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

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.
 ...
PMID:Drug-induced renal disease. 38 1

Review of clinical and pathologic data from ten fatal cases of Rocky Mountain spotted fever (RMSF) revealed the importance of acute renal failure in the clinical course and of multifocal perivascular interstitial nephritis as the principal pathologic lesion. In nine cases, Rickettsia rickettsii were demonstrated by immunofluorescence in the areas of vasculitis. Evidence was lacking for the role of disseminated intravascular coagulation, glomerulonephritis, or myoglobinuria in the pathogenesis of acute renal failure in these cases. Rickettsia-induced vascular injury led to acute renal failure by several mechanisms. Hypovolemia early in the course resulted in reversible, prerenal azotemia. Transient hypotension in midcourse produced acute tubular necrosis. In fulminant cases, preterminal circulatory collapse was associated with coma and oliguria. The interstitial nephritis could not be demonstrated conclusively to contribute to the acute renal failure.
 ...
PMID:Acute renal failure in Rocky Mountain spotted fever. 43 98

The cephalosporin antibiotics cephaloridine and cephalothin are known to cause renal damage. Experience with newer congeners is not yet sufficient to predict their potential nephrotoxocity. The renal lesion produced by cephaloridine is primarily due to the intrinsic toxicity of this drug for the cells of the proximal renal tubule and depends upon its peculiar transport characteristics. In contrast, renal injury due to cephalothin resembles that seen with the penicillins. Thus, some instances of cephalothin nephropathy appear to be toxic in nature with a histologic picture of acute tubular necrosis, whereas others exhibit signs of hypersensitivity including rash, eosinophilia, and interstitial nephritis. Among the factors alleged to contribute to the nephrotoxicity of cephalosporins is their administration with aminoglycosides. Although the physician should be aware of the possibility of a potential adverse interaction between these groups of antibiotics, the evidence is not sufficiently conclusive to warrant avoidance of the combination when it appears to be therapeutically useful.
 ...
PMID:The nephrotoxicity of cephalosporins: an overview. 65 5

Out of 152 cases of Acute renal failure (ARF) 32 patients (21%) were subjected to kidney biopsy. All patients had intrinsic ARF. Prerenal azotemia and obstructive uropathy were excluded. Histologic observations were: Crescentric glomerulonephritis in 7 (21.9%), acute endocapillary proliferative glomerulonephritis 5 (15.6%), acute interstitial nephritis 7 (21.9%), necrotizing vasculitis 4 (12.5%), acute tubular necrosis in 5 (15.6%) and membrano-proliferative GN with superimposed crescent in 2 (6.2%) while renal cortical necrosis was seen in 6.2% of cases. Prebiopsy diagnosis was correct in only 10 (31.25%) cases. The result of biopsy had altered clinical diagnosis in 22 (68.75%) patients and precise renal biopsy diagnosis resulted in therapeutic changes in 54.8% of patients with ARF.
 ...
PMID:Clinical significance of kidney biopsy in acute renal failure (ARF). 129 67

Severe exfoliative dermatitis and liver dysfunction developed in a 5-year-old girl 3 weeks after initiation of phenobarbital therapy. Liver function improved gradually after discontinuation of phenobarbital. During the convalescent stage an initially mild renal dysfunction was exacerbated by episodes of post-transfusion haemolysis. Liver biopsy revealed moderate parenchymal damage with subacute cellular infiltration. Renal biopsy demonstrated the cardinal findings of interstitial nephritis, excluding the possibility of acute tubular necrosis caused by haemolysis. Serial lymphocyte transformation studies and skin patch tests gave positive results for phenobarbital, supporting the view that these were unusual complications of phenobarbital hypersensitivity.
 ...
PMID:A case of tubulo-interstitial nephritis with exfoliative dermatitis and hepatitis due to phenobarbital hypersensitivity. 153 Aug 19

