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)

Proteinuria was studied in ten renal allograft recipients; it was defined as: (a) glomerular--characterized by predominant albumin excretion; (b) tubular--significant excretion of both albumin and low molecular weight (LMW) proteins; and (c) glomerulo-tubular or mixed type, a combination of the two. LMW protein and albumin were quantitated by polyacrylamide gel electrophoresis with sodium dodecyl sulfate. In the immediate posttransplant period, LMW protein and albumin excretion, expressed as a percentage of creatinine clearance, were high, revealing a mixed pattern, and excretion of both protein classes was higher than during both acute tubular necrosis and acute rejection crisis. Tubular proteinuria was observed in acute tubular necrosis; a glomerulo-tubular or mixed pattern of protein excretion in acute rejection crises.
Nephron 1977
PMID:Proteinuria following renal transplantation. 32 83

A 42-year-old male was hemodialyzed for 2 years with excellent control of calcium-phosphate metabolism. He received a cadaveric renal transplant but experienced a prolonged episode of acute tubular necrosis during which he could not tolerate phosphate-binding antacids. His calcium X phosphate product became markedly elevated for 20 days. Following a brief period of function, the homograft was removed on the 45th post-transplant day after severe rejection and subsequent infection. Chest X-ray was normal. Six days after graft nephrectomy, he became acutely dyspneic and markedly hypoxemic. Diffuse, flocculent pulmonary infiltrates appeared on the chest film. The patient expired 1 day later. At postmortem examination, there was severe, diffuse pulmonary alveolar calcification demonstrated by chemical and histologic examination. Although unlikely, the prolonged post-transplant period characterized by elevated calcium X phosphate product may have played a pathogenetic role. Calciphylaxis may have occurred, with hyperparathyroidism as the sensitizing agent and any of several drugs acting as challenger.
Nephron 1977
PMID:Sudden fatal pulmonary calcification following renal transplantation. 33 63

The Comrades Marathon is a gruelling test of man's stamina and only trained athletes participate. It is surprising that of over 2,000 contestants each year on a 90-km (56.25-mile) course, severe cardiac and renal damage does not occur more often. We are able, however, to report 10 cases over 9 years when renal damage did occur. 3 cases required haemodialysis; 1 had peritoneal dialysis; 2 patients had renal biopsies. Possible idiosyncratic factors are discussed as is the pathogenesis of acute tubular necrosis.
Nephron 1979
PMID:Acute renal failure in marathon runners. 50 65

Many patients with chronic pancreatitis (CP), even in the absence of intrinsic renal disease, are found to have abnormal urine, with persistent proteinuria, cylindruria, microhematuria and leukocyturia. The kidneys of 12 necropsy cases with CP showed mild to moderate arterial and arteriolar nephrosclerosis and no other significant changes. Renal biopsies were performed in 10 patients with CP without evidence of systemic disease or intrinsic renal disease, but with persistent urinary abnormalities. By light microscopy, mild arterial and arteriolar nephrosclerosis was present in 5 instances. In 1 patient, evidence of the reparative phase of acute tubular necrosis was noted. In 5 biopsies, electron microscopy revealed minimal to mild increase in mesangial matrix. Mild thickening of the glomerular basement membrane (GBM) was found in three instances but there was no clear-cut evidence of diabetic glomerulosclerosis. The presence of subendothelial electron-lucent material in 3 cases suggests the possibility of previous subclinical episodes of intravascular coagulation. The most consistent finding was the presence of lipid material in the cytoplasm of glomerular and tubular cells. The renal lesions associated with CP are mild, nonspecific and nonprogressive. Various pathogenetic factors can be invoked to account for their presence and for the urinary abnormalities found in patients with CP.
Nephron 1978
PMID:Renal lesions in chronic pancreatitis. 74 Jan 5

Renal tubular function was evaluated in vitro by kidney slice uptakes of p-aminohippurate (PAH) and tetraethylammonium (TEA) at 24 and 48 h in water-drinking rats and at 24 h in chronic saline-loaded rats after induction of acute tubular necrosis (ATN) by HgCl2 and glycerol injection. Significant correlations between decrease tubular uptake of PAH and TEA and elevated serum creatinine levels were noted in both models of ATN in water- and saline-drinking rats. However, with the same degree of impairment of PAH and TEA uptakes the creatinine was significantly lower in saline-loaded rats than in water-drinking rats in both forms of ATN. The correlation between impaired tubular function and elevated creatinine suggests that tubular damage and glomerular filtration reduction might be pathophysiologically related in ATN.
Nephron 1976
PMID:The role of tubular necrosis in the pathophysiology of acute renal failure. 94 Jun 26

