Acute Renal Failure (ARF), now referred to as acute
kidney injury (AKI) is defined as the abrupt and rapid breakdown of renal
filtration function. It primarily occurs when waste products and minerals of
the urine start accumulating in the blood. ARF is usually marked by an increase
in the serum creatinine concentration. If untreated, effects can be drastic,
resulting in permanent kidney damage, seizures, coma or even death. Apoptosis
or programmed cell death (cell suicide), is a process in which cell death occurs
in response to a variety of stimulus in a controlled regulated manner.
Acute
Renal Failure
Acute renal failure is the sudden loss in renal
filtration resulting in accumulation of uremic toxins in the blood. This
condition develops when the kidneys are not able to filter (or excrete)
balanced amounts of nitrogenous wastes in the urine. Characteristic symptoms of
ARF are vomiting, anorexia, nausea and edema. Diagnosis is made on the renal
function tests including serum creatinine. Treatment of the disease is mainly
focused on the cause of the condition and may also include management of fluid
and electrolyte as well as dialysis (in severe conditions).
Several disorders develop in the course of the
disease. In approximately all cases, levels of urea and creatinine in the blood
increase, resulting in disorders related to fluid and electrolyte imbalance.
Serious disorders that develop along with acute renal failure include
hyperkalemia and pulmonary edema.
Apoptosis
Apoptosis is a part of any normal process of growth
and development in multi-celled organisms. Also known as cell suicide,
apoptosis includes controlled cell death triggered by a variety of stimulus.
This differentiates apoptosis from another type of cell death called necrosis
(in which cell death is not regulated, leading to other potentially serious
health problems). The stimulus can be in the form of signals ordering the cells
to undergo apoptosis or intrinsic signals that are a result of cellular stress
(due to radiation or chemical exposure or viral infection). Retarded growth or
oxidative stress can also trigger cellular stress. Also, intrinsic signals that
cause apoptosis normally involve mitochondria.
Apoptosis
in Acute Renal Failure
The renal tubular cells already injured as a result
of ischemic and toxic acute renal failure, die by apoptosis. Apoptosis includes
increased cell shrinkage along with breaking up and condensation of the nuclear
chromatin. Fragmentation of the apoptotic cells leads to the formation of
apoptotic bodies (plasma membrane-bound vesicles). These bodies are quickly
phagocytosed by adjoining epithelial cells and macrophages.
Post-acute renal failure, apoptosis of the renal
tubular cells adds to the tubular cell loss and dysfunction. Medical
interventions that protect or enhance tubular cell apoptosis also play an
active role in reducing renal dysfunction and promoting recovery after ARF.
Potential
causes of Apoptosis in Acute renal failure
* Lack of Renal growth factors
* Tumor necrosis
* Oxidant stress injury
* Loss of cell-cell and cell- matrix interactions
* Ischemia, anoxia, hypoxia
* Lack of survival factors
* Cytotoxic factors
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