Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392525 (nephrolithiasis)
 2,669 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human immunodeficiency virus (HIV) patients on nucleoside or nucleotide reverse transcriptase inhibitors with HIV RNA at <1,000 copies/ml were randomized in an open-label study to administration of combined indinavir/ritonavir (IDV/RTV) at 667/100 mg every 12 h (q12h) or IDV alone at 800 mg q8h to determine the regimens' pharmacokinetics. On day 14, plasma IDV and RTV levels were determined over 24 h. Noncompartmental pharmacokinetics (minimum concentration of drug in serum [C(min)], area under the concentration-time curve from 0 to 24 h [AUC(0-24)], and maximum concentration of drug in serum [C(max)]) were expressed as geometric mean values with 90% confidence intervals (CI). The primary hypothesis was that the lower bound of the protocol-specified 90% CI for the geometric mean C(min) ratio of the combination compared to IDV alone regimen would be >/=2. Twenty-seven patients were enrolled, and 24 (15 male; average age, 42 years) completed the study. The C(min), AUC(0-24), and C(max) for IDV/RTV compared to IDV alone were 1,511 versus 250 nM, 119,557 versus 77,034 nM . h, and 10,428 versus 10,407 nM, respectively. Corresponding relationships for IDV/RTV compared to IDV alone were a 6.0-fold increase in C(min) (90% CI, 4.0, 9.3), an increase in AUC(0-24) (1.5-fold, 90% CI, 1.2, 2.0), and no increase in C(max). Adverse events were similar and generally mild, with no cases of nephrolithiasis. The geometric mean ratio of IDV C(min) for IDV/RTV compared to IDV was at least 2 by a lower bound of the 90% CI, satisfying the primary hypothesis. The C(max) was not increased, suggesting an IDV/RTV 667/100-mg toxicity profile may be similar to that of unboosted IDV.
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PMID:Pharmacokinetics of indinavir and ritonavir administered at 667 and 100 milligrams, respectively, every 12 hours compared with indinavir administered at 800 milligrams every 8 hours in human immunodeficiency virus-infected patients. 1550 42

A 2-year-old boy who was failing to thrive and who had multiple anomalies was found to have a maternally derived tandem duplication of the long arm of the X chromosome: dup(X)(q13.2-q21.2). The karyotyping interpretation was further confirmed by fluorescence in situ hybridization studies in which a double gene dosage of the X-inactivation-specific transcript (gene locus on Xq13.2) and a whole chromosome X painting on the abnormal X were noted. He suffered from hypotonia, gastroesophageal reflux, laryngomalacia, recurrent infections, immunodeficiency (IgG4 deficiency), dysgenesis of the corpus callosum, proximal renal tubular acidosis, and nephrolithiasis. His mother and elder sister also had the same rearrangement, the dup(X), on one of their X chromosomes. However, the mother was in good health, but the sister suffered from nephrolithiasis. The clinical variability in this family with the Xq duplication is reported and discussed.
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PMID:Inherited tandem duplication of the X chromosome: dup(X)(q13.2-q21.2) in a family. 1560 9

Immunomicrobiological examination was made of 656 urine and 71 blood samples from 71 patients with chronic pyelonephritis and coral nephrolithiasis. Bacteriuria in blood agar was quantified in colony-forming cells (CFC) in 1 ml of the urine. Identification of the bacterial strains was made by conventional methods. Blood samples were examined for phagocytic activity (PA) of neutrophils and phagocytic index (PI) in incomplete (30 min) and complete (2 hours) variants (S.aureus-209P), levels of IgA, IgM, IgG (in IU/ml), complement (CH50), T- and B-lymphocytes and 0-cells. Opportunistic bacteria (OB) in titer from Ig 2 to Ig 5 CFC/ml and more were identified in 428 (65.25%) samples. OB monocultures prevailed (48.6%). In exacerbation of the disease the majority of the examinees (73.0%) showed deficiency of both cellular and humoral components of antiinfection resistance system (AIRS). First-line defense against bacterial invasion was impaired as shown by incomplete neutrophil digestion in 62.0% of examinees. Among patients with humoral immunodeficiency, those with low IgM were the minority (45.0%). T-RFC and B-RFC deficiency (in 68.0 and 52.0%, respectively), low levels of IgG and IgA (66.0 and 73.0% cases, respectively) indicated deficiency of immunocompetent cells and their functional activity. The study of the AIRS established significance of its components for early and significant diagnosis of calculous pyelonephritis. Pyelonephritis in nephrolithiasis runs with deficiency of both cellular and humoral components of AIRS.
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PMID:[Some current aspects of diagnosis of calculous pyelonephritis]. 1747 91

