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)

A human proximal renal tubular epithelial antigen (designated HRTE-1) was isolated and purified from a crude tubular preparation (Fx1A) by a process of salt fractionation, DEAE anion-exchange chromatography, and Sephadex G-200 gel filtration. Utilizing 125I-HRTE-1 and a rabbit antiserum specific for the proximal tubular brush border, as determined by immunofluorescent microscopy, a radioimmunoassay by competitive protein-binding was developed. HRTE-1 was demonstrated in serum and urine and in extracts of a variety of body organs. A range of concentrations for normal random urine samples and 24-hr urine excretion rates were determined. Random urine samples from 36 patients with a variety of functional and pathologic renal disorders were assayed for the HRTE-1 antigen. Twenty-three of 24 patients with either chronic nephropathy or pre-renal azotemia had normal urinary antigen concentrations, despite wide differences in urine flow rates, the degree of existing renal function, and the amount of proteinuria. Ten of 12 patients with acute tubular necrosis, however, had statistically abnormal HRTE-1 concentrations (high in eight patients, undetectable in two). These findings suggest that HRTE-1 antigen can be detected in both normal and pathologic urines, that altered antigen concentrations can be documented in at least one renal disorder, and that quantitation of HRTE-1 in urine may have clinical value as a marker of acute rubular injury.
 ...
PMID:Radioimmunoassay for urinary renal tubular antigen: a potential marker of tubular injury. 36 38

Studies were undertaken to determine whether a hypotensive episode under variable conditions is capable of inducing experimental acute renal failure in rats. Animals were subjected to hypovolemic shock by withdrawing volumes of blood necessary to maintain a systolic pressure of 30-40 mm Hg for 105-110 min. The blood was then reinfused and the animal was allowed to recover for 48 h prior to sacrifice. In an attempt to increase the injury, a second group of animals was salt-depleted prior to injury, a third group was volume-depleted by being deprived of H2O for 72 h prior of injury, a fourth group received 7.5 mg/kg indomethacin 30 min prior to injury, and a fifth group had 30% of the blood which was removed to produce shock hemolyzed and returned following the injury. In all groups examined, light microscopy revealed a moderate to severe acute tubular necrosis localized mainly in the outer stripe of the outer zone as defined by Peter (1909). Tubular damage was confined to the medullary pars recta of the proximal tubule and only in the most severe cases did injury involve the cortical pars recta and pars convoluta. Casts were present in the distal tubules and collecting ducts. Despite these significant histologic alterations, BUN values from all experimental groups remained within control levels. These studies clearly show that extensive necrosis of the medullary pars recta can be dissociated from the development of acute renal failure.
 ...
PMID:Hypovolemic models of acute tubular necrosis in the rat kidney. 41 58

During a 4-year period, acute renal failure was observed in 27 patients (mean age 65 years) treated by various angiotensin-converting-enzyme (ACE) inhibitors for hypertension, heart failure, or a combination of both. None had significant renal artery stenosis on angiography. Overt volume depletion was present in 21 and hypotension in 12 cases. All patients received diuretic therapy and/or a low-salt diet. Other facilitating factors included cardiac failure, pre-existing chronic renal insufficiency, combined therapy with non-steroidal anti-inflammatory drugs, and diabetes mellitus. Twenty-two patients had two or more of these factors at presentation. A renal biopsy performed in 10 cases showed severe arteriosclerosis of small renal arteries in eight and acute tubular necrosis in five instances. Therapy comprised volume expansion, and withdrawal of diuretics and, except in two patients, of ACE inhibitors. Twenty-one patients recovered normal renal function, two died, and permanent renal damage remained in four. These results suggest that sodium depletion has a critical role in inducing acute renal failure, whose outcome is not always benign. A combination of diuretics and ACE inhibitors should be prescribed with caution, especially in older patients with small as well as with large renal vessel disease.
 ...
PMID:Acute renal failure after the use of angiotensin-converting-enzyme inhibitors in patients without renal artery stenosis. 131 66

