tubular necrosis


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tubular necrosis

Etymology: L, tubulus, little tube; Gk, nekros, dead, osis, condition
the death of cells in the small tubules of the kidneys as a result of disease or injury.

Acute Tubular Necrosis

A condition characterised by acute renal failure with oliguria, which returns to normal in days to weeks, with the caveat that 50% of patients die.
Aetiology Ischaemia—medical, obstetric, surgical, including transplantation (cold ischaemia); toxicity—drugs (aminoglycosides, amphotericin B, cyclosporine), chemicals (radiocontrast), pigments (myoglobin—crush syndrome, haemoglobinuria), sepsis, shock. Predisposing conditions Diabetes, liver disease, immunosuppression by toxic agents.
Management It is managed in transplanted kidneys in an expectant fashion as renal function may resume spontaneously in 2 to 4 weeks.

tubular necrosis

See Acute tubular necrosis.

tubular

1. pertaining to renal tubules.
2. pertaining to fallopian tube.

tubular backleak
leakage of tubular fluid into the interstitium of the kidney is one of the factors in the pathogenesis of acute renal failure.
tubular maxima
the concentrations of solutes at which the renal tubules are working at full capacity and further increases in concentration will not increase the function. Called also Tm.
tubular necrosis
acute necrosis of the tubular epithelium caused usually by ischemia or exposure to a nephrotoxin; in most cases the patient succumbs to uremia in a few days. See also nephrosis.
tubular proteinuria
failure of the tubules to resorb small molecule proteins excreted by the glomerulus.
tubular reabsorption
reabsorption of solutes from the glomerular filtrate by the tubules, the conservation of protein, glucose and bicarbonate, and the conservation of the water that accompanies them.
tubular transport
refers to all processes which occur with renal tubular fluid during its transport from glomerular space to renal pelvis.
tubular transport maximum
when the tubular transport maximum for a renal tubular solute is exceeded the solute appears in the urine.
References in periodicals archive ?
Table 2: Showing comparison of percentage of tubular necrosis among groups.
Table 1: The Main Histopathological Changes of Lungs and Kidneys Organs Histopathological Changes Lungs Alveolar oedema and congestion Bronchiolar congestion and haemorrhage Interstitial oedema, haemorrhage and congestion, inflammation Kidneys Tubular necrosis and haemorrhage, Glomerular haemorrhage and oedema, Interstitial necrosis, haemorrhage and congestion.
Similarly, in NLRP3 KO mice following I/R injury, an increased protection from lethal ischemic injury [56] and a reduced tubular necrosis and apoptosis, with consequent repopulation of the tubular epithelium, were observed after the reperfusion phase [84].
Renal Recovery from Acute Tubular Necrosis Requiring Renal Replacement Therapy: A Prospective Study in Critically Ill Patients.
Paraphenylene diamine induced acute tubular necrosis following hair dye ingestion.
Pathophysiology of drug-induced nephropathy Level of the nephron Action Drugs Preglomerular Afferent arteriolar Cyclosporine (afferent arteriole) constriction Glomerulus Decreased GFR NSAIDs (prostaglandins) Gold, NSAIDs Glomerulonephritis Penicillamine, cisplatin Proximal tubules Acute tubular necrosis Aminoglycosides, radiocontrast dyes Distal tubules Renal tubular ACE inhibitors, acidosis type 4 cyclosporine Tubules and ducts Crystalluria Acyclovir, sulphonamide Interstitium Interstitial nephritis Penicillin, allopurinol Renal papilla Papillary necrosis NSAIDs, analgesics Table 2.
Tubular necrosis was observed in only one mouse (12%) kidney and that too at the maximum dose i.
The renal tubules showed moderate separation hypoplasia of hemopoietic tissue as well as mild glomerular and tubular necrosis (Fig 3).
Of the 4 variants, the tubulopathy associated with the interstitial inflammatory reaction (acute tubular interstitial nephritis variant) was the most prevalent (n = 28 or 49% of all cases with proximal tubulopathy; Table 2), followed by the proximal tubulopathy without cytoplasmic inclusions (acute tubular necrosis variant) (n = 22, 39% of all cases; Table 1), proximal tubulopathy with cytoplasmic inclusions in proximal tubular cells (4 cases; approximately 8%; Table 3), and 3 cases (5% of all cases) with the "lysosomal indigestion/constipation" variant (Table 4).
Pb group: The photograph indicates a slight tubular necrosis and tubular microcalcification (beginning of lithiasis).
Histologic examination of kidneys from sham-operated animals showed no evidence of tubular necrosis (Fig.