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 ?
An important side effect of cidofovir is nephrotoxicity, which also can manifest as acute tubular necrosis.
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.
The histological profile of this study indicates that rats exposed to Pb presents a minimal tubular necrosis and tubular microcalcification, perhaps it is the beginning of nephrolithiasis, which is a disease characterized by the presence of stones in the excretory channel of kidneys.
Two cases (both falciparum oliguric renal failure) had isolated MPGN while it was seen along with changes of acute tubular necrosis (ATN) in 10 cases (falciparum 9 out of those 6 were oliguric, 3 nonoliguric and one case of nonoliguric vivax malaria).
One of the hallmarks of acute tubular necrosis is the loss of ability to concentrate urine.
In animal studies, rhAPC has been also shown to reduce liver and kidney injury by reducing renal endothelial and hepatocyte apoptosis as well as hepatic and renal tubular necrosis following reperfusion (4).
Tubular necrosis, interstitial nephritis or thrombotic angiopathy are common causes of parenchymal drug-induced renal injury.
In contrast, kidney grafts in untreated recipients demonstrated severe rejection after 35 days, characterized by cellular infiltration, interstitial hemorrhage and edema, and glomerular and tubular necrosis, as well as high antidonor antibody titers.
It is thought that one mechanism through which they cause acute tubular necrosis (and Fanconi's syndrome) is tubular mitochondrial toxicity.
Biopsies with acute injury or active proliferative changes (such as proliferative glomerulonephritis, interstitial nephritis, acute tubular necrosis, thrombotic microangiopathies, or vasculitis) were not included.
Unfortunately, the sonographic appearance of many diffuse renal parenchymal abnormalities is nonspecific, including acute tubular necrosis (ATN), acute or chronic rejection, and toxicity associated with immunosuppressive calcineurin inhibitors (cyclosporine and tacrolimus).
2) HELLP syndrome (haemolysis, elevated liver enzymes and low platelets) is a variant of severe pre-eclampsia which often complicates with renal failure, most of the time because of acute tubular necrosis (ATN) but occasionally because of RCN, through a thrombotic micro-angiopathic process.