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 urographic nephrogram is an important indicator of underlying functional and structural renal disease. With expansions in use of cross-sectional imaging, the computed tomographic (CT) nephrogram (ie, contrast material enhancement within the renal parenchyma) has assumed a greater role in the evaluation of urinary tract disorders. Both quantitative and qualitative nephrographic abnormalities are well demonstrated by CT, including global or segmental absence or persistence of the nephrogram, slowed temporal progression, striated pattern, and rim pattern. Global absence is nearly always unilateral and is most often seen with blunt abdominal trauma with renal pedicle injury. Segmental absence is attributable to focal renal infarction, most likely due to arterial emboli. Global persistence, which is much more common than segmental persistence, may be unilateral (caused by renal artery stenosis, renal vein thrombosis, or urinary tract obstruction) or bilateral (due to systemic hypotension, intratubular obstruction, or abnormalities in tubular function). Striated nephrograms may be unilateral or bilateral and are caused by ureteric obstruction, acute pyelonephritis, contusion, renal vein thrombosis, tubular obstruction, hypotension, and autosomal recessive polycystic kidney disease. The rim pattern is most often associated with renal infarction and occasionally with acute tubular necrosis and renal vein thrombosis. Careful evaluation of the CT nephrogram is an integral part of the abdominal CT examination.
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PMID:The CT nephrogram: implications for evaluation of urinary tract disease. 750 51

Tubulo-interstitial nephropathy or nephritis is suggested if renal function is deteriorated and urinary findings are slight. In most cases, the daily urinary protein excretion is less than 1 g and macrohematuria is not present. Urinary excretion of N- acetyl-beta-glucosaminidase and beta 2-microglobulin is a good indicator for tubulo-interstitial damage. Acute renal failure is caused either by acute tubulo-interstitial nephritis or acute tubular necrosis. In either case, renal biopsy is essential for diagnosis and to characterize the renal damage. In the interstitium, edema and fibrosis are seen and lymphocytes, plasma cells, polymorpholeukocytes, and/or eosinophils infiltrate. Tubular basement membrane is sometimes disrupted and lymphocytes have infiltrated inside (tubulitis).
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PMID:[Renal biopsy for diagnosis of interstitial nephritis]. 756 31

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

Tubular cells can either unergo hyperplasia or hypertrophy, two totally different growth responses. Hyperplasia with mitogenesis of tubular cells plays a central role in the regeneration of functional tubular epithelium subsequent to acute tubular necrosis. Several growth factors acting in concert are involved in this proliferative response of tubular cells. The molecular mechanisms how mitogenic signals are transduced to the nucleus are relatively well characterized. Complex oscillation patterns of cell cycle-associated proteins like cyclins and various kinases are pivotal for the progression of quiescent tubular cells through mitosis. In contrast to the mitogenic growth response of regenerating tubular cells, cellular hypertrophy is less well understood. Hypertrophic cells are arrested in the G1-phase of the cell cycle and increase their size, protein and RNA content, but do normally not replicate their DNA. Such an enlargement of tubular cells often occurs in more chronic situations of renal damage in which remnant nephrons adapt their function to the increasing need. However, evidence exists that hypertrophic tubules are finally joined into the process of maladaptation of renal function leading to tubular atrophy, interstitial scarring, and progression of renal disease. It appears that transforming growth factor-beta is involved in the hypertrophy of tubular cells. The present review will address more recent progress in understanding the mechanism of tubular growth at a cellular level. A better knowledge of the molecular factors may ultimately lead to therapeutic strategies preventing the progression of renal and speeding up renal recovery after acute renal failure.
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PMID:Cellular mechanisms of tubule hypertrophy and hyperplasia in renal injury. 756 79

