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)

The kidney is one of the organs susceptible to heavy metal intoxication. The total body burden and "saturation" level in renal tissue are important limiting factors to the onset of renal injuries. Acute or chronic exposure to many of heavy metals can induce renal tubulointerstitial injuries, including acute tubular necrosis, chronic tubulointerstitial nephritis, Fanconi syndrome, renal tubular acidosis, and renal tubular dysfunction without morphological changes. Chronic cadmium intoxication can cause irreversible Fanconi syndrome with chronic tubulointerstitial nephritis. Both urinary low-molecular weight protein excretion and urinary cadmium excretion (greater than 200-400 ppm) are the most reliable earlier markers of tubulointerstitial injury in chronic cadmium intoxication. The role of metallothionein is central to an understanding of cadmium-induced nephropathy. Acute lead intoxication in children can cause reversible Fanconi syndrome. Hypertension, hyperuricemia, and elevated serum creatinine, without Fanconi syndrome, are clinical manifestations of chronic lead exposure in adults. Nuclear inclusion body in proximal tubular cell is characteristic. Chronic exposure to inorganic germanium can cause chronic renal failure without urinary abnormalities, due to tubular degeneration and interstitial fibrosis, mainly in the thick ascending limb of Henle and distal tubulus.
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PMID:[Tubulointerstitial injuries in heavy metal intoxications]. 756 49

After transplantation the kidney is subjected to rejection and other deleterious factors including ischemic damage, acute tubular necrosis, rejection and the use of cyclosporine A (CsA) or FK506. As a result, kidney damage may be generalized with azotemia as its hallmark. These tubular syndromes may cause profound changes in the acid base balance and in the level of certain blood electrolytes and minerals. As a general rule, the renal tubular acidosis (RTA) that appears early following transplantation disappears spontaneously and is predominantly a sequela to acute renal failure. On the other hand, defects occurring in the late posttransplant period are often due to chronic rejection or CsA-induced nephrotoxicity. Secondary hyperparathyroidism, urinary tract infection and obstructive uropathy may also play a contributory urinary role in the pathogenesis of RTA. Chronic RTA following transplantation may interfere with bone metabolism and at times lead to nephrocalcinosis and nephrolithiasis. Therefore, if the condition is prolonged, a supplement of bicarbonate should be given if for no other reason that to protect the skeleton. As these patients may develop either hyperkalemia or hypokalemia, treatment with potassium supplements or potassium-sparing diuretics should be carried out with caution and under constant surveillance. Furthermore, magnesium replacement may be advisable if hypomagnesemia by decreased proximal reabsorption becomes clinically evident. Tubular dysfunction may occur following renal transplantation even in patients with maintained glomerular filtration rate and may induce a number of clinical problems including deterioration of renal graft function.
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PMID:Tubular dysfunction following kidney transplantation. 893 72

Long-term therapy with lithium may be associated with a broad spectrum of functional and structural side-effects in the kidney. Among these features, nephrogenic diabetes insipidus is the most frequent and it can be expected to occur in 20-70% of the patients. Diabetes insipidus is the result of a lithium induced resistance of collecting ducts to antidiuretic hormone. Additional functional disturbances are represented by renal tubular acidosis and consequences of hypercalcemia. Structural alterations of the kidney have a rare occurrence. In the literature, there are accounts of chronic tubulo-interstitial nephritis, acute tubular necrosis and few cases of glomerulopathies. Our report of a patient with chronic interstital nephritis is supplemented by a brief discussion of the diverse picture of the nephrotoxicity of lithium.
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PMID:[Impaired kidney function in lithium therapy]. 978 72

The spectrum of side-effects of sodium stibogluconate is well described. Patients treated with sodium stibogluconate can develop varied manifestations of renal toxicity, ranging from renal cell casts, proteinuria, renal tubular acidosis and acute tubular necrosis, resulting in acute kidney injury (AKI). We describe a 32-year-old male patient who was treated for visceral leishmaniasis with sodium stibogluconate. The patient was readmitted two weeks after completion of the treatment for evaluation of AKI. Kidney biopsy revealed marked acute interstitial nephritis. The renal dysfunction reversed totally after a course of corticosteroids. Antimonials should be recognized as a new class of agents as a possible cause of drug-induced acute interstitial nephritis.
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PMID:Sodium stibogluconate-associated acute interstitial nephritis in a patient treated for visceral leishmaniasis. 2617 51

For the pediatric nephrologist, the over-the-counter status for non-steroidal anti-inflammatory drugs (NSAIDs) is surprising due to their possible harmful side effects. These can include acute renal failure due mainly to glomerular hypoperfusion which may lead to acute tubular necrosis; more rarely in children, medullary ischemic injury and cardiovascular diseases; acute or chronic interstitial nephritis which may cause chronic renal failure. All of them may create electrolyte abnormalities: hyponatremia, hyperkaliemia, renal tubular acidosis, fluid retention causing hypertension.
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PMID:Non-steroidal Anti-inflammatory Drugs (NSAIDs) Systemic Use: The Risk of Renal Failure. 3203 4