a broad spectrum of efficacy in the treatment of seizures, including infantile spasms and myoclonic seizures. It may also have neuroprotective and antimanic effects. Its mechanism of action is not known, but it blocks sodium channels and T-type calcium channels and scavenges free radicals. [Pg.3728]

Example A study in 1,219 patients of the ATHENA (AIDS Therapy Evaluation National Centre) cohort of patients infected with HIV receiving antiretroviral therapy in the Netherlands showed a frequency of urological symptoms (including nephrolithiasis, renal colic, flank pain, hematuria, renal insufficiency, or nephropathy) of 8.3 per 100 treatment-years for indinavir compared to 0.8 per 100 treatment-years for other HIV protease inhibi-... [Pg.87]

Valencia ME J-NI, Rodriguez-Rosado R, SorianoV, Carrillo deAlbornoz ME, Gonzalez Lahoz J. Incidence of nephrolithiasis in HIV infected patients under indinavir treatment, [abstract 448]. Sixth European Conference on Clinical Aspects and Treatment of HIV Infection October 1997 Hamburg October 1997. [Pg.375]

In 1930 and 1932, two separate reports were published, each describing the successful treatment of 2 patients with hypercalcemia secondary to hyperparathyroidism with inorganic phosphate [37-38]. Due to the potential for this treatment to lead to nephrolithiasis or extraskeletal calcifications, it was not widely employed. In 1966, Goldsmith and Ingbar reported... [Pg.586]

Potential complications of long-term furosemide (frusemide) treatment in humans, in addition to the more obvious problems such as volume depletion and the development of azotemia, are potassium depletion leading to hypokalemia (see p. 353), nephrolithiasis, nephrocalcinosis and... [Pg.163]

Triamterene has been reported to cause photosensitivity reactions, increase in uric acid concentration, and blood dyscrasias.91 Nephrolithiasis may occur in susceptible patients. Megaloblastic anemia has been reported in patients with depleted folic acid stores such as those with hepatic cirrhosis. In a study conducted on rats, daily treatment of the animals with doses of 1.5, 3 and 4.5 mg/lOOg over the period of three weeks caused severe degenerative changes of renal cortical and medullary tubules resembling osmotic nephrosis.93 Reversible acute renal failure from combined triamterene and indomethacin in healthy subjects is reported.94 It is recommended that this potentially nephrotoxic association be avoided. [Pg.589]

Preminger GM, Is there a need for medical evaluation and treatment of nephrolithiasis in the age of lithotripsy Semin Urol 1994 12 51-64. [Pg.1740]

The mainstay of drug therapy for recurrent uric acid lithiasis is allopurinol. It is effective in reducing both serum and urinary uric acid levels, thus preventing the formation of calculi. Allopurinol is also recommended as prophylactic treatment in patients who wfll receive cytotoxic agents for the treatment of lymphoma or leukemia. The marked increase in uric acid production associated with cytolysis of a neoplasm predisposes a patient to the development of uric acid nephrolithiasis. [Pg.1709]

Questions are often raised regarding the indications for drug therapy for asymptomatic hyperuricemia. The purported heneflts from treatment include prevention of acute gouty arthritis, tophi formation, nephrolithiasis, and chronic urate nephropathy. The first three complications are easily controlled shonld they develop therefore antihyperuricemic therapy is not warranted to prevent these conditions. [Pg.1710]

An AIDS patient who is being treated with multiple drugs, including AZT, lamivudine, indinavir, ketoconazole, and TMP-SMX, develops breast hypertrophy, central adiposity, hyperlipidemia, insulin resistance, and nephrolithiasis. If these changes are related to his drug treatment, the most likely cause is... [Pg.223]

Uric acid nephrolithiasis calcium renal stones Malignant mesothelioma Status epilepticus Herpes simplex encephalitis Neurosyphilis Status epilepticus Cognitive dysfunction Malignant non-Hodgkin s lymphomas Treatment of PCP associated with AIDS Acanthamoeba keratitis Peripheral arterial occlusive disease Congenital or acquired protein C deficiency Respiratory distress syndrome associated with prematurity... [Pg.524]

Candidates for teriparatide treatment include women who have a history of osteoporotic fracture, who have multiple risk factors for fracture, or who failed or are intolerant of previous osteoporosis therapy. Teriparatide should not be used in patients who are at increased baseline risk for osteosarcoma (including those with Paget s disease of bone, unexplained elevations of alkaline phosphatase, open epiphyses, or prior radiation therapy involving the skeleton). Full-length PTH(l-84), which is in clinical trials, has not been associated with osteosarcomas. Other adverse effects have included exacerbation of nephrolithiasis and elevation of serum uric acid levels. [Pg.678]

Thiazide diuretics, which reduce urinary excretion of Ca, sometimes are employed to treat calcium nephrolithiasis and may be useful for the treatment of osteoporosis see Chapter 61). Thiazide diuretics also are a mainstay for treatment of nephrogenic diabetes insipidus, reducing urine volume by up to 50%. The mechanism of this paradoxical effect remains unknown. Since other hahdes are excreted by renal processes similar to those for Cl", thiazide diuretics may be useful for the management of Br" intoxication. [Pg.492]

Wasserstein AG, Rak I, Reife RA. Nephrolithiasis during treatment with topiramate. Epilepsia 1995 36(Suppl 3) S153. [Pg.65]

Coe, F.L. Nephrolithiasis. Pathogenesis and treatment. Year Book Medical Publishers 1978, pp 95- Chicago and London. [Pg.51]

The results of this study indicate that excessive purine intake is a major cause for hyperuricosuria among stone patients. Therefore, restriction of dietary purines is of therapeutic value in the treatment of nephrolithiasis. [Pg.71]

Out of 529 inpatients with nephrolithiasis, in 30.4% these stones consisted of pure uric acid (Table 4). In 133 of 161 patients with uric acid stones, which means in almost 83%, the concrement had led to a congestion of the descending urinary tract this occurred on both sides in 15 cases. As can also be seen from Table 4, in more than 20% of the cases a treatment with a uricosuricum — generally Benzbromaron — had been started. [Pg.101]

F. L. Coe, Nephrolithiasis pathogenesis and treatment. Year book of Medicine. Year book Publishers Inc. Chigago, London. (1978). ... [Pg.200]

Jocham D, Brandi H, Chaussy C, Schmiedt E. Treatment of nephrolithiasis with ESWL. In Gravenstein JS, Peter K, eds. Extracorporeal Shock Wave Lithotripsy... [Pg.615]


See other pages where Nephrolithiasis treatment is mentioned: [Pg.291]    [Pg.291]    [Pg.199]    [Pg.131]    [Pg.199]    [Pg.154]    [Pg.1031]    [Pg.361]    [Pg.390]    [Pg.163]    [Pg.802]    [Pg.1715]    [Pg.1043]    [Pg.255]    [Pg.456]    [Pg.824]    [Pg.1041]    [Pg.116]    [Pg.692]   
See also in sourсe #XX -- [ Pg.1708 ]




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