Therapeutic use of gentamicin (GM) in a clinical setting may result in nephrotoxicity, most commonly presenting as acute tubular necrosis (ATN). We have previously observed decreased plasma pyridoxal 5'-phosphate (PLP) levels in rabbits given therapeutic doses of GM and endeavor in this study to determine if vitamin B6 supplementation (B6S) could protect against the nephrotoxicity of GM. Twenty-one rabbits were randomly assigned to 1 of 7 treatment groups of 3 rabbits each. Three of the groups received 10 mg GM/kg with either 10 mg B6S, 100 mg B6S or 0.9% saline. Three of the groups received 40 mg GM/kg with either 10 mg B6S, 100 mg B6S, or normal saline. The control group only received 100 mg B6S. All treatments were administered im once daily for 5 d. Blood was drawn for chemical assays on day 0 prior to any treatments and 2 h after each respective treatment on days 1, 3 and 5. After 5 d, the rabbits were euthanatized and kidneys were excised for histological evaluation by light microscopy. At the 40 mg GM/kg/d dose, significant mild to moderate ATN was observed in the saline controls, which was prevented by either dose of B6S. Only a few animals given 10 mg GM/kg/d showed any renal pathology and that was minimal. Unexpectedly, 1 rabbit given only 100 mg B6S/d but no GM had interstitial nephritis with focal ATN. We conclude that vitamin B6 can protect against the nephrotoxicity of GM in rabbits, but that further study is needed on the possible nephrotoxicity of high doses of B6S.
 ...
PMID:Effect of vitamin B6 supplementation on gentamicin nephrotoxicity in rabbits. 162 59

There is a growing number of hospitalised patients who develop a drug-induced renal problem because increasing numbers of potent drugs have been added to the therapeutic arsenal in recent years. The 3 clinical syndromes that can be recognised in drug-induced nephropathy are acute renal failure, chronic interstitial nephritis and the nephrotic syndrome. The first can be caused by prerenal problems, acute interstitial nephritis, acute tubular necrosis and intratubular obstruction. The most important drugs that cause prerenal failure are NSAIDs, captopril and cyclosporin. NSAIDs inhibit the synthesis of prostaglandins, and consequently vasoconstriction of the afferent arteriole leads to lowering of the glomerular filtration rate (GFR); captopril blocks the formation of angiotensin II (which also leads to a lower GFR), and should be used with caution in patients with stenotic renal arteries; cyclosporin causes vasoconstriction of the afferent arteriole, which is probably mediated by the sympathetic system. Combinations of these drugs result in increased nephrotoxicity. The drugs most likely to cause acute interstitial nephritis are antibiotics and NSAIDs. Normally, signs of an allergic reaction are also present. Acute interstitial nephritis is usually self-limiting, but in some studies it is claimed that steroids may promote recovery. Four important causal agents of acute tubular necrosis are aminoglycosides, amphotericin B, radiocontrast agents and cyclosporin. Approximately half of the cases of drug-induced renal failure are related to the use of aminoglycosides: generally, 10 days after start of treatment a nonoliguric renal failure develops, with recovery after withdrawal of the drug in almost all cases. The aminoglycosides are particularly nephrotoxic when combined with other nephrotoxic drugs. 80% of amphotericin B-treated patients develop renal insufficiency, a percentage that increases as the cumulative dose exceeds 5g. It is because of its unique antifungal properties that there are still some indications for the use of this highly nephrotoxic drug; the high percentage of nephrotoxicity can probably be prevented in part by sodium loading. The nephrotoxicity of radiocontrast agents is largely dependent on renal function: from 0.6% in patients with normal renal function to 100% in patients with a serum creatinine above 400 mumol/L. Diabetes mellitus does not add greatly to the risk of radiocontrast nephrotoxicity. The nephrotoxicity of cyclosporin is dose-dependent and reversible, although there are some reports of irreversibility after long term use. Cyclosporin can also result in nephrotoxicity in combination therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Drug-induced nephrotoxicity. Aetiology, clinical features and management. 204 84