Acetaminophen is the most commonly reported drug overdose in the United States. Acute renal failure occurs in less than 2% of all acetaminophen poisonings and 10% of severely poisoned patients. At the therapeutic dosages, acetaminophen can be toxic to the kidneys in patients who are glutathione depleted (chronic alcohol ingestion, starvation, or fasting) or who take drugs that stimulate the P-450 microsomal oxidase enzymes (anticonvulsants). Acute renal failure due to acetaminophen manifests as acute tubular necrosis (ATN). ATN can occur alone or in combination with hepatic necrosis. The azotemia of acetaminophen toxicity is typically reversible, although it may worsen over 7 to 10 days before the recovery of renal function occurs. In severe overdoses, renal failure coincides with hepatic encephalopathy and dialysis may be required. Recognition of acetaminophen nephropathy requires the following: (1) a thorough drug history, including over-the-counter medications such as Tylenol or Nyquil; (2) knowledge of the risk factors that lessen its margin of safety at therapeutic ingestions, i.e., alcoholism; and (3) consideration of acetaminophen in the differential diagnosis of patients who present with combined hepatic dysfunction and ATN.
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PMID:Acute renal failure due to acetaminophen ingestion: a case report and review of the literature. 757 69

This report describes a patient with acute renal failure that resulted from the ingestion of djenkol beans. Features of acute djenkolism include nausea, vomiting, bilateral loin pain, gross hematuria, and oliguria. The blood urea level was 16.2 mmol/L and the serum creatinine was 460 mumol/L. Phase contrast microscopy of the urinary sediment indicated that the hematuria was nonglomerular. Ultrasound of the kidneys showed slightly enlarged kidneys with no features of obstruction. Renal biopsy showed acute tubular necrosis similar to the single animal study reported in the literature. With conservative therapy, which included rehydration with normal saline and alkalinization of the urine with sodium bicarbonate, the acute renal failure resolved. Based on its chemistry, djenkol bean-associated acute renal failure may be analogous to acute uric acid nephropathy.
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PMID:Djenkol bean poisoning (djenkolism): an unusual cause of acute renal failure. 781 May 35

Among a spectrum of renal disorders encountered in patients infected with the human immunodeficiency virus (HIV), the lesion studied most often has been the glomerular disease known as HIV-associated nephropathy. Of the other coincidental renal perturbations reported, the most significant are a heterogenous group encompassing potentially reversible acute renal failure (ARF), primarily acute tubular necrosis. While HIV-associated nephropathy may frequently be seen in asymptomatic HIV-seropositive individuals, acute tubular necrosis almost always is encountered in patients with clinical acquired immunodeficiency syndrome (AIDS). We analyzed our decade's experience in the management of 146 HIV disease patients with ARF (132 AIDS patients and 14 HIV-seropositive patients) and compared it with a contemporaneous group of 306 non-HIV subjects with ARF. All patients evaluated for ARF between January 1984 and December 1993 by the Renal Division at Kings County Hospital Center, Brooklyn, NY, were reviewed. Only those patients with ARF who reached a serum creatinine concentration of 530 mumol/L or higher were included in the analysis. Ninety-one percent of 146 HIV disease patients with ARF were less than 50 years old compared with only 33% of the 306 non-HIV subjects (P < 0.001). Septicemia was directly or indirectly responsible for 75% of patients with ARF in the AIDS group and for 39% in the non-HIV subjects (P < 0.006). Urinary tract obstruction was the cause of ARF in 54 of 306 (17%) non-HIV patients compared with none in the HIV group (P < 0.00001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Outcome of severe acute renal failure in patients with acquired immunodeficiency syndrome. 787 16

Thromboxane synthase (TS) catalyzes the formation of thromboxane (TxA2) in monocytes/macrophages, platelets, and various tissues. TxA2 is likely to play a role in graft dysfunction due to its vasoconstrictive and platelet aggregatory properties. We studied the expression of TS in 7 normal native kidneys, 29 consecutive renal allograft biopsies (performed for rising serum creatinine, n = 23, and delayed graft function, n = 6), and one transplant nephrectomy specimen with severe acute rejection. TS expression was determined by immunocytochemistry using a monoclonal antibody against human TS, Kon-7. Histologic grading of the transplant biopsy specimens was based on the Banff classification. The degree of TS staining was graded in the glomeruli, interstitium, tubules and vessels from 0 to 3+. Of 29 biopsies, 13 had chronic nephropathy (CN), 6 had acute rejection (AR) with chronic nephropathy (AR/CN), 4 had acute rejection (AR), and 6 had acute tubular necrosis (ATN). TS staining of native kidneys showed sporadic interstitial cells. The biopsy and transplant nephrectomy specimens showed significant staining, predominantly in the glomeruli and interstitium. Positively staining cells appeared to be of macrophage/monocyte lineage by morphology. The mean glomerular staining grade was significantly increased in specimens with AR (2.3 +/- 0.9) and the mean interstitial staining was increased in specimens with AR/CN (2.2 +/- 0.9). Follow-up renal function 6 months post-biopsy showed that patients with higher TS staining grades had a faster decline in graft function. In conclusion, TS expression is increased in patients with acute rejection with or without chronic nephropathy and is associated with more rapid deterioration in function.
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PMID:Thromboxane synthase expression in renal transplant patients with rejection. 787 51

