Acute tubular necrosis (ATN) is a condition resulting from tubular cell apoptosis contributing to renal failure (1-3). It can result due to insult from extensive injury such as acute blood loss or septic shock, a specific renal disease such as glomerulonephritis, nephrotoxic drugs or bacterial products, or hypoxia (1-3).
ATN is identified via a rising serum urea creatinine and can be classified as pre-renal, renal or post-renal (1). If identified early, corrective action can stop damage and possible hyperkalemia (1).
Managing ATN includes caring for patient by replacing extra cellular fluid when necessary, controlling an underlying infection that may be cause, monitoring body fluid volume closely and via dialysis (1). Recovery involves three phases: initial oliguric phase (impairment), diuretic phase (high-urine output) and recovery phase (return of complete renal function) (1).
Glomerulonephritis is an inflammation of the glomeruli, which causes progressive renal damage that can lead to ATN and renal failure (4-6). The disease is mainly caused by infection such as streptococcal infection (7;8). In post-streptococcal glomerulonephritis, symptoms can include sudden hypertension, proteinuria, edema and hematuria (9). The inflammatory response causing the damage to the kidneys is thought to be related to hypersensitive immune response (9). Maintenance generally can include treatment of underlying disease, balancing electrolytes and fluids, and possible peritoneal dialysis (10).
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