Although a wide variety of disease processes can result in a failure of renal excretory function, the vast majority of cases with "acute renal failure" (ARF) are due to the syndrome of acute tubular necrosis (ATN). The syndrome is usually initiated by an acute injury to the proximal renal tubular epithelial cells by ischemic or nephrotoxic events. This is followed by progressive and often rapid increases in the concentration of blood urea nitrogen (BUN) and serum creatinine. In the average case, the failure of renal excretory function persists for 1 to 3 weeks, to be followed by recovery. Oliguria (urine volume less than 400 ml) is present in about half of the patients. The pathogenesis of the retention of nitrogenous waste in human ATN is the subject of controversy, but the balance of data in most patients suggests that the predominant mechanism is a profound secondary vasoconstriction in response to tubular cell injury. This may represent a teleologically appropriate response to prevent catastrophic losses of fluid that would occur, if the normally high rates of glomerular filtration continued, in the face of reduced tubular reabsorptive capacity. The mechanisms by which the tubular cell injury is communicated to the vasculature, and the mediators of the hemodynamic changes, remain to be established. The differential diagnosis in a patient with ARF, usually involves exclusion of an obstruction to the urinary tract as an initial step. The next step is to differentiate the patients with ATN from those who have renal hypoperfusion in response to events in the systemic circulation, but who otherwise have functionally and structurally intact kidneys, i.e., prerenal ARF. The kidneys of patients with prerenal ARF exhibit the normal renal response to an acute reduction in renal blood flow and glomerular filtration rate (GFR). This consists of avid reabsorption of the filtered salt and H2O, so that a small amount of concentrated and NaCl-poor urine is elaborated. The tubular cell injury in ATN syndromes prevents this response from maximally occurring, so that the urine is isosmotic and relatively rich in NaCl.
 ...
PMID:Acute renal failure. 264 37

Non-narcotic analgesics have acute and chronic effects on the kidney. Until quite recently chronic effects have received much more attention than acute effects. Renal papillary necrosis attributed to prolonged intake of analgesic compounds was first described from Switzerland in the 1950s, and subsequently in many countries including Scandinavia, Australia, Belgium and Canada. Renal papillary necrosis is now accepted as an effect of over-the-counter analgesic compounds and has also been recorded with many individual non-steroidal anti-inflammatory drugs (NSAIDs). Evidence suggests that uroepithelial tumours also occur as a complication of prolonged abuse of analgesic compounds. Clinical evidence associating renal papillary necrosis with compound analgesics and NSAIDs has been backed up by experimental evidence showing that these drugs cause renal papillary necrosis in animals. Acute effects of non-narcotic analgesics have been described mainly in association with aspirin and NSAIDs. In high renin states, including salt-depleted normal subjects, NSAID administration may be associated with an acute decrease in renal function, which is more obvious in patients who have underlying renal disease. Clinical syndromes which occur in association with NSAIDs include oedema, hyperkalaemia and acute renal failure and the acute nephrotic syndrome. Acute renal failure may be associated with acute interstitial nephritis and the nephrotic syndrome or may be due to acute tubular necrosis. Patients who have the nephrotic syndrome show fusion of foot processes of glomerular epithelial cells on electron microscopy as well as acute interstitial nephritis. Patients who suffer these episodes of acute renal function deterioration associated with NSAIDs recover slowly after withdrawal of the drugs, and the recovery may not be complete.
 ...
PMID:Effects of non-narcotic analgesics on the kidney. 355 79

