Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is almost ironic that one of the major organs that serves to maintain the "internal milieux" by secretion of various toxic agents, can itself become injured in the process. The pattern of morphologic renal injury is nonspecific and can involve any of the components of the kidney, although the injury and subsequent morphologic changes are most commonly noted in the tubules and/or interstitium. Of course, unless the drug/toxin is commonly or regularly noted to be associated with tubular and/or interstitial injury, the association of the drug with the renal changes may be missed and the correlation may not necessarily identify causation. For example, if a drug is associated with a renal injury in a given individual, it may be quite difficult to prove that the drug is the cause of the injury. This scenario is somewhat reminiscent of the test question-is it "true-true-related," or "true-true-unrelated"? Sometimes it is only by the accrual of a great many examples or correlations, and or dissection of the pathophysiology, can it be shown that the drug is directly related to the observed morphologic (and subsequent clinical) injury. Renal changes induced by chemicals can affect the tubules, interstitium or both. This review of chemically induced nephropathy in humans considers acute tubular necrosis, interstitial nephritis, and tubulointerstitial nephritis or nephropathy. Because the tubules and the interstitium are so intimately related, injury to 1 of these 2 components may eventually lead to injury of the other, resulting in tubulointerstitial disease.
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PMID:Chemical-induced nephropathy: a review of the renal tubulointerstitial lesions in humans. 1550 66

Adult patients deficient in carnitine palmitoyltransferase II (CPT II) cannot generate sufficient amounts of energy, which results in rhabdomyolysis and acute renal failure (ARF). Its genetic basis has been recognized; but histopathologic changes, especially electron microscopic changes, have scarcely been described. The study subject is a patient with ARF caused by repetitive nontraumatic rhabdomyolysis. The acylcarnitine profile of serum and enzyme assay on skin fibroblasts confirmed the diagnosis of CPT II deficiency. Renal biopsy specimens were examined microscopically and immunohistochemically. The histological diagnosis was interstitial nephritis with acute tubular necrosis caused by rhabdomyolysis. Myoglobin in tubules was detected by means of immunohistochemistry and electron microscopy. The genetic structure of CPT II was analyzed in the patient and his family. Eight pairs of polymerase chain reaction (PCR) primers were designed to cover the coding region. Each PCR-amplified gene product was subjected to DNA sequencing, which unveiled heterozygosity at the CPT II locus consisting of a deletion of cytosine and thymine at codon 408, resulting in a stop signal at 420, as well as a mutation of arginine to cysteine at codon 631. The frame shift at 408 has never been described before. DNA sequencing of the family showed the deletion mutation from the mother and the point mutation from the father. We describe renopathological findings in a patient with CPT II deficiency associated with rhabdomyolysis, which suggested the pathological role of myoglobin casts in the development of tubular necrosis. Genetic analysis of the patient identified a novel variant of the CPT II gene.
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PMID:Carnitine palmitoyltransferase II deficiency due to a novel gene variant in a patient with rhabdomyolysis and ARF. 1575 83

NSAIDs are commonly used drugs. Even with the advent of selective COX-2 inhibitors, nephrotoxicity still remains a concern. The adverse effects of NSAIDs are mediated via inhibition of prostaglandin synthesis from arachidonic acid by non-specific blocking of the enzyme cyclooxygenase leading to vasoconstriction and reversible mild renal impairment in volume contracted states. When unopposed, this may lead to acute tubular necrosis and acute renal failure. NSAIDs also produce interstitial nephritis with or without nephrotic syndrome secondary to minimal change disease. Although this presents as acute renal failure, it can progress in some cases to chronic renal failure. Papillary necrosis has been incriminated in the development of chronic renal failure secondary to NSAIDs. In patients on long term NSAIDs without acute or chronic renal failure, subclinical renal dysfunction such as reduced creatinine clearance and impaired urine concentrating ability has been shown to be present. Although this sub-clinical dysfunction is reversible on withdrawal of NSAIDs, some reports have suggested a persistent residual dysfunction. Even with a wide range of NSAIDs at our disposal, a renal safe NSAID is yet to be discovered.
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PMID:NSAIDs and kidney. 1584 59

