Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016199 (flank pain)
 2,189 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The extensive use of selective histamine H2 receptor antagonists provides a unique opportunity to describe very rare adverse drug reactions. Although mild elevation of serum creatinine level following the administration of cimetidine is relatively common, acute interstitial nephritis (AIN) is a rare hypersensitivity reaction. There have been 25 published reports of AIN associated with H2 antagonist therapy and we also identified 16 cases from the Australian Adverse Drug Reaction Advisory Committee (ADRAC) database. AIN was reported most commonly following cimetidine administration. AIN was supported by renal biopsy in 28 patients and by rechallenge in 6. H2 antagonist-induced AIN was more commonly reported in men older than 50 years. In the majority of cases the onset was within 2 weeks of initiation of therapy (1 day to 11 months). The clinical manifestations were nonspecific including sterile pyuria, elevated erythrocyte sedimentation rate, fatigue, proteinuria and leucocytosis whereas rash, arthralgia and flank pain were rarely reported. There were 170 cases of hepatotoxicity following H2 antagonist administration reported to ADRAC. These were more common following ranitidine and included cholestatic, hepatocellular and mixed reactions. Hepatotoxicity was proven following liver biopsy in several cases published in the literature and in 15 cases reported to ADRAC. Hepatotoxicity recurred upon rechallenge in 6 cases. Generally, renal and hepatic adverse effects resolved quickly after cessation of H2 antagonist therapy and did not require specific treatment. Nephrotoxicity and hepatotoxicity following administration of an H2 antagonist is rare and a high index of suspicion is necessary for early detection. Now that many H2 antagonists are available over the counter, awareness of these conditions and early detection with cessation of H2 antagonist therapy would appear paramount.
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PMID:Nephrotoxicity and hepatotoxicity of histamine H2 receptor antagonists. 1121 86

This case report describes a 32-year-old woman treated with indinavir who developed mild to moderate flank pain, malaise, and low-grade fever. Sterile pyuria preceded increased serum creatinine levels. Workup revealed persistent pyuria, normal-sized kidneys, a normal intravenous pyelography, and negative urinary cultures. Renal biopsy showed interstitial nephritis and chronic inflammation. Collecting ducts contained crystals. Two months after treatment with indinavir was discontinued, serum creatinine levels returned to normal and pyuria disappeared. Sterile pyuria in patients taking indinavir may help to identify patients at risk for renal dysfunction and interstitial nephritis. Markedly increasing the fluid intake above the recommended dosage may ameliorate or even reverse the process of tubulointerstitial disease.
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PMID:Persistent flank pain, low-grade fever, and malaise in a woman treated with indinavir. 1136 24

A 56-year-old male with DM and HTN presented with flank pain and nausea. Review of systems was negative, physical examination was notable for mild hypovolemia and laboratory revealed BUN 51 mg/dl, creatinine (Cr) 5.1 mg/dl (baseline 1.5), Westergren ESR 122 mm/h, fractional excretion of sodium 0.2% and UA positive for blood and protein. Despite volume resuscitation the Cr continued to rise. Urine sediment analysis revealed granular casts, renal tubular epithelial cells and a negative Hansel's stain. Hemodialysis was initiated with Cr 13.7 mg/ dl for dyspnea and dysgeusia. Subsequent laboratory data revealed 2 separate positive anti-GBM antibody titers and prednisone therapy was initiated. Renal biopsy was performed for further diagnostic, therapeutic and prognostic information and demonstrated interstitial nephritis with linear IgG and albumin deposition consistent with diabetic nephropathy. Follow-up antibody titers were negative. prednisone was discontinued and Cr stabilized with conservative therapy. Anti-GBM antibody disease is characterized by circulating IgG antibodies directed against the glomerular basement membrane, specifically the alpha-3 (IV) collagen chain. Anti-GBM nephritis is a rapidly progressive, isolated glomerulonephritis in association with circulating anti-GBM antibodies. A positive immunofluorescence (IF) test is considered diagnostic in the appropriate clinical setting. Therapies include immunosuppressive agents to suppress new antibody production and plasmapheresis to eliminate circulating antibodies. Anti-GBM antibody is not rapidly cleared by steroid therapy and the recovery of renal function is rare if initiation Cr is greater than 7 mg/dl. This case demonstrates that the current ELISA for alpha-3 (IV) collagen is not pathognomonic for anti-GBM nephritis and that renal biopsy with IF for IgG and albumin may be indicated to prevent administration of potentially toxic treatment.
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PMID:Diabetic nephropathy with interstitial nephritis presenting with a false-positive anti-GBM antibody. 1203 99

Reversible acute kidney injury very rarely complicates the course of immunoglobulin A (IgA) nephropathy. We report an atypical case of reversible acute kidney injury, gross hematuria, and severe bilateral flank pain as the presenting triad of IgA nephropathy. Renal biopsy revealed mesangial IgA deposition without glomerular crescents. The patient's renal dysfunction, mediated by red cell tubular obstruction, interstitial nephritis, and tubular necrosis, resolved without intervention. We conclude that IgA nephropathy should be considered in the differential diagnosis for transient acute kidney injury with gross hematuria, and should be appropriately treated based on known prognostic factors.
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PMID:Atypical triad of IgA nephropathy: reversible acute kidney injury, gross hematuria, and severe bilateral flank pain. 2850 88

Urinoma, defined as the urine leakage beyond the urinary tract, is commonly induced by blunt trauma or urinary tract obstruction by stone, intra-abdominal malignancy, or retroperitoneal fibrosis. Spontaneous urinoma is rare and parenchymal pathologic change is rarely mentioned when urinoma is found. We present a case of a 28-year-old woman with bilateral flank pain induced by spontaneous urinoma. The lady received chronic analgesics because of migraine. After intravenous ketorolac injection, bilateral perirenal urinoma developed. Renal biopsy showed acute interstitial nephritis associated with nonsteroid anti-inflammatory drug (NSAID). After discontinuing the medication, urinoma subsided, and the patient was discharged with normal serum creatinine. This was the first case of urinoma induced by NSAID-related interstitial nephritis, and pathophysiology and management of spontaneous urinoma are discussed.
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PMID:Spontaneous perirenal urinoma induced by NSAID-associated acute interstitial nephritis. 2961 38


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