The resistive index (RI), calculated from the duplex Doppler waveform, was compared with clinical and laboratory findings and the results of renal biopsy in 41 patients with nonobstructive (medical) renal disease. Kidneys with active disease in the tubulointerstitial compartment had a mean RI of 0.75 +/- 0.07. This was statistically significantly different (p less than .01) from the RI in kidneys with disease limited to the glomeruli (mean RI of 0.58 +/- 0.05). Acute tubular necrosis resulted in an elevated RI (mean RI = 0.78 +/- 0.03) as did vasculitis/vasculopathy (mean RI = 0.82 +/- 0.05). Patients with hypertension, proteinuria, or hematuria did not have kidneys with a significantly higher RI than did patients without these clinical factors. Kidneys found to be abnormally echogenic did not have an RI significantly different from kidneys of normal echogenicity. There was a weak correlation between creatinine level and RI value, reflected by a linear correlation coefficient of 0.34. In patients with normal renal RIs, the mean creatinine level was 1.7 +/- 1.7, whereas in those with abnormal RI values (greater than or equal to 0.70), the mean creatinine level was 3.7 +/- 3.6. We conclude that some forms of nonobstructive renal disease can produce changes in the Doppler waveform detectable by RI measurement. The production of Doppler waveform changes is strongly influenced by the site of the main disease within the kidneys. Active disease within the tubulointerstitial compartment (acute tubular necrosis, interstitial nephritis) or vasculitis/vasculopathy generally resulted in an elevated RI, whereas disease limited to the glomeruli, no matter how severe, did not significantly elevate the RI. Degree of renal dysfunction as indicated by serum creatinine level probably affects the Doppler waveform to some degree, but the relationship is weak.
 ...
PMID:Intrarenal arterial Doppler sonography in patients with nonobstructive renal disease: correlation of resistive index with biopsy findings. 211 Jul 32

Drug-induced renal disease is a common problem. Drugs cause several renal syndromes, such as prerenal azotemia, fluid and electrolyte abnormalities, acute tubular necrosis, acute interstitial nephritis, and chronic interstitial nephritis. Acute renal failure due to acute tubular necrosis is the most common syndrome and is most frequently caused by aminoglycoside antibiotics, radiographic contrast agents, and amphotericin B. Avoidance of these drugs in volume-depleted or hypotensive patients with preexisting renal disease or in those receiving multiple nephrotoxic drugs is the most effective way to reduce nephrotoxicity. Acute interstitial nephritis is an immune process that is most commonly caused by penicillins, diuretics, allopurinol, nonsteroidal anti-inflammatory drugs, cimetidine, and sulfonamides. Prompt recognition of the disease and cessation of the responsible drug are usually the only necessary therapy. Chronic interstitial nephritis is most often seen after prolonged use of several different types of analgesic agents, including aspirin, acetaminophen, and nonsteroidal anti-inflammatory drugs. These patients develop recurrent papillary necrosis and eventually chronic renal failure. They are also at risk of developing transitional cell carcinomas of the urinary collecting system. Some patients who are receiving cyclosporine also develop chronic renal failure due to interstitial fibrosis.
 ...
PMID:Drug-induced nephropathies. 219 61

Medullary tubules in renal biopsies from twelve patients suffering from ischemic acute tubular necrosis (ATN) and nine patients with allergic, drug-induced acute interstitial nephritis (AIN) were investigated by electron microscopy using quantitative and semiquantitative methods. For comparison, 12 biopsies from patients without renal disease or with minimal change nephropathy were studied. The mean scores for reduction of brush border and basolateral infoldings of the cell surface were significantly increased in the straight part of the proximal tubule and the thick ascending loop of Henle (straight part of the distal tubule) compared with medullary controls, and these changes were significantly greater than the scores for the corresponding convoluted tubules in the cortex. The numbers of missing tubular epithelial cells (indicating sites of cellular desquamation) were significantly increased in the thick ascending loop of Henle in ATN as well as in AIN and in the straight proximal tubule in ATN. This single cell lesion also occurred in the collecting duct. These findings are discussed in the light of recent experimental data indicating the importance of medullary tubules for the pathogenesis of ATN.
 ...
PMID:Ultrastructure of medullary tubules in ischemic acute tubular necrosis and acute interstitial nephritis in man. 228 9


1 2 3 4 5 6 7 8 9 10 Next >>