Nephrotoxicity of sodium arsenate was evaluated in dogs to determine the pathophysiologic basis for renal lesions caused by this heavy metal. Examination of biopsy specimens indicated that the low dose of the As salt (0.73 mg/kg of body weight) produced histologic changes consisting of mild degeneration and vacuolation of renal tubular epithelium. Vacuolation involved mainly the ascending thick portion of the nephron. Clinical pathologic changes were not demonstrable at this dosage level according to glomerular filtration rate (creatinine clearance), fractional reabsorption of sodium, potassium, and chloride; plasma osmolar and free water clearance; and urinalysis. The medium dose (7.33 mg/kg) resulted in alterations determined by urinalysis, but did not markedly affect other clinical pathologic measurements. Histopathologic changes were equal to or greater than those seen with the low dose. Tubular necrosis was observed in the cortical portion of the nephron and the ascending thick limb. The high dose (14.66 mg/kg) consistently produced marked changes in all parameters evaluated. Clinical pathologic alterations were compatible with acute tubular necrosis involving all segments of the nephron. Histologically, moderate glomerular sclerosis and severe tubular necrosis were observed. During recovery from the high dose of As, a gradual compensatory healing process was observed that was evident in all clinical pathologic parameters and was confirmed from sequential renal biopsy specimens.
 ...
PMID:Nephrotoxicity of sodium arsenate in dogs. 668 17

This patient had severe dehydration and renal failure presumed to be extrarenal. After volume replacement, the course was not typical for simple extrarenal azotemia or acute tubular necrosis. Tubular handling of salt and water may not provide adequate criteria to evaluate the cause of reduced glomerular filtration rate.
 ...
PMID:Acute renal failure: a diagnostic dilemma. 685 13

Renal nerves contribute to the genesis of at least four disease processes. 1. Excess renal nerve activity contributes significantly to salt and water retention by patients with congestive circulatory failure. 2. Circumstantial evidence suggests that dopamine production may be deficient in a group of patients with idiopathic edema. Aldosterone secretion is high in this group and it has been shown that dopamine exerts a tonic inhibitory effect on angiotensin-stimulated aldosterone secretion. 3. Excess renal nerve activity probably plays a crucial role in the transition from hypotension and pre-renal failure to ischemic acute tubular necrosis. 4. Without doubt hyperactivity of renal nerves causes systemic hypertension in a variety of animal disease models. There is also good reason to believe that this occurs in some forms of human hypertension. The effects of the sympathetic nervous system on renal vascular resistance, renin release, tubular electrolyte reabsorption and aldosterone secretion are discussed in the context of these four diseases.
 ...
PMID:Nervous disorders of renal function. 688 67

There are specific clinical settings in which each of the urine electrolytes may be diagnostically useful. The urine sodium alone is not efficient in differentiating prerenal azotemia from acute tubular necrosis, but if urine sodium is coupled with some measure of the renal concentrating ability, e.g., the urine:plasma creatinine ratio. discrimination between these two conditions is much improved. Usefulness of the urine sodium in other settings (evaluation of hyponatremia, prediction of acute rejection in renal transplant recipients, index of salt balance) is controversial. Urine potassium may be useful in the evaluation of hypokalemia of obscure etiology and, occasionally, in the form of the urinary Na/K ratio, as a guide to diuretic therapy. Urine chloride is assuming importance in the differential diagnosis of metabolic alkalosis, particularly when Bartter's syndrome is a consideration.
 ...
PMID:Measurement of urine electrolytes: clinical significance and methods. 702 36

Prerenal failure is traditionally accompanied by oliguria and represents the normal renal adaptation to retain salt and water and correct the prerenal state. Nonoliguria occurring in the setting of acute renal failure usually represents acute tubular necrosis (ATN) since the kidney has lost its ability to extract salt and water. We report nine cases of patients with acute renal failure occurring in the setting of impaired systemic hemodynamic states and yet who were nonoliguric without strong evidence for ATN. The common defect in these subjects with "polyuric prerenal failure" was a blunted urinary concentrating ability. Polyuria and renal failure occurring despite evidence for impaired systemic hemodynamics may not necessarily be ATN, may still be prerenal, and should be recognizable and promptly reversible if treated appropriately.
 ...
PMID:Polyuric prerenal failure. 738 98


1 2 Next >>