Familiarity with renal issues that can challenge the care of patients with human immunodeficiency virus (HIV) should expedite diagnosis and therapeutic interventions. Among the most common problems are electrolyte and acid-base imbalances from many opportunistic infections or their treatments, including hyponatremia, hyperkalemia, hypokalemia, and hypo- and hypercalcemia. Acid-base disturbances, simple or mixed, can be due to underlying sepsis, opportunistic infections, or the therapy thereof. A recent report of seven patients with HIV with type B lactic acidosis failed to identify a satisfactory etiology. Elevations in creatinine or diminishing urine output should alert the physician to the possibilities of prerenal azotemia or acute tubular necrosis, which can result from progression of prerenal azotemia or can occur secondary to administered nephrotoxins, such as certain antibiotics and radiocontrast agents. Agents associated with nephrotoxicity include aminoglycosides, antifungal, antiviral, and radiocontrast agents, and nonsteroidal anti-inflammatory pain medications. Although prerenal azotemia and acute tubular necrosis are the most frequent causes of acute renal failure, the differential diagnosis should include acute interstitial nephritis, obstructive nephropathy, and glomerulopathies such as hemolytic uremic syndrome, thrombotic thrombocytopenia purpura, the newly described IgA nephropathy, and, in certain populations, HIV nephropathy.
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PMID:The spectrum of kidney diseases in patients with human immunodeficiency virus infection. 792 95

Magnesium is an essential cation, involved in many enzymatic reactions, as a cofactor to adenosine triphosphatases. It is critical in energy-requiring metabolic processes, as well as protein synthesis and anaerobic phosphorylation. Serum Mg concentration is maintained within a narrow range by the kidney and small intestine since under conditions of Mg deprivation both organs increase their fractional absorption of Mg. If Mg depletion continues, the bone store contributes by exchanging part of its content with extracellular fluid (ECF). The serum Mg can be normal in the presence of intracellular Mg depletion, and the occurrence of a low level usually indicates significant Mg deficiency. Hypomagnesemia is frequently encountered in hospitalized patients and is seen most often in patients admitted to intensive care units. The detection of Mg deficiency can be increased by measuring Mg concentration in the urine or using the parenteral Mg load test. Hypomagnesemia may arise from various disorders of the gastrointestinal tract, conditions affecting Mg renal handling, or cellular redistribution of Mg. The gastrointestinal causes include the following: protein-calorie malnutrition, the intravenous administration of Mg-free fluids and total parenteral nutrition, chronic watery diarrhea and steatorrhea, short bowel syndrome, bowel fistula, continuous nasogastric suctioning, and, rarely, primary familial Mg malabsorption. The renal causes include Bartter's and Gitelman's syndrome, post obstructive diuresis, post acute tubular necrosis, renal transplantation, and interstitial nephropathy. Many therapeutic agents cause renal Mg wasting and subsequent deficiency. These include loop and thiazide diuretics, aminoglycosides, cisplatin, pentamidine, and foscarnet. Magnesium deficiency is seen frequently in alcoholics and diabetic patients, in whom a combination of factors contributes to its pathogenesis. Hypomagnesemia is known to produce a wide variety of clinical presentations, including neuromuscular irritability, cardiac arrhythmias, and increased sensitivity to digoxin. Refractory hypokalemia and hypocalcemia can be caused by concomitant hypomagnesemia and can be corrected with Mg therapy. The dose and route of administration of Mg in the treatment of hypomagnesemia is dictated by the clinical presentation, the degree of Mg deficiency, and the renal function.
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PMID:Magnesium deficiency: pathophysiologic and clinical overview. 777 97


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