ATN

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Acute Tubular Necrosis (ATN)

In ATN, the urine cannot be concentrated because the tubule cells are damaged.

It produce urine of similar osmolality to blood (about 300 mOsm/L) called isosthernuria (renal tubular concentrating defect)

Urine osmolality becomes inappropriately low

Dehydration should normally increase urine concentration (osmolality)

In ATN + dehydration, the body inappropriately loses sodium (UNa >20) and water (UOsm < 300)

Healthy person with fluid overload --> low urine osmolality or dilute urine

Healthy person with dehydration -->> high urine osmolality or concentrated urine

Ischemic acute tubular necrosis (ATN) as a result of hypotension from hemorrhage. The clinical course of ATN may be divided into initiation, maintenance (Oliguric), and recovery phases.

  1. The initiation phase of ATN corresponds with the original ischemic or toxic insult and lasts about 36 hours. During this phase, there is only a slight decrease in urine output as renal tubular cell damage begins.

  2. During the maintenance phase, tubular damage is fully established and patients commonly have Oliguria, fluid overload, and electrolyte abnormalities (hyperkalemia, metabolic acidosis). This second phase of ATN usually lasts 1-2 weeks, during which the glomerular filtration rate (GFR) stabilizes at a level well below normal. With a rise in serum creatinine. Light microscopy in this stage shows tubular epithelial necrosis, denudation of the tubular basement membrane, and casts containing degenerating cells and debris.

  3. The recovery phase of ATN is characterized by re-epithelization of tubules. The GFR recovers relatively quickly as the tubules clear of casts and debris, However, the tubular cells recover more gradually, resulting in transient polyuria and loss of electrolytes due to impaired tubular resorption and decreased renal concentrating ability. The majority of patents eventually experience complete restoration of renal function.

Analgesic-induced nephropathy can present with florid nephrotic range proteinuria. This often results from nonsteroidal anti-inflammatory medications which cause a reversible decline in renal blood flow and glomerular filtration rate due to the inhibition of vasodilatory prostaglandin production.