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Pathophysiology

Acute tubular necrosis (ATN) follows a well-defined three-part sequence of


initiation, maintenance, and recovery (see below). The tubule cell damage and
cell death that characterize ATN usually result from an acute ischemic or toxic
event. Most of the pathophysiologic features of ischemic ATN, as described
below, are shared by the nephrotoxic forms.

Initiation phase
Ischemic ATN is often described as a continuum of prerenal azotemia. Indeed,
the causes of the two conditions are the same. Ischemic ATN results when
hypoperfusion overwhelms the kidneys autoregulatory defenses. Under these
conditions, hypoperfusion initiates cell injury that often, but not always, leads to
cell death.

Injury of tubular cells is most prominent in the straight portion of the


proximal tubules and in the thick ascending limb of the loop of Henle,
especially as it dips into the relatively hypoxic medulla. The reduction in the
glomerular filtration rate (GFR) that occurs from ischemic injury is a result not
only of reduced filtration due to hypoperfusion but also of casts and debris
obstructing the tubule lumen, causing back-leak of filtrate through the damaged
epithelium (ie, ineffective filtration).

The earliest changes in the proximal tubular cells are apical blebs and loss of the
brush border membrane followed by a loss of polarity and integrity of the tight
junctions. This loss of epithelial cell barrier can result in the above-mentioned
back-leak of filtrate.

Another change is relocation of Na+/K+ -ATPase pumps and integrins to the apical
membrane. Cell death occurs by both necrosis and apoptosis. Sloughing of live
and dead cells occurs, leading to cast formation and obstruction of the tubular
lumen (see the image below).
Photomicrograph of a renal biopsy specimen shows renal medulla, which is
composed mainly of renal tubules. Features suggesting acute tubular necrosis
are the patchy or diffuse denudation of the renal tubular cells with loss of brush
border (blue arrows); flattening of the renal tubular cells due to tubular dilation
(orange arrows); intratubular cast formation (yellow arrows); and sloughing of
cells, which is responsible for the formation of granular casts (red arrow). Finally,
intratubular obstruction due to the denuded epithelium and cellular debris is
evident (green arrow); note that the denuded tubular epithelial cells clump
together because of rearrangement of intercellular adhesion molecules.
Photomicrograph of a renal biopsy specimen shows renal medulla, which is
composed mainly of renal tubules. Features suggesting acute tubular necrosis
are the patchy or diffuse denudation of the renal tubular cells with loss of brush
border (blue arrows); flattening of the renal tubular cells due to tubular dilation
(orange arrows); intratubular cast formation (yellow arrows); and sloughing of
cells, which is responsible for the formation of granular casts (red arrow). Finally,
intratubular obstruction due to the denuded epithelium and cellular debris is
evident (green arrow); note that the denuded tubular epithelial cells clump
together because of rearrangement of intercellular adhesion molecules.

In addition, ischemia leads to decreased production of vasodilators (ie, nitric


oxide, prostacyclin [prostaglandin I2, or PGI2]) by the tubular epithelial cells,
leading to further vasoconstriction and hypoperfusion. On a cellular level,
ischemia causes depletion of adenosine triphosphate (ATP), an increase in
cytosolic calcium, free radical formation, metabolism of membrane
phospholipids, and abnormalities in cell volume regulation. The decrease or
depletion of ATP leads to many problems with cellular function, not the least of
which is active membrane transport. With ineffective membrane transport, cell
volume and electrolyte regulation are disrupted, leading to cell swelling and
intracellular accumulation of sodium and calcium. Typically, phospholipid
metabolism is altered, and membrane lipids undergo peroxidation. In
addition, free radical formation is increased, producing toxic effects.
Damage inflicted by free radicals apparently is most severe during
reperfusion.

Maintenance phase
The maintenance phase of ATN is characterized by a stabilization of GFR at a very
low level, and it typically lasts 1-2 weeks. Complications (eg, uremic and others; see
Complications) typically develop during this phase.
The mechanisms of injury described above may contribute to continued nephron
dysfunction, but tubuloglomerular feedback also plays a role. Tubuloglomerular
feedback in this setting leads to constriction of afferent arterioles by the macula
densa cells, which detect an increased salt load in the distal tubules.
Recovery phase
The recovery phase of ATN is characterized by regeneration of tubular epithelial
cells. [2] During recovery, an abnormal diuresis sometimes occurs, causing salt and
water loss and volume depletion. The mechanism of the diuresis is not completely
understood, but it may in part be due to the delayed recovery of tubular cell function
in the setting of increased glomerular filtration. In addition, continued use of diuretics
(often administered during initiation and maintenance phases) may also add to the
problem.
Pathophysiologic mechanisms of selected types of nephrotoxicity
Nephrotoxicity can result from various drugs, such as aminoglycosides,
amphotericin, calcineurin inhibitors, foscarnet, ifosfamide, cisplatin, and crystal-
forming drugs. Additionally, conditions such as multiple myeloma and
rhabdomyolysis can cause nephrotoxicity. Acute kidney injury (AKI) can result, and
the pathophysiologic mechanism for renal injury differs among the agents and
conditions.
AKI is observed in about 5% of all hospital admissions and in up to 30% of patients
admitted to the intensive care unit (ICU). ATN is the most common cause of AKI in
the renal category, and the second most common cause of all categories of AKI in
hospitalized patients, with only prerenal azotemia occurring more frequently.

