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)

A 9-year-old castrated male domestic shorthair cat with dysuria, anorexia, vomiting, and lethargy was admitted to the veterinary teaching hospital. A large, firm mass was palpable in the ventral cervical region. Hypercalcemia, azotemia, and nonregenerative anemia were evident on serum biochemical analysis and CBC, and multiple uroliths were detected by abdominal radiography. At necropsy, light microscopy of the ventral cervical mass revealed a parathyroid adenocarcinoma. Light microscopy of sections of the kidneys revealed multifocal, chronic, lymphocytic/plasmacytic, tubulointerstitial nephritis, as well as moderate multifocal acute tubular necrosis. On quantitative analysis, the uroliths were composed of calcium oxalate. Determination of serum calcium concentration is indicated in cats with calcium oxalate urolithiasis to aid in detection of primary hyperparathyroidism.
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PMID:Calcium oxalate urolithiasis in a cat with a functional parathyroid adenocarcinoma. 775 34

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

The present report describes a rare case of hematophagic histiocytosis associated with acute renal failure. A 32-year-old woman was referred to us from a local hospital because of progressive deterioration of renal function, jaundice and a bleeding tendency. The physical findings at admission revealed hyperemic conjunctivae, gingival bleeding, hepatomegaly, and generalized myalgia. Laboratory data indicated a decrease in platelet count, azotemia and hyperbilirubinemia. Marked elevation of serum triglycerides and ferritin was also noted. Histiocyte proliferation with phagocytosis of erythrocytes and platelets was observed in a bone marrow aspirate. A renal biopsy specimen exhibited lesions generally observed in acute tubular necrosis: degeneration and necrosis of tubular epithelial cells; round cell infiltration and edema in the interstitium; and unremarkable glomeruli. The serum titer to coxsackievirus B1 rose from < 4x at admission to 16x after recovery from the illness, suggesting that this virus may have been the causal organism of the accompanying infection. The patient's symptoms improved rapidly with supportive therapy, and complete restoration of renal function was achieved in 20 days. The morphological characteristics of the bone marrow aspirate and the clinical course were compatible with hematophagic histiocytosis.
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PMID:A case of hematophagic histiocytosis associated with acute renal failure. 833 3

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55

During the first month after bone marrow transplantation, approximately 15% of patients develop acute renal failure (ARF). This usually occurs in the setting of hepatic veno-occlusive disease (VOD). Prior clinical data have suggested that this form of ARF has a hemodynamic basis, analogous to the hepatorenal syndrome (HRS). If so, then proximal tubular injury would not be expected. To directly test this hypothesis, enzymuria (N-acetyl-beta-D-glucosaminidase [NAG]) was quantitated in the following groups of patients within the first 35 days after BMT: (1) VOD+ARF (serum creatinine level > 1.5 mg/dL; N = 10); (2) VOD with relatively normal renal function (serum creatinine level < 1.5 mg/dL; N = 11); and (3) patients without hepatic or renal complications (BMT controls; N = 12). For comparison, NAG was also quantitated in the following groups of non-BMT patients: (1) toxic/ischemic acute tubular necrosis (ATN) (N = 10); (2) jaundice without azotemia (N = 5); and (3) HRS (N = 6). Urine samples from eight healthy subjects established normal NAG concentrations (2.5 +/- 0.5 microU/mg urinary creatinine; mean +/- SE). All non-BMT patients with ATN had markedly elevated NAG levels (61 +/- 12; P < 0.001), validating the test as a marker of tubular damage. NAG concentrations were significantly elevated in all of the control BMT patients (24 +/- 3; P < 0.01), and the presence of VOD was associated with further striking increments (approximately 50 times normal). However, the degree of enzymuria was virtually identical for VOD patients with (125 +/- 27) and without (122 +/- 17) ARF. Jaundice in a non-BMT setting was associated with only mild NAG elevations (11 +/- 2). However, striking enzymuria was noted in all HRS patients (61 +/- 20), equaling the levels seen with ATN. The following conclusions were derived: (1) subclinical tubular injury, as defined by enzymuria, appears to be ubiquitous after BMT; (2) VOD dramatically increases the extent of enzymuria; (3) the degree of enzymuria in VOD patients is not correlated with renal dysfunction, implying that the associated ARF has a large hemodynamic component; and (4) HRS and ATN manifest comparable degrees of enzymuria, suggesting that substantial tubular damage exists in both of these forms of ARF.
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PMID:Marked enzymuria after bone marrow transplantation: a correlate of veno-occlusive disease-induced "hepatorenal syndrome". 874 94

