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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indinavir sulfate is a protease inhibitor that has been found to be extremely effective in increasing CD4+ cell counts and in decreasing HIV-RNA titers in patients with HIV and AIDS. However, patients receiving indinavir also have been noted to have a significant risk for developing urolithiasis. Published reports of indinavir urolithiasis estimate its incidence at between 4 and 13%. Indinavir has a high urinary excretion with poor solubility in a physiologic pH solution. Consequently, patients develop urinary stones that are principally composed of indinavir or of a mixture of indinavir and other substances, such as calcium oxalate. Similar to other forms of urolithiasis, acute flank pain and hematuria are the typical symptoms of indinavir urolithiasis. Indinavir urolithiasis is unique in that computed tomography, which was once thought to be efficacious in identifying all urinary calculi, is not useful in imaging stones that are composed of pure indinavir. Indinavir urolithiasis generally responds to a conservative regimen of hydration, pain control, and the temporary discontinuation of the medication. Only a minority of patients need surgical intervention. Approximately 10% of patients ultimately need to discontinue indinavir therapy altogether. Indinavir is an antiviral agent that has a significant role in the treatment of AIDS. Although urolithiasis is a significant side effect of indinavir use, limiting its clinical application is not the answer. Rather, physicians need to know more about indinavir urolithiasis to help their patients cope with its potential complications.
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PMID:Indinavir urolithiasis. 1114 25

Indinavir sulfate is a protease inhibitor used of the treatment of primary HIV infection either as monotherapy or as part of antiretroviral treatment schemes. Approximately 10% of all patients develop urolithiasis with radiolucent stones consisting of indinavir. We present our results of the treatment in 11 HIV positive patients (9 men, 2 women), who developed Indinavir lithiasis after 5-8 months of antiretroviral therapy. Following the initial procedures (spasmoanalgetic drugs, ureteroscopy, double J-stent or nephrostomy), the patients were further treated by increasing diuresis and urinary acidification. All the patients responded well to the treatment, the obstruction was releieved and their renal function was restored to normal.
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PMID:Treatment of indinavir sulfate induced urolithiasis in HIV-positive patients. 1254 31

Indinavir sulphate is a protease inhibitor that has been found to be extremely effective in increasing CD4+ cell counts and in decreasing HIV-RNA titers in patients with HIV and AIDS. However, patients receiving indinavir also have been noted to have a significant risk of developing urolithiasis. Indinavir has high urinary excretion with poor solubility in a physiologic pH solution. The typical symptoms of indinavir urolithiasis are similar to other forms of urolithiasis. Indinavir urolithiasis is unique in that computed tomography, which was once thought to be efficacious in identifying all urinary calculi, is not useful in imaging stones that are composed of pure indinavir. Indinavir urolithiasis generally responds to a conservative regimen of hydration, pain control, and temporary discontinuation of the medication. Only a minority of patients need surgical intervention.
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PMID:[Renal lithiasis due to indinavir]. 1268 14

Drug-induced calculi represent 1-2% of all renal calculi. The drugs reported to produce calculi formation may be divided into two groups. The first one includes poorly soluble drugs with high urine excretion that favours crystallisation in the urine. Among poorly soluble molecules, triamterene was the leading cause of drug-containing urinary calculi in the 1970s, and it is still currently responsible for a significant number of calculi. In the last decade, drugs used for the treatment of HIV-infected patients, namely indinavir and sulfadiazine, have become the most frequent cause of drug-containing urinary calculi. Besides these drugs, about twenty other molecules may induce nephrolithiasis in patients receiving long-term treatment or high doses. Calculi analysis by physical methods, including infrared spectroscopy or x-ray diffraction, is needed to demonstrate the presence of the drug or its metabolites within the calculi. The second group includes drugs that provoke urinary calculi as a consequence of their metabolic effects. Here, diagnosis relies on careful clinical inquiry because physical methods are ineffective to differentiate between urinary calculi induced by the metabolic effects of a drug and common metabolic calculi. The incidence of such calculi, especially those resulting from calcium/vitamin D supplementation, is probably underestimated. Although drug-induced urinary calculi most often complicate high-dose, long-duration drug treatments, there also exist specific patient risk factors in relation to urine pH, urine output and other parameters, which provide a basis for preventive or curative treatment of calculi. Better awareness of the possible occurrence of lithogenic complications, preventive measures based on drug solubility characteristics and close surveillance of patients on long-term treatment with drugs with lithogenic potential, especially those with a history of urolithiasis, should reduce the incidence of drug-induced nephrolithiasis.
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PMID:Drug-induced renal calculi: epidemiology, prevention and management. 1487 Nov 69