Selective cyclooxygenase-2 (COX-2) inhibitors are relatively newer anti-inflammatory drugs that produce comparable antiinflammatory and analgesic effects to the nonselective nonsteroidal antiinflammatory drugs (NSAIDs); but with fewer symptomatic gastric and duodenal ulcers. Limited data are available concerning the toxicity associated with COX-2 inhibitors outside the gastrointestinal tract. The NSAIDs have been known for their nephrotoxic potentials including minimal-change disease (MCD) with interstitial nephritis. Although the recent data suggests that COX-2 inhibitors may have the same adverse renal effect as NSAIDs, there is only one case report describing minimal change disease and acute interstitial nephritis (AIN) associated with a COX-2 inhibitor, celecoxib. We are reporting a case of MCD and acute tubular necrosis (ATN) but without interstitial nephritis in a patient treated with celecoxib. Although the proteinuria in our patient resolved completely after discontinuation of celecoxib, the renal function did not. We suggest that heightened suspicion of this side effect of COX-2 inhibitors should be maintained in all patients taking this class of drugs who present with nephrotic syndrome.
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PMID:Cyclooxygenase-2 inhibitor-associated minimal-change disease. 1590 98

Toxic nephropathy is an important cause of reversible renal injury. This article focuses on the nephrotoxicity of several new therapeutic compounds. Selective cyclooxygenase-2 inhibitor is associated with sodium retention, hypertension, ankle edema, and acute renal failure. The incidence of renal complication is similar to conventional nonsteroidal anti-inflammatory drugs. Bisphosphonates, especially when used in high dose for prolonged duration, can cause toxic acute tubular necrosis and renal failure. Pamidronate is also associated with a specific form of collapsing focal segmental glomerulosclerosis similar to one found in patients with human immunodeficiency virus (HIV) infection. Acyclic nucleoside phosphonate, a new group of antiviral agents, can cause Fanconi-like syndrome and progressive renal impairment. On the other hand, indinavir, a potent protease inhibitor for the treatment of HIV infection, can cause crystalluria, renal stone, acute tubular obstruction and chronic interstitial nephritis. Intravenous immune globulin and hydroxyethyl starch, a new plasma expander, are associated with acute renal failure with characteristic renal histology known as osmotic nephrosis. In short, physicians should be cautious about possible renal toxicity during the use of any new therapeutic agents.
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PMID:Nephrotoxicity related to new therapeutic compounds. 1595 51

In the developing world, up to 80% of the population uses traditional medicine for primary health care. In industrialized countries, adaptations of traditional medicine, termed "complementary" or "alternative" medicine (CAM), are used by a growing number of patients for preventive or palliative care. However, alternative medicine (AM) may be an important risk for the development of acute and chronic kidney injury because of several factors: nonconventional preparations rarely meet the required essential standards of consistency in composition and biological activity; many of these products contain undisclosed over-the-counter or prescription drugs or can be adulterated with hormones and glandular extracts; herbal preparations can be contaminated by pesticides and heavy metals; and because of errors in plant identification and confusing terminology, opportunities for mistakes and deliberate substitution can occur. Furthermore, there is a lack of reports of adverse events and drug interactions because of a lack of professional surveillance, and specific data on systemic and kidney toxicity are not easily available. Kidney injury/kidney syndromes caused by AM consist of acute tubular necrosis/toxicity (eg, Fanconi's syndrome), acute interstitial nephritis, papillary necrosis, hypertension, kidney stones, urinary retention, chronic tubulointerstitial nephritis with fibrosis, urinary tract carcinoma, and acute rejection of the kidney transplant. To improve the care for patients using AM, extension of physicians' knowledge about its possible hazards and toxicity is essential. This review deals with acute and chronic kidney toxicity caused by animal-, plant-, and mineral-based, nonconventional medicine and kidney failure caused by drug interactions with AM.
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PMID:Kidney injury from alternative medicines. 1601 Jun 41