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

Boutonneuse spotted fever is a summer and late spring infection caused by Rickettsia Conorii mainly in Middle East countries adjacent to the mediterranean coast (1). Malignant forms have been described in debilitated patients associated with prerenal azotemia, acute tubular necrosis or renal vasculitis (2, 3). We report for the first time to our knowledge, the association of an extracapillary glomerulonephritis with a Boutonneuse spotted fever. This observation suggest that Rickettsia Conorii, as other bacteria, could participate to the development of glomerulonephritis.
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PMID:[Occurrence of extracapillary glomerulonephritis during Mediterranean boutonneuse fever]. 897 53

We report a 66-year-old man with minimal change nephrotic syndrome (MCNS) that was associated with reversible acute renal failure (ARF) caused by acute tubular necrosis (ATN). He had a subacute onset of proteinuria and progressive azotemia. Hemodialysis (HD) was required to improved azotemia. Renal biopsy revealed minor glomerular abnormalities associated with ATN. While continuing HD, steroid therapy was started, which subsequently allowed the patient to be weaned from HD and relieved from NS. In this patient, histological examination and clinical course suggested that ATN was probably induced by hypovolemia due to MCNS.
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PMID:Acute renal failure associated with minimal change nephrotic syndrome in an elderly adult. 930 42

Acute renal failure (ARF) is a life-threatening disease that often causes multiple organ dysfunction. The accurate and rapid diagnosis of the cause of ARF is particularly important for selecting the appropriate therapy. Ultrasound Doppler is a noninvasive diagnostic method that has recently been introduced to clinical nephrology. We report the diagnostic value of Doppler ultrasound in differentiating acute tubular necrosis (ATN) from prerenal azotemia by comparing this study with the fractional excretion of sodium (FENa), renal failure index (RFI), and urinary/serum creatinine (Cr) ratio. Doppler ultrasound was able to differentiate prerenal azotemia from ATN, equivalent to FENa, RFI, and the urinary/serum Cr ratio. Doppler ultrasound does not require blood or urine samples and can be performed at the bedside. Of note, Doppler is unaffected by changes in Na or Cr in urine or serum after diuretics or hemodialysis. Furthermore, one can predict recovery from ATN by Doppler findings. Thus, we consider Doppler ultrasound an effective diagnostic tool in ARF.
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PMID:Differential diagnosis of prerenal azotemia from acute tubular necrosis and prediction of recovery by Doppler ultrasound. 1073 94

Human immunodeficiency virus-associated nephropathy (HIVAN) is a clinicopathological entity characterised by proteinuria, rapidly developing azotemia and histologically by collapsig variant of focal and segmental glomerulosclerosis with acute tubular necrosis and mild interstitial inflammation. Untreated, it may result in end stage renal disease (ESRD) in as little as four months. The incidence of HIVAN continues to increase and is the single most common cause of chronic renal disease in HIV-1 seropositive patients. It affects predominantly black individuals. Exact pathogenesis is still not clear but a great deal of progress has been made in the recent past by studies on transgenic mouse model, renal cell cultures and from study of human biopsy material. Current considerations revolve around the role of HIV or protein in renal epithelium and the effects of cytokines, including transforming growth factor-beta and basic fibroblast growth factor on renal structures. Different modalities of treatment with corticosteroids, zidovudine or angiotensin converting enzyme inhibitors have been tried with modest success.
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PMID:Human immunodeficiency virus-associated nephropathy. 1183 70


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