The raw carp bile has both nephrotoxic and hepatotoxic effects which are not well known. Recently, we studied 13 patients who had toxic acute renal failure and toxic hepatitis after ingestion of raw bile of carp in 3, grass carp in 8 and silver carp in 2 cases. The purpose of this report is to alert physicians to this very rare cause of toxic acute renal failure and hepatitis. All patients presented initially with gastrointestinal upset after eating. These symptoms were followed by oliguria in 7 patients (54%), hematuria was noted in 10 (77%) and jaundice in 8 patients (62%). Elevation of blood urea nitrogen, creatinine and transaminases lasted for about 3 weeks. The severity of the symptoms depended on the amount of bile ingested. All the patients recovered with conservative therapy and hemodialysis. Biopsy of the kidney revealed findings compatible with acute tubular necrosis similar to that produced by other nephrotoxins. Biopsy of the liver revealed findings consistent with acute toxic hepatitis. Both suggest toxic effects of carp bile as a cause of toxic acute renal failure and hepatitis.
Nephron 1990
PMID:Toxic acute renal failure and hepatitis after ingestion of raw carp bile. 224 75

We have performed a retrospective review of the incidence and etiologies of acute renal failure (ARF) in 105 adult patients receiving liver transplants. The prevalence of chronic renal failure was also determined. ARF occurred in 94.2% of these patients. Acute tubular necrosis was the leading cause of ARF and was associated with the highest mortality. Factors associated with increased mortality included: (1) peak serum creatinine greater than 3 mg/dl, (2) multiple liver transplants and (3) the need for dialysis. Pretransplant renal failure did not increase mortality. Chronic renal failure developed in 83% of patients at latest follow-up (mean: 30.5 +/- 7.9 months).
Nephron 1990
PMID:Acute and chronic renal failure in liver transplantation. 236 25

Recently we reported that maintaining rats on restricted dietary protein regimens prior to renal ischemia will significantly improve postischemic survival rates. This effect required a week or more of maintenance on a restricted protein diet prior to the renal insult and appeared to be independent of the postischemic dietary protein regimen. The present study was designed to evaluate the role of systemic toxicity in this protection. Adult male Sprague-Dawley rats were pair-fed by weight on restricted or high isocaloric protein diets for 8-10 days prior to 45 min of renal ischemia induced by renal pedicle clamping. When placed on a normal dietary protein regimen immediately following ischemia, the rats preconditioned to restricted dietary protein exhibited significantly less acidosis, less hyperkalemia, lower blood urea nitrogen values, and improved survival rates compared with rats preconditioned on a high dietary protein regimen. In order to separate the possible effects of prior dietary protein regimen on acute tubular necrosis suffered during renal ischemia from its effects on the uremic response, bilateral nephrectomies were performed on rats preconditioned for 14 days to low, normal, and high dietary protein regimens. Although all of the rats were placed on the same dietary protein regimen immediately following bilateral nephrectomy, those that had previously been on a lower dietary protein regimen exhibited a significantly reduced uremic response and lived longer. These findings indicate that dietary protein regimen prior to renal ischemia is a risk factor which can have a significant lingering effect on the severity of postischemic systemic toxicity.
Nephron 1990
PMID:Dietary protein regimen prior to renal ischemia significantly affects the postischemic uremic response. 237 Sep 27

Three healthy adult males developed acute renal failure following cocaine abuse. Muscle pain, tenderness, elevated levels of serum muscle enzymes, heme-positive urine and the presence of pigmented granular casts in urine all indicated occurrence of rhabdomyolysis. One of them developed acute compartmental syndrome of the left leg and required emergency fasciotomy. The course of renal failure and fast recovery were suggestive of acute tubular necrosis in all 3 patients. A possible role of cocaine in the aggravation of renal and/or muscle ischemia has been speculated.
Nephron 1989
PMID:Acute renal failure following cocaine abuse. 231 44

The effects of intramuscular glycerol on ischemic acute renal failure was investigated in dogs. Anesthetized dogs received a bilateral 120-min renal artery obstruction (RAO) alone, RAO plus 5 ml/kg of 50% glycerol or RAO plus 5 ml/kg of 75% glycerol. Control groups received the glycerol injection, but not RAO. Renal histopathology was minimal in dogs receiving glycerol alone. In RAO dogs, those receiving 50% glycerol showed diffuse acute tubular necrosis (ATN), while those receiving 75% glycerol had severe ATN with extreme mortality. Changes in serum creatinine, creatinine clearance, and fractional excretion of sodium were consistent with the histopathologic changes. We conclude that myoglobinuria, of a degree insufficient to cause renal failure itself, can interact with renal ischemia to significantly exacerbate the renal damage produced.
Nephron 1989
PMID:Myoglobinuria exacerbates ischemic renal damage in the dog. 279 46


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