We describe the first case of efavirenz-induced urolithiasis in a 47-year-old HIV-positive patient. Urinary obstruction led to pyelonephritis and septic shock, requiring emergency ureteral catheterisation. The subsequent clinical course was favourable, allowing the patient's discharge on day 5. A 7 mm, radio-translucent, non-crystalline, beige stone was extracted during catheterisation. Stone analysis by Fourier transform infrared spectrometry, liquid chromatography and mass spectrometry revealed a stone composed of efavirenz (EFV) metabolites M4, M5, M8 (as described by Mutlib et al. in 1999) and approximately 50% of unspecified proteins. EFV is a non-nucleoside reverse transcriptase inhibitor introduced to European markets in 1999. It is principally metabolised by cytochrome P450 3A4 and 2B6. Of the dose, 14-34% is excreted in the urine, 1% as unchanged drug. The patient had been taking 600 mg EFV per day for 3 years. As EFV-induced urolithiasis has not been reported so far, we would like to draw the attention of the medical community to this potentially severe complication.
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PMID:Efavirenz-induced urolithiasis. 1662 85

Three HIV-seropositive patients were diagnosed with urolithiasis related to the use of indinavir. The first patient was a 45-year-old white male with severe haemophilia who presented with fever and flank pain referred to the glans penis. Ultrasound and intravenous pyelography (IVP) revealed a concrement in the left renal pelvis. Discontinuation of indinavir and acidification of the urine did not reduce the stone load. Percutaneous nephrolithotripsy was then performed. The second patient, a 41-year-old white male, presented at the emergency ward with flank pain and fever. Ultrasound examination showed dilatation of the left kidney. A percutaneous nephrostomy catheter was inserted. Antegrade contrast imaging showed a concrement in the proximal ureter. The patient underwent extracorporeal shock wave lithotripsy. A second antegrade image made a few days later showed no evidence of stone material. The third patient was a 56-year-old white male with a previous history of indinavir-associated urolithiasis. He presented at the emergency ward with flank pain and haematuria. A CT urography showed dilatation of the right kidney and distal portion of the right ureter with no evidence of concrement. The symptoms resolved after a percutaneous nephrostomy catheter was inserted and the antiviral medication was modified. The catheter was removed 2 weeks later. At last follow-up, none ofthe 3 patients had symptoms of urolithiasis. These cases illustrate that, although conservative therapy for indinavir-related urolithiasis can be sufficient, minimally invasive endourological surgery is sometimes necessary.
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PMID:[Three patients with indinavir-related urolithiasis]. 1787 43

The prevalence of HIV continues to grow in the United States and worldwide. HIV-positive patients experience many genitourinary disease processes. With improvements in HIV therapy, patients have questions and concerns pertaining to their quality of life. This article reviews conditions such as HIV-related urinary tract infections, urolithiasis, voiding dysfunction, fertility, sexual dysfunction, HIV-related nephropathy, malignancies, and occupational exposure and prophylaxis. Knowledge of the various HIV manifestations of genitourinary conditions and their treatment options benefits clinicians and improves patient outcomes.
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PMID:HIV-AIDS: urologic considerations. 1806 Oct 24

In recent years the nature of HIV infection has been dramatically transformed from an invariably fatal disease to a chronic disorder with a relatively benign course. Disease progression from HIV to AIDS and HIV-related mortality can be reduced effectively by several years of treatment with highly active antiretroviral therapy (HAART). For patients who do not have access to HAART, HIV infection continues to be a lethal disorder characterized by opportunistic infection with uncommon organisms (e.g. mycobacteria, fungi, parasites and viruses), as well as lethal malignancies such as Kaposi sarcoma, non-Hodgkin lymphoma and squamous cell carcinoma of the penis or cervix. In patients receiving HAART, urologic complications are likely to be caused by adverse effects of antiretroviral medication (e.g. indinavir urolithiasis) or disorders associated with aging, such as benign prostatic hyperplasia and prostate cancer. Prospective clinical trials have shown that adult male circumcision can reduce the rate of female to male HIV transmission by more than 50%; however, the development of preventive or curative modalities with 100% efficacy remains elusive.
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PMID:Urologic complications of HIV and AIDS. 1913 4

Here, we report a case of chronic granulomatous tubulo-interstitial nephritis related to atazanavir crystals in a HIV type-1-infected patient. Renal function in this patient was partially recovered after atazanavir withdrawal and steroid therapy. Many reports have described atazanavir-associated urolithiasis, but this is the first case that describes chronic granulomatous nephropathy.
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PMID:Chronic interstitial nephritis in an HIV type-1-infected patient receiving ritonavir-boosted atazanavir. 2131 Nov 16

Several observational studies have identified tenofovir as an independent risk factor for kidney impairment. Conversely, randomized trials have only demonstrated minor tenofovir-related changes in kidney function, but these studies included patients with normal kidney function and with low underling risk for progression of their renal function, had limited size, and limited follow-up. Several potential mechanisms of tenofovir nephrotoxicity are known. Atazanavir can, equally to indinavir, cause urolithiasis, but both drugs have also been associated with chronic kidney disease (CKD) and fast declining eGFR in persons without clinical symptoms of urolithiasis, especially when the plasma drug concentration is boosted by concomitant ritonavir use. In 2012, only a minority of HIV-positive individuals are affected by drug-induced nephrotoxicity. However, in the future, the clinical impact and hence the requirement for more research in this area will likely increase due to ageing and continued cART exposure of the HIV-positive population.
Curr HIV/AIDS Rep 2012 Jun
PMID:HIV therapies and the kidney: some good, some not so good? 2237 Sep 68


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