Introduction

Dialysis is a procedure to remove waste products and excess fluid from


the blood when the kidneys stop working properly. It often involves
diverting blood to a machine to be cleaned.

Normally, the kidneys filter the blood, removing harmful waste products and
excess fluid and turning these into urine to be passed out of the body.

Why do I need dialysis?


If your kidneys aren't working properly, for example because you have
advanced chronic kidney disease (kidney failure), the kidneys may not be able to
clean the blood properly. Waste products and fluid can build up to dangerous
levels in your body.

Left untreated, this can cause a number of unpleasant symptoms and eventually
be fatal. Dialysis filters out unwanted substances and fluids from the blood
before this happens.

How long will I need dialysis for?

It depends. In some cases, kidney failure may be a temporary problem and


dialysis can be stopped when your kidneys recover.

But often, someone with kidney failure will need a kidney transplant. It's not
always possible to carry out a kidney transplant straight away, so dialysis may
be needed until a suitable donor kidney becomes available.

If a kidney transplant isn't suitable for you, for example because you're not well
enough to have a major operation, dialysis may be needed for the rest of your
life.

What happens during dialysis

There are two main types of dialysis: haemodialysis and peritoneal dialysis.

Haemodialysis

Haemodialysis is the most common type of dialysis and the one most people are
aware of.

During the procedure, a tube is attached to a needle in your arm. Blood passes
along the tube and into an external machine that filters it, before it's passed
back into the arm along another tube.

This is usually carried out three days a week, with each session lasting around
four hours.

Peritoneal dialysis

Peritoneal dialysis uses the inside lining of your abdomen (the peritoneum) as
the filter, rather than a machine. Like the kidneys, the peritoneum contains
thousands of tiny blood vessels, making it a useful filtering device.
Before treatment starts, an incision is made near your belly button and a thin
tube called a catheter is inserted through the incision and into the space inside
your abdomen (the peritoneal cavity). This is left in place permanently.

Fluid is pumped into the peritoneal cavity through the catheter. As blood passes
through the blood vessels lining the peritoneal cavity, waste products and excess
fluid are drawn out of the blood and into the dialysis fluid. The used fluid is
drained into a bag a few hours later and replaced with fresh fluid.

Changing the fluid usually takes about 30-40 minutes and normally needs to be
repeated around four times a day. If you prefer, this can be done by a
machine overnight while you sleep.

Read more about how dialysis is performed.

Which type of dialysis is best?

In many cases, you'll be able to choose which type of dialysis you want to have.

The two techniques are equally effective for most people, but each has its own
advantages and drawbacks. For example:

haemodialysis means you'll have four treatment-free days a week,


but the treatment sessions last longer and you may need to visit hospital
each time
peritoneal dialysis can be done quite easily at home and can
sometimes be done while you sleep, but it needs to be done every day

If you're able to choose the type of dialysis you prefer, your care team will
discuss the pros and cons of each option with you to help you make a decision.

Read more about the advantages and disadvantages of both types of dialysis.

Side effects of dialysis

Haemodialysis can cause itchy skin and muscle cramps. Peritoneal dialysis can
put you at risk of developing peritonitis (infection of the thin membrane that
surrounds your abdomen).

Both types of dialysis can make you feel exhausted.

Read more about the possible side effects of dialysis

Life on dialysis
Many people on dialysis have a good quality of life. If you're otherwise well, you
should be able to:

continue working or studying


drive
exercise
go swimming
go on holiday

Most people can remain on dialysis for many years, although the treatment can
only partially compensate for the loss of kidney function and having kidneys that
don't work properly can place a significant strain on the body.

Sadly, this means that people can die while on dialysis if they don't have a
kidney transplant, particularly elderly people and those with other health
problems. Someone who starts dialysis in their late 20s can expect to live for up
to 20 years or longer, but adults over 75 may only survive for two to three years.

However, it's important to be aware that survival rates of people on dialysis have
improved over the past decade and are expected to continue improving in the
future.

ANTIIOTIK AKUT KOLES Management includes hospital admission, IV fluids, and analgesics,
such as an NSAID (ketorolac) or opioid. Nothing is given orally, and nasogastric suction is
instituted if vomiting or an ileus is present. Parenteral antibiotics are usually initiated to treat
possible infection, but evidence of benefit is lacking. Empiric coverage, directed at gram-negative
enteric organisms, involves IV regimens such as ceftriaxone 2 g q 24 h plus metronidazole 500
mg q 8 h, piperacillin/tazobactam 4 g q 6 h, or ticarcillin/clavulanate 4 g q 6 h.

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