We report the cases of two patients who developed acute renal failure following multiple wasp stings. Both patients required dialysis and recovered within 4 weeks. The kidney biopsy from one patient showed acute tubular necrosis with interstitial nephritis. One patient had complete recovery of renal function on follow-up, while the other was lost to follow-up.
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PMID:Acute renal failure following multiple wasp stings. 1622 51

Acute renal failure is an unusual complication of wasp stings. We report three cases who developed acute renal failure after multiple wasp stings (Vespa magnifica). Two patients had evidence of intravascular haemolysis and rhabdomyolysis whereas one patient investigation showed no evidence of intravascular haemolysis or rhabdomyolysis. All three cases had impaired liver functions. Oligo-anuria was seen in all three of the patients and all of them required dialytic support. One patient died of massive gastrointestinal bleeding while the remaining two recovered completely. Although acute renal failure after wasp stings is typically caused by acute tubular necrosis in the setting of haemolysis or rhabdomyolysis, in some patients, renal failure may result from a direct nephrotoxic effect or acute interstitial nephritis from a hypersensitivity reaction to the wasp venom.
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PMID:Wasp envenomation-induced acute renal failure: a report of three cases. 1635 36

Acute renal failure is a very rare complication seen during the course of non- fulminant hepatitis A. Several mechanisms have been postulated in the pathogenesis of renal failure. Firstly, there is insufficiency of renal blood flow due to developing endotoxemia or cryoglobulinemia, secondly mesangial proliferative glomerulonephritis or interstitial nephritis occurs due to immune complexes and finally there is acute tubular necrosis caused by the direct cytopathic effect of the virus or due to immune complexes. The following case report describes a 17 year old male patient admitted with complaints of appetite loss and severe weight loss due to anorexia nervosa. During the second week of admission, he developed hepatitis A infection which was complicated by acute renal failure requiring hemodialysis therapy. Hepatorenal parameters returned to normal values by the fifth week of admission in this case of biopsy proven acute tubular necrosis. In this case, the possible negative effects of malnutrition on the liver and kidneys were not observed. The present authors emphasize that during the course of non- fulminant hepatitis A, renal functions should be closely monitored and renal biopsy should be performed if acute renal failure occurs.
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PMID:Acute oligo-anuric renal failure during the course of non-fulminant hepatitis A in a patient with anorexia nervosa. 1637 99

From July 1998 to July 1999, 45 cases of acute renal failure were treated at Bir Hospital, Kathmandu. Out of which 24 were male and 21 were female. Age ranged from 11 months to 84 years with mean age being 35 years and 9 cases were below 10 years. Four cases with pre-renal azotaemia and twenty five cases of acute tubular necrosis (ATN) accounted for 64% of all cases. These were due to gastroenteritis 10, sepsis 6, post surgical 1, trauma 1 and obstretical complications 5. Multiple hornet stings were responsible for acute renal failure in 3 cases, acute urate nephropathy in 1 case and miscellaneous causes in 2 cases. Glomerulonephritis / vasculitis accounted for 17.7%, acute interstitial nephritis 4.4%, haemotytic uraemic syndrome (HUS) 6.6%, and post renal azotaemia in 6.6% of all cases. Mean serum creatinine was 8 mg/dl, mean blood urea 190 mg/dl. Eight cases were treated only conservatively, eighteen received haemodialysis, fourteen received peritoneal dialysis, three received both and two refused for dialysis. Average duration of hospital stay was 13.6 days. Out of the forty-five cases twenty-nine recovered normal renal function, ten expired, two recovered partially, two progressed to chronic renal failure and two left against medical advice. Overall mortality was 22.2%. Common causes of acute renal failure in our setting were gastroenteritis (22%) and sepsis (20%). HUS was exclusively seen in children following bacillary dysentery. Multiple hornet stings is an important cause of acute renal failure in our country.
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PMID:Acute renal failure in a tertiary care center in Nepal. 1655 67


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