Many pathogens are thought to be involved in the development and progression of chronic kidney disease (CKD). The mechanism of kidney damage due to infection includes direct invasion of pathogens and deposition of antigen-antibody complex by immunological reaction. As to renal dysfunction induced by bacterial infection, some cases of poststreptococcal glomerulonephritis present progressive decline of glomerular filtration rate (GFR). Methicillin resistant Staphylococcus aureus (MRSA)-related glomerulonephritis and infectious endocarditis are known to cause acute renal failure, which clinicians often find difficulty in the treatment. Chronic pyelonephritis by repetitive vesicoureteral reflux or nephrolithiasis also cannot be disregarded. Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are the most recognized etiology of virus associated nephropathy, and the representative histological changes are membranous nephropathy and membranoproliferative glomerulonephritis, respectively. Furthermore, morbidity of human immunodeficiency virus (HIV) associated nephropathy is increasing, reflecting the prolonged survival of HIV-infected patients. Thorough preventive/therapeutic strategies should be taken against these infections for improving clinical outcome.
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PMID:[Infection and chronic kidney disease]. 1878 11

The widespread introduction of highly active antiretroviral therapy (HAART) in the mid-1990s dramatically altered the course of human immunodeficiency virus (HIV) infection, with improvements in survival and reductions in the incidence of AIDS-defining illnesses. Although antiretroviral therapy has been shown to reduce the incidence of both AIDS-defining and non-AIDS conditions, long-term exposure to HAART may also be associated with significant toxicity. This article reviews the potential nephrotoxicity of specific antiretroviral agents and the impact of antiretroviral therapy on related metabolic disorders. The antiretroviral agents most strongly associated with direct nephrotoxicity include the nucleotide reverse transcriptase inhibitor, tenofovir, and the protease inhibitor indinavir, although other agents have been implicated less frequently. Tenofovir and related nucleotide analogs have primarily been associated with proximal tubular dysfunction and acute kidney injury, whereas indinavir is known to cause nephrolithiasis, obstructive nephropathy, and interstitial nephritis. Kidney damage related to antiretroviral therapy is typically reversible with early recognition and timely discontinuation of the offending agent, and nephrologists should be familiar with the potential toxicity of these agents to avoid delays in diagnosis.
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PMID:Antiretroviral medications: adverse effects on the kidney. 2000 91

Nephrolithiasis is a known side effect of indinavir sulfate, a protease inhibitor used in the treatment of human immunodeficiency virus (HIV). The duration of its side effects, however, has not been well defined. We present a case where a patient presented with symptomatic indinavir-induced nephrolithiasis 3.5 years after discontinuing indinavir. We use this case to illustrate the pathophysiology of indinavir stones and hypothesize how they can occur years after discontinuation by discussing the pharmacokinetics of the drug.
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PMID:Indinavir-induced nephrolithiasis three and one-half years after cessation of indinavir therapy. 2045 37

Crystalline nephropathy can occur following treatment with multiple therapeutic agents. We describe a human immunodeficiency virus (HIV)-infected patient treated for 2 years with combination antiretroviral therapy including atazanavir (ATV). Kidney biopsy revealed a crystalline nephropathy associated with diffuse chronic and granulomatous interstitial inflammation. Following the biopsy, treatment with ATV was discontinued and kidney function returned to pretreatment baseline levels. ATV, which has a well-established association with nephrolithiasis, is a rare but important cause of crystalline nephropathy. Recognition of this association and prompt withdrawal of the offending agent are critical to optimize outcomes.
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PMID:Atazanavir-Associated Crystalline Nephropathy. 2857 22

Drug-induced calculi represent 1-2% of all renal calculi. The drugs reported to produce calculi may be divided into two groups. The first one includes poorly soluble drugs with high urine excretion that favour crystallisation in the urine. Among them, drugs used for the treatment of patients with human immunodeficiency, namely atazanavir and other protease inhibitors, and sulphadiazine used for the treatment of cerebral toxoplasmosis, are the most frequent causes. Besides these drugs, about 20 other molecules may induce nephrolithiasis, such as ceftriaxone or ephedrine-containing preparations in subjects receiving high doses or long-term treatment. 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. Some drugs may also provoke heavy intra-tubular crystal precipitation causing acute renal failure. Here, the identification of crystalluria or crystals within the kidney tissue in the case of renal biopsy is of major diagnostic value. The second group includes drugs that provoke the formation of urinary calculi as a consequence of their metabolic effects on urinary pH and/or the excretion of calcium, phosphate, oxalate, citrate, uric acid or other purines. Among such metabolically induced calculi are those formed in patients taking uncontrolled calcium/vitamin D supplements, or being treated with carbonic anhydrase inhibitors such as acetazolamide or topiramate. Here, diagnosis relies on a careful clinical inquiry to differentiate between common calculi and metabolically induced calculi, of which the incidence is probably underestimated. Specific patient-dependent risk factors also exist in relation to urine pH, volume of diuresis and other factors, thus providing a basis for preventive or curative measures against stone formation.
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PMID:Drug-Induced Kidney Stones and Crystalline Nephropathy: Pathophysiology, Prevention and Treatment. 2926 83


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